8.11: Why It Matters- Cell Division - Biology

8.11: Why It Matters- Cell Division - Biology

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Why learn about the various stages of cell division?

Cell division is key to life: from the moment we are first conceived, we are continually changing and growing. Cell division takes occurs by a strict cycle, with multiple stages and checkpoints to ensure things don’t go awry.

Perhaps most importantly, without cell division, no species would be able to reproduce—life would simply end (or would have ended a long time ago). Every human, as well as every sexually reproducing organism, begins life as a fertilized egg (embryo) or zygote. Trillions of cell divisions subsequently occur in a controlled manner to produce a complex, multicellular human. In other words, that original single cell is the ancestor of every other cell in the body. Single-celled organisms use cell division as their method of reproduction.

New insight into brain development disorder

IMAGE: During cell division, DNA must be copied and distributed between daughter cells. A cellular structure called the mitotic spindle pulls apart the DNA-containing structures, the chromosomes. The photo shows a. view more

Credit: Cell Biology Utrecht University

"Biological processes are determined by molecules in our cells. We can only understand the factors that determine health and disease and find medicines to control these factors by zooming into this molecular world", explains research leader Prof. Anna Akhmanova.

The researchers began their studies by focusing on the protein ASPM. "We knew that the genetic form of microcephaly is most often caused by defects in this protein. But a surprising discovery was that ASPM appears to work closely together with another protein, called katanin", tells Akhmanova.

Essential for healthy development

It appears that precisely this collaboration is important for cell division, and therefore for the normal development of brain cells. "The interaction between ASPM and katanin is required for the proper balance between cell division and their specialisation into nerve cells. When the balance sways too much in one direction or the other, too few brain cells are produced", Akhmanova adds.

For developing brain cells, this balance is especially crucial, because once they become nerve cells, they cannot divide. If new cells develop into nerve cells too quickly, not enough cells are formed, and the brain remains small.

During cell division, DNA must be copied and distributed between daughter cells. A cellular structure called the mitotic spindle pulls apart the DNA-containing structures, the chromosomes. The photo shows a microscopic image of DNA (blue) in a spindle. The protein ASPM appears to play a key role in this process, as it is located at the 'poles' (yellow) in the spindle.

The study shows how ASPM does its work at the molecular level, and why it is so important. In cooperation with the protein katanin, ASPM is responsible for the regulation of the organisation and positioning of the spindle. "It is this positioning that helps to determine how the daughter cells develop: will they become copies of new cells, or will they develop into nerve cells", Akhmanova explains.

The fact that a deviation in the protein ASPM leads to microcephaly can now be better understood at the molecular level. However, the results of this study provide a much broader insight, which may make it possible to explain or find other causes of the disorder.

Akhmanova's fascination for brain development is not limited to disease, however. "Even apes, our closest relatives, have much less brain capacity than we do. Our brain makes us what we are. This means the development of our brain is evolutionarily very special."

  • Website Cell Biology
  • This research is an example of Science for Life, a theme within Utrecht University's interdisciplinary research programme Life Sciences.

"Microtubule minus-end regulation at spindle poles by an ASPM-katanin complex"
Kai Jiang*, Lenka Rezabkova*, Shasha Hua*, Qingyang Liu*, Guido Capitani, A. F. Maarten Altelaar*, Albert J. R. Heck*, Richard A. Kammerer, Michel O. Steinmetz and Anna Akhmanova*
* Utrecht University
Nature Cell Biology 24 April 2017, http://dx. doi. org/ 10. 1038/ ncb3511

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

Plant Growth and Development Class 11 Important Questions Very Short Answer Type

Question 1.
What is known as growth? Describe in brief different phases of growth.
According to Miller, ‘Growth is the permanent change in the size, weight and volume in the cell and organs of the body’.
Phases of growth :
1. Ceil division phase: In this phase one cell divides to form many cells.
2. Cell enlargement phase: The newly formed cell increases in size and attains maturity. Large vacuoles develop within the cell.
3. Cell differentiation and morphogenesis: Here cells differentiate into tissue and formation of different organs begin.

Question 2.
What are plant hormones?
Plant hormones are the organic chemical substances which regulate growth and other physiological functions in plants at a site away from its place of production and active in very minute quantity e.g., Auxin, Gibberellin.

Question 3.
What is Florigen?
Florigen is a flowering hormone which is produced in presence of proper photoperiod by the phytochromes present in the plasma membrane of leaf cells. The hormone is then transported to the floral bud region where it induces flowering.

Question 4.
Write the name of hormone which accelerates the cell division.

Question 5.
What is 2,4-D? Also elaborate it.
It is an artificial growth hormone. 2,4-D stands for 2,4-dichlorophenoxyacetic acid.

Question 6.
Write the name of apparatus used for measuring plant growth.

Question 7.
What are growth inhibitor hormones? Write two functions.
Abscisic acid (ABA) and Ethylene are top two plant growth inhibitor hormones. For their function

Functions of abscisic acid :
1. It induces dormancy in buds and seeds as opposed to gibberellic acid which breaks dormancy.
2. It promotes senescence of leaves, appearance of abscission layer, leaf-fail and ageing which can be effectively reverted by application of cytokinins.
3. It inhibits lettuce seed germination but this can also be reversed by kinetin.
4. It inhibited gibberellin induced growth in various tests and is believed to be a powerful gibberellin antagonist.

Ethylene hormone was discovered by scientist Burg (1962) which is a gaseous hormone.
Main functions of ethylene :

  1. Triple response: Ethylene gas inhibits stem growth, helps in swelling of stem and destroys geotropism.
  2. Flowering: It decreases flowering but in pineapple it induces flowering.
  3. Sex modification: It increases number of female flower and decreases number of male flowers in plants.
  4. Ripening of fruits: It is used in ripening of fruits, therefore nowadays ethephone (schloroethyl phosphoric acid which produces ethylene gas) is used for ripening fruits at industrial level.

Question 8.
Elaborate I.A.A. and describe at least one function of it.
I. A. A. is Indole Acetic Acid. It controls the growth of plants.

Question 9.
Write the name of hormones which initiate flowering.

Question 10.
Name the hormone that exists in gaseous state.

Question 11.
Why it is beneficial in some plants to cut the tip of newly formed branches?
Cutting of branches, initiates growth of lateral buds which results into formation of more new branches and the plant becomes more dense.

Question 12.
Name two artificial plant hormones.

Plant Growth and Development Class 11 Important Questions Short Answer Type

Question 1.
What do you mean by growth-regulating substance? Name any three growth regulator substances.
The chemical substances which regulates growth and development in organisms are called as growth regulating substances. Actually, these are the organic substances which are naturally produced in the plants to control the growth and other physiological functions at a site away from its place of production and are active in extremely minute quantities and called as hormones. Three plants hormones are :

Question 2.
Give four functions of cytokinin hormone.
Functions of cytokinin :

  1. Activates cell division.
  2. Helps in the expansion of green leaves.
  3. Accelerates protein synthesis.
  4. Inhibition of the breakdown of leaf pigments and nucleic acid. Chemically they are derivatives of adenine with furfuryl group at 6th position.

Question 3.
Is any leafless plant can react with photoperiodism? Yes or No? Why? (NCERT)
No, because flowering in some plants not only depend on light or dark period but it depends on duration of light. At the apical bud, floral but develops but it can not experience photoperiodism. Leaves can experience light or dark period. A hormone florigen is responsible for flowering. It travels from leaf to floral bud only when leaf is exposed to required period of light, Gibberellin and Anthesin hormones together induce flowering.

Question 4.
Give four functions of auxin.
Functions of auxin :

  1. Helps to increase in height of plants.
  2. It induces root development.
  3. It induces production of parthenocarpic fruits.
  4. It prevents defoliation of leaves and induces flowering.
  5. Weed eradication.

Question 5.
Give importance of abscisic acid.
Functions of abscisic acid :
1. It induces dormancy in buds and seeds as opposed to gibberellic acid which breaks dormancy.
2. It promotes senescence of leaves, appearance of abscission layer, leaf-fail and ageing which can be effectively reverted by application of cytokinins.
3. It inhibits lettuce seed germination but this can also be reversed by kinetin.
4. It inhibited gibberellin induced growth in various tests and is believed to be a powerful gibberellin antagonist.

Question 6.
Give four functions of gibberellin hormone.
Functions of gibberellin :

  1. Parthenocarpic fruits may be produced by their application in tomato, pear, apple etc.
  2. Induces stem elongation by promoting growth of intemodes.
  3. Flower development in lettuce, barley etc.
  4. Seed germination by breaking their dormancy.
  5. Buds development.

Question 7.
Give four main functions of ethylene hormone.
Ethylene hormone was discovered by scientist Burg (1962) which is a gaseous hormone.
Main functions of ethylene :

  1. Triple response: Ethylene gas inhibits stem growth, helps in swelling of stem and destroys geotropism.
  2. Flowering: It decreases flowering but in pineapple it induces flowering.
  3. Sex modification: It increases number of female flower and decreases number of male flowers in plants.
  4. Ripening of fruits: It is used in ripening of fruits, therefore nowadays ethephone (schloroethyl phosphoric acid which produces ethylene gas) is used for ripening fruits at industrial level.

Question 8.
Write short note on apical dominance?
Apical dominance: In many plants where apical bud grows, axillary bud do not grow i.e., apical bud dominates growth of axillary bud. Actually apical bud produces a hormone which is transported to different parts of phloem and it inhibits growth of axillary bud. The hormone is auxin. On the other hand cytokinin induces growth of axillary bud.

Question 9.
What is phytochrome? Give its importance in plants.
Phytochrome: It is well established that short day plant does not produce flower if the dark period is interrupted by a brief flash of light. It has been observed that the wavelength of 660 in the orange red colour is the most effective wavelength for inhibiting the process of flowering. Far red light on the contrary, does not break up a long night into two short nights. Besides, far red radiation of a wavelength of 740 has been found to reverse the effect of red light by Borthwick et al (1952) and Downs (1956) and is termed as red-far red reversible photoreaction.

If a brief flash of red light in the mid-night is followed by a brief flash of far red radiation, its inhibitory effect is counteracted and flowering takes place. If far red radiation is followed further in sequence by red light, flowering will again be inhibited, i.e., the radiation is last used in the sequence, will determine the response of the plant. This discovery ultimately resulted in the discovery of the pigment is called as phytochrome by Butter et al (1959), since light energy cannot be effected unless it is absorbed by a pigment.
The main characteristics of the pigment are :

  1. Proteinaceous in nature.
  2. Located in plasma membrane.
  3. Found in all green plants.
  4. Exists in two different forms :(a) Red light-absorbing forms designated as PR and
    (b) Far-red light-absorbing forms designated as PFR .
  5. Both of these forms are photochemically interconvertible.
  6. On absorbing red light (660-665 nm) PR form is converted into PFR form.
  7. On absorbing far-red light (730-735 nm) PFR form is converted into PR form.
  8. The PFR form of the pigment gradually changes into PR form in dark.

Spectrophotometric examination of the pigment by Briggs suggests that most of the phytochrome is found in inactive form. According to Hartman the biologically active form of phytochrome is some unknown derivative of PFR. He has suggested a different scheme of phytochrome action.

Question 10.
Why Abscisic acid is called as tension hormone? (NCERT)
Abscisic acid is called as tension hormone due to following reasons :

  • It prevents growth in plants.
  • It induces leaf fall making the leaves weak.
  • It prevents effect of gibberellin hormone.
  • It prevents seed germination.

Question 11.
Short day plant and long-day plants show flowering together in one place. Explain it. (NCERT)
1. Short-day plants: Need a short daylight period ranging between 8-10 hrs and a continuous dark period exceeding 12hours(14to 6his.),i.e., Xanthium, Soyabeans, Tobacco, Gossipium, Coffee etc. The salient features of such plants are given below :

  • These plants require a relatively long period of darkness for flowering. It is generally longer than a certain critical length. If dark period is less, no flowering would result. If this period is interrupted even with a small exposure, the plants will not flower.
  • No flowering occurs if a weak intensity of light is given to those plants.
  • No flowering under alternating cycles of short dark and light period.
  • They are also termed as long night plants because length and continuity of night determine the flowering.

2. Long day plants: These plants require a longer daylight (14 -16hrs) for flowering, e.g., Supuracea etc. They are characterised by the following :

  • They require a photoperiod of more than a critical length. They require either a small period of darkness or no darkness for flowering.
  • Flowering is full in continuous light.
  • Darkness has inhibitory impact on these plants.
  • They can be induced to flowering by short photoperiods but accompanied by shorter dark period.

Question 12.
Growth in flowering plants can not be described under one parameter. Why? (NCERT)
Growth at cellular level in flowering plants is the result of growth in the proto¬plasm, which can not be measured. Thus growth in plants is measured by some other ways.
Some way of measurements are: Increase in fresh weight, dry weight, lengthwise area, volume and number of cells. At the root tip meristems produces more than 17,500 new cells by cell division per hour, whereas in watermelon at cell division stage growth is slow because cells increases in number without increasing in volume by multiplication, later growth become 3,50,000 times than previous time due to cell elongation. Increase in length of pollen tube per unit time can be measured easily. In dorsiventral leaves, growth in surface area of leaves is measured.
Thus, from above examples, it is clear that growth in plants can not be described under one parameter.

Plant Growth and Development Class 11 Important Questions Long Answer Type

Question 1.
What is growth? Describe various stages of cell growth.
Growth: Growth is a vital process in which organism increase in its size, weight, volume and structure.
Stages of Growth :
1. Cell division: During this stage the cells divide and redivide by mitotic division for a definite period depending upon the organ of the plant in which growth is taking place.

2. Cell elongation phase: During this phase the newly formed cell increase in size due to their internal metabolic activities. In this phase cell wall materials and water increases 5 to 10 times of their original value

3. Cell differentiation phase: During its structural, qualitative and quantitative changes takes place and cells attain final definite shape, structure, function and properties.

Question 2.
What are photoperiodism and vernalization? Give their economic importance. (NCERT)
1. Photoperiodism: The growth and development of large number of plants is dependent upon the duration of light availability called Photoperiodism. The reproductive growth and flowering is mainly controlled by light period and temperature. The flowering requires a certain day length, i.e., the relative length of day and night which is called as photoperiod.

Economic importance of photoperiodism :

  • The knowledge regarding photoperiodism is important for hybridization.
  • Characterization and structure of florigen is useful for industrial purposes.
  • It is an excellent example of physiological preconditioning of plants.
  • Induction to flowering may be used in horticulture.
  • By this process plants which produces fruits once in a year, can produce fruits twice in a year.

2. Vernalization: It has been observed that if seeds of winter seasonal plants are kept at 0-5° C temperature for some days and then sown during spring season, flowering occurs in them like other spring seasonal plants. This phenomenon is called as vernalization.

If vernalized seeds are kept at high temperature for some time then vernalization effect is lost. This process is called as devernalization. It is believed that stimuli is received by apical meristem and vernalin hormone which is a gibberellin type hormone is secreted, which is transported to growth region.
In Siberia where soil remain cover by ice for 10 months, wheat is produced by this process in two months.
Economic importance of vernalization :

  1. By this process winter plants can be converted into spring plants.
  2. Crops can be protected from natural harm effects.
  3. Flowering can be done in plants in short period of time.
  4. Crops can be produced in short period of time by this process.

Question 3.
In higher plants growth and differentiation is open. Explain it. (NCERT)
In higher plants growth can be represented by a sigmoid curve (S-shaped curve).
There are three phases of this curve :

  1. Lag phase: When the rate of growth is very slow.
  2. Log phase: It is the phase of rapid growth.
  3. Steady phase: Growth slows down at this stage or reaches to an equilibrium as cell division stops.
    When cell losses its division capacity, they proceed towards cell differentiation to produce different tissues to perform different functions. The growth of a cell, tissue, organ, organ system or an organism follow same pattern of growth, thus it is open, whereas development is flexible. Actually, development is the sum total of growth and differentiation.

Question 4.
Write short note on following :
(a) Arithmetic growth (NCERT)
(b) Geometrical growth
(c) Sigmoid growth rate
(d) Absolute and relative growth rate.
(a) Arithmetic growth: After mitosis division one cell undergoes arithmetic growth by regular cell division, whereas the second cell differentiate and mature. It occurs in a constant rate.

(b) Geometrical growth: In geometrical growth both the cells produced by mitosis undergoes cell division. But due limited nutrient supply gradually growth rate become slow, at last it reaches to steady state.

(c) Sigmoid growth rate: If a graph drawn between increase in size of the organism versus time then ‘S’ shaped curve is obtained called as sigmoid curve. It has three phases :

  1. Lag phase: When the rate of growth is slow in initial stage.
  2. Log phase: When the rate of growth is fast or rapid.
  3. Steady phase: When rate of growth reaches to an equilibrium because rate of production of cells become equal to cell death.

(d) Absolute and relative growth rate: Measurement and comparison of complete development in unit time is called as Absolute growth rate, whereas measurement of growth per unit time by any other given way is called as relative growth rate.

Question 5.
Define Growth, Differentiation, Development, De-differentiation, Re-differentiation, Meristem and growth rate. (NCERT)

  1. Growth: It is the irreversible or progressive increase in size, shape, volume and weight of an organism.
  2. Cell differentiation: After cell division and cell elongation a cell undergoes differentiation. The cell differentiates, change in shape, position and get modified, matured as permanent cells to perform specific function. This phenomenon is called as differentiation.
  3. Development: Development is the gradual growth of the living body in its life cycle.
  4. De-differentiation: Differentiated cells regain their cell division capacity in some specific condition. This phenomenon is called as De-differentiation.
  5. Re-differentiation: New cells formed by de-differentiated cells losses their cell division capacity again and become permanent tissue by differentiation to perform specific function. This is called as re differentiation.
  6. Meristems: Group of similar, immature plant cells, which can show regular cell division to form new cells are called as meristems.
  7. Growth rate: Increase in size, dry weight, volume or number of cells of the living organism per unit time is called as growth rate.

Question 6.
If you are asked to do following works which plant hormone can be used?
(a) To produce root in a twig of plant. (NCERT)
(b) To ripe fruit fast.
(c) To prevent falling of premature leaves.
(d) For growth of axillary bud.
(e) To promote flowering in rose.
(f) To close stomata soon.
(a) Auxin,
(b) Ethylene,
(c) Gibberellin,
(d) Cytokinin,
(e) Gibberellin,
(f) Abscisic acid.

Question 7.
What will happen if: (NCERT)
(a) GA3 is provided to seedlings of rice.
(b) Dividing cells stops cell division.
(c) Keeping a decay fruit with unripen fruits.
(d) If you forget to add cytokinin in the culture medium of plant.
(a) Rice plant will increase in height.
(b) Cells when loss capacity to divide, differentiate to form different tissues to perform specific function.
(c) If a decay fruit is kept with unripen fruits then all fruits will decay.
(d) If cytokinin is not added to culture medium of plant then it may affect formation of chlorophyll in the young leaves, growth of lateral branches, growth of adventitious branches. In absence of cytokinin abscission of leaves may occur.

Question 8.
What are synthetic growth hormone? What are their importance in agriculture?
Synthetic growth hormone or growth regulator :
As hormone regulates growth in organisms therefore they are called as growth hormone. Following are few examples of growth regulators, their importance in agriculture are as follows:
1. Morpactins: It is a synthetic hormone and derivative of fluorine-carboxylic acids. It induces growth of axillary bud by inhibiting growth of stem, leaf lamina etc. It increases production of oranges.

2. Malic Hydrazide (MH): It is a synthetic hormone which inhibit growth of grass, shrubs and trees. It inhibits germination of potato and onion thus they can be kept for long period of time.

3. Cycocel (CCC): Chemically it is chloroethyl-trimethyl ammonium chloride. It is used to kill weeds.
4. Synthetic Auxin (IBA and N.A.A.): It prevents defoliation of fruits and leaves.
5. Alpha naphthalene acetic acid: It is a synthetic hormone used for inhibiting growth of buds in godown of potato. Therefore potatoes can be kept for long time.
6. 2, 4 Dichlorodiphenoxy acetic acid: It is used to kill weeds.
7. Ethaphone: Chemically it is 2-chloroethyl phosphoric acid. It is used for ripening fruits like banana, grapes, mango at industrial level.

Question 9.
What is flowering hormone? Describe various types of flowering hormones in plants.
Flowering hormones: Flowering hormones are the hormones which induces flowering by the effect of temperature and light.
There are two types of flowering hormones :

1.Vernalin: It induces flowering by regulating vernalization process. As a result of vernalization, i.e. when apical bud receives winter stimuli produces vernalin hormone which acts like gibberellin and induces flowering.

2. Florigen: Phytochrome pigments found in the green leaves after absorbing light rays produces florigen hormone which is transported to growing region, where it induces flowering process.

Question 10.
Describe various factors which affect growth.
Factors affecting growth :
1. Food supply: It affects the rate of growth firstly because it provides growth material to the growing region and secondly because it provides potential energy to the growing region.

2. Water supply: It has a direct relationship with the rate of growth because it is necessary for all the metabolic activities of protoplasm and for increasing the turgidity of the cell for cell enlargement.

3. Oxygen supply: Oxygen increases growth as it helps in respiration to convert potential energy into kinetic energy required for the vital activities of protoplasm.

4. Temperature: It affects growth in a way that growth occur between 4-45°C, optimum activity takes place at 28-33°C.

5. Light: All the three aspects of light intensity, quality and periodicity affects growth. High intensity of light induce dwarfing of the plant and increases the loss of water. Weak light intensity reduces the rate of overall growth and also photosynthesis. Different colour (wavelength) also affects the growth of plants. In blue-violet colour light, intermodal growth is pronounced while green colour light reduces the expansion of leaves. The red colour favours elongation.

Infrared and ultraviolet are detrimental to growth. There is a remarkable effect of the duration of light on the growth of vegetative as well as reproductive structure.
6. Growth hormones: Now it is well established that the growth of plant is controlled by certain organic compounds present in very minute quantities. These compounds are called hormones, phytohormones or growth-promoting substances.

Plant Growth and Development Class 11 Important Questions Objective Type

1. Choose the correct answers:

Question 1.
Gibberellins was first extracted from :
(a) Gibberella fujikuroi
(b) Gelidium
(c) Gracelaria
(d) Aspergillus.
(a) Gibberella fujikuroi

Question 2.
Storage sprouting of potato can be prevented by :
(a) IAA
(b) Malic hydrazide
(c) Cytokinins
(d) Gibberellins.
(b) Malic hydrazide

Question 3.
The following is a naturally occurring growth inhibitor :
(a) IAA
(b) ABA
(d) GA3.
(b) ABA

Question 4.
The following hormone is concerned chiefly with cell division in plants :
(a) IAA
(b) Kinin (zeatin)
(c) GA3
(d) 2,4-D.
(b) Kinin (zeatin)

Question 5.
Gibberellic acid has been successfully employed to induce flowering :
(a) In short-day plants under long-day conditions
(b) In long-day plant under short-day conditions
(c) For some plants
(d) None of these.
(b) In long-day plant under short-day conditions

Question 6.
The leaves of Mimosa pudica drop down on touch because :
(a) The plant has nervous system
(b) The leaves are very tender
(c) The leaf tissues are injured
(d) The turgor of the leaf changes.
(d) The turgor of the leaf changes.

Question 7.
Vernalization is :
(a) Growth curve in response to light
(b) Recurrence of day and night
(c) Effect of day length on plant growth
(d) Acceleration of the ability of flower by low-temperature treatment.
(d) Acceleration of the ability of flower by low-temperature treatment.

Question 8.
Effect of length of the day on flowering is called :
(a) Phototropism
(b) Photoperiodism
(c) Photorespiration
(d) Photo-oxidation.
(b) Photoperiodism

Question 9.
In plants the hormone associated with cell division is :
(a) GA
(b) 2,4-D
(c) IAA
(d) Kinin.
(d) Kinin.

Question 10.
(a) A hormone that stimulate cell division
(b) A process of cell division
(c) A form of cell movement ‘
(d) A substance that produces dormancy.
(a) A hormone that stimulate cell division

Question 11.
Three main growth inducing hormones in plants are :
(a) Auxin, Gibberellin and Ethylene
(b) Gibberellin, Cytokinin and Abscisic acid
(c) Ethylene, Abscisic acid and cytokinin
(d) Auxin, Gibberellin and cytokinin.
(d) Auxin, Gibberellin and cytokinin.

Question 12.
Cytokinesis induces:
(a) Cell division
(b) Cell elongation
(c) Stem elongation
(d) Parthenocarpy.
(d) Parthenocarpy.

4. ……………………….. hormone is used to increase length of genetically dwarf plants.

8. Bakani disease of rice is caused by a fungus known as ……………………….. .
Gibberella fuji kuroi

9. Growth occurs per unit time period in the living organisms is called as ……………………….. .
Growth rate

10. In ……………………….. growth after mitosis division only one daughter cell shows regular cell division.

Column ‘A’ Column ‘B’
1. Florigen (a) IAA
2. Abscission (b) Protein
3. Delay in senescence (c) Cytokinin
4. Aleuron layer (d) ABA
5. Auxin (e) Flowering.

1. (e) Flowering.
2. (d) ABA
3. (c) Cytokinin
4. (b) Protein
5. (a) IAA.

Column ‘A’ Column ‘B’
1. Dormin (a) Auxin
2. GA3 (b) Abscisic acid
3. Zeatin (c) Gibberellin
4. 2,4-D (d) Cytokinin
5. Termination of seed dormancy (e) Gibberellin.

1. (b) Abscisic acid
2. (c) Gibberellin,
3. (d) Cytokinin
4. (a) Auxin
5. (e) Gibberellin.

1. Name the tissues responsible for growth in plants.
Meristematic tissue

2. Write the name of various phases of growth.
Cell division stage, Cell elongation stage, Cell maturation stage

3. Elaborate the term 2,4-D. Also write one function of it.
2, 4 di phenoxy acetic acid, it is a growth hormone and used as weedicide

4. Elaborate the term IAA and write one function of it.
Indole acetic acid, used in development of seedless fruits

5. Name the hormone which is found in gaseous state.

6. Name the apparatus used for measurement of plant growth.

7. Name the growth regulator which help to stop germination of potato and onion.
Malic hydrazide

Advanced Computing, Mathematics and Data Research Highlights

Wide-field immunofluorescence imaging of human mammary epithelial cells using antibodies against the EGFR (red) and the manose-6-phosphate receptor (M6PR green). The cell nuclei were counterstained with DAPI (blue). Most of the EGFR in these cells is located at the cell surface with a minority localized in intracellular vesicles. The M6PR are localized primarily to certain compartments within the cell.

Results: In biological research, a typical process would be to conduct experiments and then analyze the collected data to reach conclusions. A new model-based analysis approach from computational biology scientists at Pacific Northwest National Laboratory demonstrates that integrating computations into experimentation enables researchers to obtain more robust quantitative information about cell kinetics.

The process uses a computational model to generate predictions about the dynamics of cell receptors in different cellular compartments. The model predicted that the time scales of receptor (de)activation kinetics on the cell surface and the interior compartments were comparable. This finding initially appeared contrary to what would have been expected based on existing literature however, follow-up experiments validated that the computational predictions were actually correct.

The work is featured on the November cover of Molecular BioSystems.

Why It Matters: In human cells, signaling (i.e. telling the cell what to do such as releasing hormones or regulating a cell cycle) is initiated by external cues, and cell receptors facilitate the relay of the received information to regulatory elements in the cell. Since knowing their differential cellular signaling patterns can provide clues about the potential effectiveness of drug responses and treatment strategies, determining whether surface and internal receptors function the same way is important. Current data indicate that surface and internal cell receptors may have differing response and activation kinetics, that is, they may respond differently when exposed to the same stimulus. But using the new model, PNNL scientists predicted that the receptors would actually have similar deactivation kinetics. Laboratory measurements of receptor phosphorylation levels&mdashwhich indicate the level of their activity&mdashshowed that, in fact, deactivation rates were roughly the same for both the internal and surface receptors.

Methods: The PNNL team developed mathematical models for epidermal growth factor receptor (EGFR) signaling to predict how the activated receptors were spatially distributed within cells. In order to maintain simplicity, model development and the design of future experiments were integrated from the beginning. The model was constructed to predict the receptor phosphorylation levels in a cell under specific conditions for the immediate-to-short (minute-to-hours) response durations. The team then performed the validation laboratory tests to determine the actual EGFR phosphorylation levels in cells, both for all the cell receptors and for only the internal receptors. The difference between these two measurements provided the information about the surface receptors.

What's Next: When receptors receive a cue to initiate a signal, the signal is transmitted "downstream" along signaling pathways to trigger the next phase of activity. Such signal propagation occurs through transient protein-protein interactions and may involve a large number of associated proteins. The PNNL team is now investigating how different ways for initiating a signal translate into different response patterns at the level of downstream proteins. Additionally, they are looking at how differential signaling, i.e., variations in signaling patterns when conditions change, may be regulating cell decision-making, thus resulting in different responses based on the cell&rsquos observed properties.


This research was funded by a National Institutes of Health grant.

Research Team: Harish Shankaran, Yi Zhang, William B. Chrisler, Jonathan A. Ewald, H. Steven Wiley, and Haluk Resat&mdashPNNL

Reference: Shankaran H, Y Zhang, WB Chrisler, JA Ewald, HS Wiley and H Resat. 2012. "Integrated Experimental and Model-based Analysis Reveals the Spatial Aspects of EGFR Activation Dynamics." Molecular BioSystems 8(11):2868-2882. DOI:10.1039/C2MB25190F.

Part 2: Escalating Infectious Disease Threat

00:00:01.19 Hi I'm back from my second lecture now. This is going to be
00:00:05.04 quite different from the first one you heard. First one was the
00:00:08.18 the science that goes on in my lab. This talk is why I do that
00:00:12.20 science and why we all have to be aware of what's going on
00:00:17.15 in this global village that we live in. It has become clear
00:00:23.22 that the global infectious disease threat is real and something we
00:00:29.00 have to worry about. Today infectious diseases are the leading
00:00:34.02 cause of death worldwide and the third leading cause of death
00:00:39.02 in the United States. Now the diseases that predominate
00:00:43.11 we all know about and have heard about. Of course they include
00:00:46.27 HIV/AIDS. They include acute lower respiratory infections,
00:00:52.05 diarrheal diseases, tuberculosis, malaria but since 1973,
00:00:59.17 at least 29 previously unknown diseases have emerged. Now
00:01:06.27 20 diseases have re-emerged in new places where they never
00:01:11.24 were before and are sitting in new ecosystems. And the question
00:01:17.13 of course is, "Why is this happening?" Where do new diseases
00:01:20.24 come from? Why are we facing such an escalation?
00:01:25.10 And in point of fact, this is due to the very dramatic changes in the
00:01:31.01 society and in the environment in which we live. There's been an
00:01:36.01 explosion population growth, spreading poverty, global warming,
00:01:40.29 and urban migration, and what we're finding is new pathogens in
00:01:47.29 new places and old pathogens in new places. And what do we mean by,
00:01:54.26 "How is this happening?" So if we have urban migration,
00:01:58.25 which means we're moving into our forests, a typical disease that
00:02:03.06 is now blooming all over the place is Lyme disease, carried by a tick.
00:02:07.28 And that was due to deforestation to make way for new homes.
00:02:12.17 And this causes a tick bite that's carrying this bacterial infection
00:02:17.09 is quite devastating. Another that we of course all know about is
00:02:22.00 HIV/AIDS that is growing and spreading in all urban populations.
00:02:28.29 Another interesting one is called Hantavirus. This virus was unknown.
00:02:33.29 It's new to us. And it appears in the American far West in
00:02:39.07 Utah and Arizona. It's carried by mice and rats. This is a very
00:02:44.18 nasty virus with a 60% kill rate. And we're still trying to understand it.
00:02:49.24 Another one that's coming out of the forests in Africa is
00:02:55.21 caused by a virus, and it's Ebola. And that is a very difficult virus
00:03:00.28 to deal with. Now we have also the different kinds of changes in our environment.
00:03:10.01 For example, Mad Cow disease, which you've all read about and
00:03:14.07 heard about, which is caused not by a bacterium, not by a virus,
00:03:19.12 but by a protein that changes conformation and goes into a
00:03:23.28 state that causes a very severe neurological brain defect.
00:03:28.23 And why did this somehow get out of the box? And if you remember
00:03:34.05 in England several years ago, there was just an outbreak
00:03:39.10 of Mad Cow disease, and it turned out to be due to the fact
00:03:43.02 that the production of the foodstuffs that we feed all of our
00:03:48.02 livestock was made differently. We were feeding them various kinds of
00:03:54.22 vegetable, mineral, and animal refuse and this time they would
00:04:00.22 include the nervous structure--the brains and the nerves. And that's
00:04:05.24 where these prions were. And then it wasn't until the mandate
00:04:09.24 came down to change the preparation of food for our livestock that
00:04:14.20 this epidemic was dropped down. And this had to be changed worldwide.
00:04:18.16 So this is another example of us trying to survive in large populations
00:04:24.09 and feed everybody by changing the way in which we carry
00:04:27.22 out what we do. The other thing that's happened is that
00:04:31.04 there's been a resurgence of very drug-resistant tuberculosis.
00:04:36.27 And in South Africa now, there are strains of the bacillus that
00:04:43.11 causes tuberculosis that are resistant to every known antibiotic
00:04:48.12 and it's a particularly virulent strain with a very high kill rate.
00:04:52.14 So the crowding, urban mixing of people and pathogens has given
00:05:00.21 us a bloom of bacteria that are resistant to antibiotics. Now
00:05:08.20 we also know that we have international travel everywhere.
00:05:15.02 It's increased. If we have a disease outbreak in Kuala Lumpur,
00:05:19.09 in a day, the person that gets on that airplane with an infectious
00:05:24.21 disease can be in Chicago in that same day. So that we are
00:05:30.01 rapidly moving all over this globe, and there's an incredibly rapid spread
00:05:34.29 of disease, reminding of us that no country is an island. And we now
00:05:40.00 live in a global village, which means that all the countries on this globe
00:05:45.00 have to now coordinate, collaborate, and help one another
00:05:50.08 to identify diseases and to disseminate things that will help
00:05:55.08 squash down an outbreak of some kind. Now, one other thing that
00:06:00.23 happens when this guy picks up a disease in Kuala Lumpur and
00:06:05.07 winds up in Chicago--now the people in Kuala Lumpur may have
00:06:08.25 been living with this disease for a little while and they've built up immunity.
00:06:11.28 But the people in Chicago have no immunity to this and so it's
00:06:15.24 a bigger problem. Now the part of this that's difficult is that we have
00:06:21.25 asymptomatic travel. You get on a plane and you feel fine but in fact
00:06:27.02 you're infected. And of the big problems with a possible influenza
00:06:32.23 epidemic is if you catch flu bug--influenza--you are asymptomatic
00:06:40.08 for at least two days. And during that period of time, you are
00:06:44.07 infectious. So you don't know what you're transferring. And that is
00:06:48.28 what leads you to pandemic. Now another problem of course is
00:06:54.29 the loss of control of our national borders. And we're really not very
00:07:01.08 good at carrying out our quarantine laws. It's difficult to do this.
00:07:08.04 And we are going to return to this later in my talk because in many diseases--
00:07:14.29 effective quarantine laws are the only thing that we're going to
00:07:19.25 use to protect ourselves. Now every one of these issues is something
00:07:25.21 that is being worked on and understood by many countries
00:07:30.22 coordinated by the World Health Organization. The final issue that
00:07:36.25 is almost making where we live now a perfect storm is that
00:07:41.20 while we have increased globalization, while we have increased
00:07:46.10 population, while we have increased urbanization, and the migration of
00:07:51.04 pathogens into new ecological niches, we have the rise of
00:07:55.15 antibiotic-resistant pathogens. So let me tell you what an
00:07:59.22 antibiotic is. An antibiotic is a small compound either made
00:08:03.24 in a laboratory or made by some living creature and when
00:08:08.01 this compound is made, what it does is kill the pathogen.
00:08:15.16 It kills the bacterial pathogen. Perhaps I should just remind you
00:08:19.12 of the difference between a bacterial pathogen and a viral
00:08:23.07 pathogen. A virus is not a living cell. A virus just has a protein
00:08:29.24 coat and the genetic material sits inside this coat. And it
00:08:34.27 cannot make more of itself. The only way it can make more of itself
00:08:39.24 is if it infects a host cell--one of our cells, one of the cells that are
00:08:45.08 of a rat, or a monkey, or some other animal. And then it gets in there
00:08:49.07 co-opts the machinery of that cell and makes many more of itself.
00:08:53.17 That's a virus. A bacterial cell is this little tiny living cell that can grow
00:09:00.17 and divide and respond to its environment and figure out if it's
00:09:04.22 a pathogen how to get into a host cell and make you very ill.
00:09:09.05 So that's a bacterial cell. Antibiotics are specific for bacterial cells,
00:09:16.00 not viral infections. And what has happened is that we have had
00:09:22.14 a history of various kinds of antibiotics, which were first discovered
00:09:30.11 in 1946 with penicillin. Then soon after that, we had strep and staph
00:09:38.23 infections that would be very sensitive to penicillin. Today, 80%
00:09:44.29 of all strains of staph--staphylococcus--are resistant to penicillin.
00:09:51.03 This was quite a shock to us. In 1950 we had more antibiotics that
00:10:00.25 would infect multiple bugs--streptomycin, chloramphenicol,
00:10:06.07 tetracycline. Then in 1953 there was a Shigella outbreak in Japan
00:10:12.15 and it resulted in the appearance of a strain of dysentery bacillus
00:10:16.22 that was resistant not just to one antibiotic but to many. And that
00:10:22.04 was a red flag. And people started becoming somewhat concerned.
00:10:27.07 Up now to 1982, when we had the last new class of antibiotics--the quinolones--
00:10:34.22 resistance is rising, really, in a frightening manner. Cipro, to which
00:10:41.08 we were eating like candy when there was an anthrax scare in
00:10:45.24 the United States, has caused enormous resistance to that particular drug.
00:10:51.16 In 1998, vancomycin, which is considered by many an antibiotic of
00:10:58.01 last resort for staph infections and other kinds of pathogens,
00:11:01.25 we are now seeing the emergence of resistance to Vancomycin as well.
00:11:06.12 Now what happens when something becomes resistant to an antibiotic
00:11:11.18 is that it turns out that these bugs are very, very smart and what they
00:11:16.15 have learned how to do is if they see a drug coming towards
00:11:21.28 it, like arithrimycin, it figures out how to spit it out. Or if the
00:11:29.00 antibiotic manages to get into the bug, the bacteria have figured out
00:11:34.28 a way of chemically modifying that antibiotic so that it's no longer
00:11:38.23 working. And they also have figured out how to change the target
00:11:43.16 of that antibiotic in that particular cell so it doesn't work any longer.
00:11:47.26 So these bugs are very smart and we're in a war with them and
00:11:53.03 the bugs are winning. And what we need is to understand how to make
00:11:57.22 new and better antibiotics. If I just look at staph infections in the
00:12:03.12 United States, in 1957 100% sensitive to penicillin. 1982-- fewer
00:12:12.04 than 10% of all staph cases could be cured by penicillin.
00:12:16.06 1993-- only vancomycin survived as an effective antibiotic. And today, as I
00:12:23.13 told you, there are strains that are resistant to everything. So
00:12:27.18 one of the questions is, "Why is antibiotic resistance growing so rapidly?"
00:12:32.03 And in fact, what we're seeing is that antibiotics are put into animal
00:12:38.17 feed, into aerosols for fruits and vegetables. Of the 50 million
00:12:43.09 pounds of antibiotics produced annually in the U.S., 40% go into
00:12:49.23 livestock. So how does this resistance arise? Let's say you
00:12:55.06 have 10 to the ninth (10^9) bacterial cells all resistant to a particular antibiotic.
00:13:00.15 One of those 10^9 cells has a mutation that makes it resistant.
00:13:07.12 All the others will be killed by that antibiotic, but that one
00:13:12.00 will happily grow and divide and then you have a bloom of an
00:13:16.18 antibiotic-resistant pathogen. By feeding antibiotics in huge quantities
00:13:23.14 to all of our livestock, we are increasing the chances of that one
00:13:30.05 guy to develop antibiotic resistance. Another reason that things--
00:13:36.10 this resistance--is growing so rapidly is that there are growing numbers
00:13:40.28 of immunocompromised people. And this is really partly due to
00:13:45.10 the wonders of medicine and also to new infectious diseases.
00:13:48.20 Chemotherapy patients have very, very low immunity. They're infected
00:13:53.21 by many different bacteria and they grow and divide and develop
00:13:57.04 resistance. Transplant patients, AIDS patients, even just aging populations--
00:14:04.05 if you're over 65, your immune system is going to hell in a handbasket.
00:14:09.20 And so you have to really realize that you are particular sensitive to
00:14:14.17 bacterial infections and again you become a reservoir for increased
00:14:19.19 antibiotic resistance. There's also the excessive use of antibiotics,
00:14:24.04 over-prescription and then unregulated over-the-counter sales. So these
00:14:29.22 are all very serious problems. Of course, as I told you before,
00:14:34.02 international travel has us all over the place. And so if you get
00:14:38.08 a multi-drug-resistant strain of streptomycin in Spain, you wind up
00:14:46.13 with it in South Africa in four days if somebody is traveling rapidly.
00:14:50.03 So we have complete and rapid dissemination. Now what I'm
00:14:53.26 going to turn to is the story of where new bugs come from.
00:15:00.23 Where do new pathogens come from? And the story I'm going to tell you
00:15:05.22 is one of E. coli 0157. It's a new and pervasive pathogen. It's a food
00:15:12.16 contaminant that is now the leading cause of kidney failure
00:15:15.26 in children. Now the first time I told this story was in a very
00:15:19.28 unusual scenario. It was during Bill Clinton's administration.
00:15:25.27 And he became very worried about genetic engineering--
00:15:30.20 in other words, what we can do in the lab now in building new
00:15:34.01 groups of genes and perhaps altering a pathogen or altering some other
00:15:39.15 normal process. And he was worried. He wanted to know how
00:15:43.11 worried we should be about malevolent forces actually creating
00:15:48.12 new pathogens. And he wanted to understand what was happening.
00:15:53.27 And I was part of a group of six people who were invited to speak
00:15:58.20 with President Clinton and his whole cabinet. And the story I
00:16:03.00 told them really was that genetic engineering, yes we can do
00:16:09.04 in the lab, but the bugs and the various kinds of critters in the
00:16:15.14 natural world are much better genetic engineers than we are and
00:16:19.15 the example is E. coli 0157. Now, this is a picture of a virus
00:16:27.18 and I'm going to show you and tell you how this figured in
00:16:32.06 to the genetic engineering that was carried out by E. coli 0157.
00:16:37.13 So where did it come from? E. coli 0157 was first isolated
00:16:44.08 from a 50-year-old woman in California, who came down with
00:16:49.09 severe gastric distress and bloody diarrhea. She survived but
00:16:54.11 she was quite ill. Then in 1980, 14 children were admitted to a Toronto
00:17:01.03 hospital with the same symptoms. Of these, two children died
00:17:05.24 and the rest were left with severe kidney damage. Again
00:17:10.03 the bug, the bacterium, isolated from one of these kids
00:17:15.18 was the same as that found in that 50-year-old woman and
00:17:20.15 upon analysis, the very surprising development was that this
00:17:27.01 E. coli cell, which is a bug that grows in all of our gastric system
00:17:33.12 and is quite harmless, had picked up a gene--a particular gene--
00:17:40.14 from another bug, a pathogen called Shigella that coded for a toxin.
00:17:46.13 So now we had taken an E. coli cell and put in a gene that made it
00:17:52.04 a pathogen. That is genetic engineering. In 1981, in White City,
00:17:58.08 California 12 people eating at a local hamburger place became
00:18:02.13 ill with the same symptoms. 1982 in Michigan--again a local hamburger
00:18:08.03 place--E. coli 0157 was found in its meat patties. 1993--Jack-in-the-box
00:18:17.01 restaurants in the Northwest--hundreds became ill. Four kids died.
00:18:22.14 And this continues on and on. It was found in 1996 in contaminated
00:18:27.24 apple juice and lettuce. And that turned out because the E. coli cell
00:18:32.15 picked up not only your gene for the toxin but a gene that makes
00:18:35.25 it resistant to acid. So it could grow in an acidic environment,
00:18:39.18 which normal E. coli does not. 1997--there was again a huge
00:18:45.10 recall of contaminated hamburger meat. And in 2007, just a couple
00:18:51.00 months ago, contaminated spinach was found. And that came
00:18:56.02 from the runoff from livestock, which were not too far away.
00:19:01.20 So it turns out that now, there are 25 to 30 outbreaks per year
00:19:09.00 in the United States alone of E. coli 0157 contamination
00:19:13.18 and 5% of our dairy cows carry this pathogen. So how did this
00:19:20.13 happen? How do we think that this occurred? So what I'm showing you
00:19:25.00 here is a bacterial virus. Remember I told you that a virus
00:19:30.08 has a protein head, and that's shown here. That's the head.
00:19:34.12 This is its tail, and there's DNA in this head. And this over here
00:19:39.10 shows you what the virus looks like. This over hear shows you a
00:19:43.26 diagram of this virus. Looks like a moon lander, doesn't it?
00:19:46.29 And what this moon lander does is it lands on a bacterial cell
00:19:51.13 and it injects the DNA, the genetic material, right into the
00:19:57.05 bacterial cell that it hits. And this is how we believe this happened.
00:20:02.12 Okay. In this diagram I show you a Shigella bacterial cell. The blue
00:20:09.03 circle indicates the chromosome--the single chromosome.
00:20:13.10 And the little moon lander up there indicates the virus.
00:20:17.10 So the virus injects its DNA, and that's that little circle in the
00:20:22.13 center of the head, into the cell. Once that DNA gets into the
00:20:27.00 cell, it codes for things that chop up that blue chromosome.
00:20:31.13 You chop up that blue chromosome and the little piece
00:20:35.02 that contains that Shigella gene, then gets put into the head
00:20:40.27 of a new virus. And so this new bacterial virus contains
00:20:46.09 its own DNA and a little bit of that Shigella DNA. And that little bit
00:20:51.24 contains the gene that causes a toxin. Now what happens is
00:20:58.14 that that same virus hits an E. coli cell. And we believe this
00:21:05.04 happened during an epidemic of dysentery in Central America
00:21:10.18 when both E. coli and Shigella were mixed. And this virus injected
00:21:16.04 its DNA into the harmless E. coli. And this piece of DNA got
00:21:21.10 incorporated into the DNA of this E. coli, creating E. coli 0157.
00:21:29.15 That, folks, is genetic engineering. That happens naturally.
00:21:34.05 So now let me tell you a second story. And the second story
00:21:38.25 deals with why it's so difficult when we're first faced with something
00:21:44.20 that we haven't seen before in a given country to decide whether this
00:21:48.24 is a natural outbreak. Is it a malevolent deed? Where is it coming
00:21:54.26 from? And this is an interesting story. Now West Nile virus
00:22:02.00 causes an encephalitis-type disease. But it had never been found
00:22:06.26 in the Western hemisphere. And this is several years ago now.
00:22:12.14 And the way it started was that birds in the Bronx zoo started to die.
00:22:17.25 And they had an encephalitis-type infection. And a vet in the Bronx zoo
00:22:24.02 sent her tissue samples to the CDC--Center for Disease Control--
00:22:28.21 and they were pretty overwhelmed because the CDC never has
00:22:32.17 enough money to do everything they have to do and they sort of
00:22:36.16 said, "Yeah, we'll get to this. Birds are dying." Well, at the same time
00:22:40.27 there was an increasing number of human patients in New York City,
00:22:44.22 which were exhibiting and dying from an encephalitis-type disease.
00:22:49.22 People thought it was the mosquito-born St. Louis encephalitis virus.
00:22:55.04 They didn't really know. Then the chief of Emergency Management
00:23:01.07 in New York City managed to co-opt the entire supply of "Off."
00:23:07.02 "Off" is something that kills mosquitoes and flying bugs, and he
00:23:11.15 just sprayed "Off" all over the city and he stopped the epidemic
00:23:15.21 cold. Meanwhile, the lady vet at the Bronx Zoo was still trying
00:23:21.08 desperately to find out why her birds were dying. Waiting to hear
00:23:25.15 something from the CDC, and the weeks were going on and she
00:23:29.23 happened to go to a wedding on the West Coast and sitting
00:23:34.01 next to her at this wedding was a virologist. And not particularly
00:23:39.15 interested in dancing, they started talking about this odd thing
00:23:43.23 that was happening to her birds at the zoo. And he said, "Look,
00:23:48.01 why don't you send me some of her tissues, and I'll try to figure out what
00:23:51.02 you've got." And that's what happened. He very rapidly identified
00:23:55.17 this as West Nile Virus. Now everyone's initial reaction was,
00:24:01.26 "This couldn't be. We don't have West Nile Virus in the Western
00:24:04.18 hemisphere!" But at about that time, in Fort Collins, the CDC had
00:24:10.06 in fact identified this as well as West Nile Virus. It just took too long.
00:24:18.23 And this was our first experience with trying to rapidly identify
00:24:23.18 something new. Now, interestingly, concurrently while all of this
00:24:28.18 was going on, an Iraqi defector had reported that Saddam Hussein
00:24:34.24 was developing a strain of West Nile Virus as a biological warfare
00:24:39.22 agent and was preparing to release it. This was never confirmed.
00:24:44.12 Was this a BW event? We don't know. Did this come into the United
00:24:50.08 States on a 747 that a mosquito happened to crawl into? We don't
00:24:55.22 know. We don't know the answer, but what's important--what one
00:25:00.20 has to remember--is anything we do to identify a new outbreak
00:25:05.28 will be relevant no matter what the source is--malevolent or natural.
00:25:11.10 The problem is to understand what we've got and to rapidly
00:25:15.19 understand how we can analyze these things and identify the
00:25:20.04 agents. Now, this is changing. And this is changing particularly because
00:25:26.08 of what we found with SARs. Now that's happened fairly recently.
00:25:30.22 SARs is Severe Acute Respiratory Syndrome. It's caused by a
00:25:36.14 corona virus, which is an RNA virus. It's similar to the viruses that
00:25:42.17 cause the common cold. It has a very high potential for natural evolution
00:25:47.21 so it can change itself a lot. Now with SARs--it's an interesting story
00:25:54.21 because this is an infection that first started predominantly in
00:25:59.08 Hong Kong and Beijing and Guangdong Province in China. But
00:26:03.26 very rapidly appeared in Toronto. And what happened there
00:26:08.11 is that we had a highly infectious agent that exemplifies this
00:26:13.08 global village we live in. There was a scientific meeting in Hong Kong.
00:26:17.02 Someone got sick. They wound up in Toronto and it was all
00:26:20.11 over the place. But SARs is an example in which we were much better
00:26:24.26 at identifying the agent rapidly by sequencing. We were also
00:26:30.26 able to realize that the only thing that would be effective
00:26:34.14 was quarantine. And this is interesting because in fact
00:26:40.06 Singapore was very effective in quarantine. They said, "This is
00:26:45.24 what we have to do to stop this." Whereas Hong Kong and Toronto
00:26:49.16 were not. Ultimately it stopped. The dealing with this was very effective.
00:26:58.17 And actually there were very few deaths if you look at it in a global way.
00:27:03.12 But the effect on the economy was enormous. And so this tells
00:27:08.03 us that even a minor outbreak is going to have severe economic
00:27:12.25 implications globally. And what it did do though was help the World
00:27:18.23 Health Organization build a network of reporting, of understanding, of
00:27:25.07 diagnosing outbreaks of diseases everywhere in the world. So
00:27:29.16 that we would know how to respond and deal rapidly with them.
00:27:33.05 Now what I'm going to do is end this talk with a discussion of something
00:27:38.14 that's facing us all right now. And that's Asian bird flu H5N1.
00:27:45.22 This causes influenza. Influenza is with us all the time, various
00:27:50.25 different kinds of strains. This is a particularly frightening
00:27:54.03 one. However, there is no strong evidence as yet of human-
00:27:59.09 to-human transmission. Right now, this is a disease of birds--
00:28:04.26 local fowl, poultry, wild birds. Our concern is that H5N1, which
00:28:13.01 mutates rapidly, will ultimately go from person to person.
00:28:19.16 Now, let me tell you a little bit about this virus because it's relevant.
00:28:24.22 Each virus has a single strand of RNA containing 8 genes.
00:28:31.00 Each gene encodes a single protein. This very high mutagenicity
00:28:36.20 rate, in other words changing the kind of protein that's made
00:28:40.24 from each gene, can happen by reassorting the genes by
00:28:44.22 single-base mutations. And it just changes rapidly. That's
00:28:48.11 why we get flu shots every year. And basically at this time
00:28:54.14 we know that the transmission of H5N1 goes from ducks to
00:29:00.20 either wild birds or to some cats, tigers, lions, leopards, house pets
00:29:06.25 with a fairly easy transmission. However, from wild birds to humans
00:29:14.10 does occur. It's not easy. You need very personal contact.
00:29:19.15 And humans to humans--there's not strong evidence of that yet.
00:29:25.15 Our concern is that it might happen. And so what is H5N1 mean
00:29:31.03 anyway? "H "stands for hemaglutinin and that is a protein that sits
00:29:38.00 on top of that cage that the RNA sits into. The function of
00:29:43.05 that hemaglutinin is to allow the virus to bind to the host cell
00:29:48.23 and allow entry of the RNA to do its bad stuff. "N" stands for
00:29:55.21 neuraminidase. Neuraminidase is another kind of protein
00:29:59.05 that's also sitting on the surface of the cell and it allows
00:30:02.28 newly formed viruses to escape and infect other cells. We have
00:30:09.03 two anti-virals out there now. One is called Tamiflu.
00:30:12.25 The other is Relenza. And the neuraminidase is the target for both
00:30:17.13 of these. And in fact, the best way to use something like Tamiflu
00:30:23.04 is if you've not been infected yet, it will give you 80% protection
00:30:28.12 for awhile. If you've been infected, it will drop the viral load so that
00:30:34.05 you're not as contagious. You'll still get sick but you won't
00:30:37.09 be as sick. Now if we look at the history of flu viruses, the most serious
00:30:46.04 flu pandemic occurred in 1918 and that influenza was H1N1.
00:30:53.20 It killed 40 million people worldwide and H1N1 means a particular
00:31:00.06 derivative of the hemaglutinin and the neuraminidase. 1957
00:31:05.26 flu was H2N2--killed about 2 million people. 1968--H3N2 killed about
00:31:13.19 a million. I know that one very well because I caught that one.
00:31:16.20 And let me tell you--a real flu infection is no fun. Their current
00:31:22.10 Asian bird flu is H5N1 as I've said. Scary thing about this guy
00:31:27.11 is that right now it has a 50% kill rate, which is enormous.
00:31:32.06 And humans have no immunity against H5, whereas we have some
00:31:37.10 against H1, H2, and H3, which has been around for awhile.
00:31:42.14 So what needs to be done? How are we going to deal with this?
00:31:48.10 Let me just tell you first that using something like Tamiflu
00:31:56.10 is best done in my opinion not by sprinkling Tamiflu amongst
00:32:02.21 the 30 million people in the world but rather using it where there's
00:32:07.23 a hot spot. Now that we have an entire network of reporting
00:32:15.16 coming all over the world, keeping their eyes out for hot spots
00:32:20.00 of sudden break outs of H5N1, possibly being passed from human to
00:32:26.02 human, then our Tamiflu has to get there immediately. And then
00:32:31.27 what you do, is you cordon off the area, quarantine, treat with
00:32:36.18 Tamiflu, and start vaccines. Now clearly the vaccine we have now
00:32:41.26 is to the H5N1 that only goes between birds and possibly cats.
00:32:48.06 What we will ultimately need--if this happens--if it mutates to
00:32:53.08 human-to-human is that we then have to get a new vaccine
00:32:59.11 that will be against that particular variant. And a lot of work
00:33:04.04 is going on right now by many small companies and many
00:33:06.27 large pharmaceutical houses to be ready to make this as quickly as
00:33:11.13 possible. Now one thing that is important to realize is that
00:33:18.27 vaccines are made in eggs. I mean zillions of eggs. If you go to one of these
00:33:24.13 vaccine production places, it's astonishing. It's like a football field
00:33:28.05 of eggs. And virus gets injected into these eggs and then a high titer
00:33:34.14 of more viruses made that's impaired. You kill it. You then make
00:33:39.03 the vaccine. The reason that we use eggs is that you get a very high
00:33:43.17 titer. One thing that I can't stress too strongly is that in fact
00:33:49.22 you can't get flu from a flu shot. It's dead. But you certainly can
00:33:56.26 get immunity. But people seem to think that vaccines are an
00:34:03.17 absolute panacea. It's not true. Flu vaccines are 70-90% effective
00:34:10.15 in young healthy people and only 40-60% effective in people over
00:34:17.11 65. So that the flu alone is not going to save us. But there are
00:34:23.20 many things that we can do to help ourselves. One of the things
00:34:28.26 we have to do is that we have to stockpile face masks--the kind
00:34:32.19 you buy in the hardware store for painters--syringes, medical
00:34:38.23 supplies, food, and water. Currently we do not have in the United States
00:34:44.06 enough ventilators if we were to have a pandemic. So it's extremely
00:34:48.05 important that we learn how to deal with large amounts of people
00:34:54.13 becoming ill. So what if we do get a pandemic? What does a
00:34:57.19 country do? And what I'm going to do is end with sort of an
00:35:01.27 economic part and that is in ordinary times economic logic does
00:35:07.07 not dictate pandemic preparedness. We all keep low inventories.
00:35:12.29 We don't want redundancy in reserves. We have lots of offshore
00:35:20.00 drug production because it's cheaper. We don't guarantee the
00:35:24.11 purchase of flu drug as we do with other kinds of weapons.
00:35:27.16 In fact we have just in-time delivery with no surge capacity.
00:35:32.24 Now what does this mean if you have a pandemic? The supply
00:35:38.10 chain is very thin. Every hospital contains only 30 days of drugs.
00:35:42.19 We have, in a pandemic, workers becoming ill. Drug company
00:35:49.22 workers, the production of new vaccines and new drugs will become
00:35:53.09 less. And in fact, we'll have borders closed and embargos. They
00:35:59.13 can't get in. Truck drivers get sick. Things can't be delivered.
00:36:03.13 We then have to say, "Alright, what do we need to do to deal
00:36:09.05 with this?" We need scaled-up manufacturing and stockpiling of
00:36:13.27 vaccines and anti-viral drugs, as well as antibiotics because
00:36:18.18 many people die of flu infection by a secondary bacterial infection.
00:36:24.02 So we need antibiotics. There's a pneumococcal vaccine that is
00:36:29.02 something people should all have that helps. We need better
00:36:32.19 surveillance and epidemiology on a global scale, very accurate
00:36:37.06 reporting of case clusters. We need actual procedures for drug
00:36:42.02 delivery and most important, we need quarantine laws. Not only
00:36:47.09 here in the United States but everywhere in the world. And
00:36:50.09 our population has to understand what these population laws,
00:36:55.17 what these quarantine laws, are before we're faced with the
00:37:00.22 absolute disaster of a pandemic. And you have to know what
00:37:06.24 you're supposed to do in a quarantine, where you'll get your medicines,
00:37:10.21 who will see you. And this can't be done just at a national level.
00:37:15.01 It has to be done in cities and towns where groups of people
00:37:19.03 can work together. That's probably the strongest thing. Now
00:37:23.28 let me just end by turning this back to what are the things that needs
00:37:28.25 to be done with this emerging infectious diseases with the way
00:37:33.16 in which our world has changed and the basic science that's
00:37:37.05 going on. So we have now a real need to increase basic research
00:37:44.14 to understand these viral and bacterial pathogens. We have to
00:37:48.21 identify genes essential for the pathogen's survival. We have to
00:37:53.09 sequence and compare bacterial and viral genomes. We have to
00:37:57.16 identify virulence factors and resistance genes and understand
00:38:03.06 how they work. And as I said in my previous lecture, by understanding
00:38:09.01 how the bacterial cell carries out all of its functions to let them grow
00:38:14.17 and divide, we have identified new targets and designed new
00:38:19.19 antibiotics. That's just one lab. And this has to happen in many
00:38:23.05 many more. The second thing that we have to do is design
00:38:26.12 and stockpile new vaccine strategies and in fact make combination
00:38:31.27 antibiotics where you have a particular drug that kills the bug
00:38:37.19 but in that same pill or shot you've got a compound that prevents
00:38:43.00 the resistance from being expressed. And then finally for epidemic
00:38:47.21 control, we have to develop techniques for very fast--hours, not
00:38:52.28 days, not like what happened with West Nile or even the slowness
00:38:57.13 of SARs, which was much better--to identify causative agents.
00:39:02.08 To do this, we have to exploit viral and bacterial DNA sequence-
00:39:07.01 based technologies. We need, as I keep saying, an increased
00:39:11.02 network of surveillance and reporting protocols and finally
00:39:14.19 return to the historical use of quarantine. If we all work together
00:39:20.07 and if we realize that we are not just independent islands
00:39:24.26 and separate countries, we work together as a global village
00:39:28.25 and help us combat these things. So with that, I'd like to thank
00:39:33.10 you very much.

  • Part 1: Dynamics of the Bacterial Chromosome

Animal coloration research: why it matters

While basic research on animal coloration is the theme of this special edition, here we highlight its applied significance for industry, innovation and society. Both the nanophotonic structures producing stunning optical effects and the colour perception mechanisms in animals are extremely diverse, having been honed over millions of years of evolution for many different purposes. Consequently, there is a wealth of opportunity for biomimetic and bioinspired applications of animal coloration research, spanning colour production, perception and function. Fundamental research on the production and perception of animal coloration is contributing to breakthroughs in the design of new materials (cosmetics, textiles, paints, optical coatings, security labels) and new technologies (cameras, sensors, optical devices, robots, biomedical implants). In addition, discoveries about the function of animal colour are influencing sport, fashion, the military and conservation. Understanding and applying knowledge of animal coloration is now a multidisciplinary exercise. Our goal here is to provide a catalyst for new ideas and collaborations between biologists studying animal coloration and researchers in other disciplines.

This article is part of the themed issue ‘Animal coloration: production, perception, function and application’.

1. Introduction

Since its foundation at the turn of the nineteenth century by luminaries including Alfred Russel Wallace, Edward Poulton, Abbot Thayer and Charles Darwin, animal coloration research has contributed to an increasing breadth of scientific disciplines. Use of colour phenotypes as genetic markers to study developmental processes and natural selection in the wild was critical to the early development of genetics and evolutionary theory. Later, Hugh Cott's [1] important volume on the adaptive coloration of animals changed the way we think about the functional significance of colour patterns. As technologies advanced, biologists turned their attention to colour perception, particularly of ultraviolet wavelengths, recognizing that other animals see the world very differently compared to humans. Most recently, the discovery of photonic crystals in nature [2] has led to a surge of research on structural coloration and its biomimetic applications. Both the diversity of areas encompassing modern animal coloration research and the rapid pace of developments in each make it a particularly exciting interdisciplinary field.

This volume provides an entry point to recent developments in the main areas of animal coloration research: colour production, perception, function and evolution. All the topics covered in this special issue touch on the interdisciplinary nature of such research, which now straddles optical physics, genetics, physiology, psychology, functional morphology, behavioural ecology and evolution [3]. But animal coloration research not only draws on many disciplines, it also contributes to fundamental knowledge in those disciplines and generates solutions to societal problems. Contributions to this themed issue primarily focus on advances related to fundamental knowledge. However, many novel connections between basic and applied research are emerging, especially in terms of colour production, perception and function, and we highlight these here.

2. Production of colour

Colour in nature is remarkably diverse and often visually stunning. It is produced by both chemical pigments, which absorb certain wavelengths of light, and by physical structures on the scale of hundreds of nanometers, which manipulate light in varied ways. Such structural colour is of particular interest for the development of artificial materials because it can be astonishingly vivid, produces a range of optical effects (iridescence, polarization, metallic sheens, anti-reflection) and has specific features. First, structural coloration is durable, lasting as long as structures remain intact. Second, the remarkable range of optical effects is produced by few types of renewable material (e.g. chitin, keratin, guanine [4,5]). Third, biological materials are self-assembled, such that highly ordered structures are produced within such materials through local cellular processes. Last, animal surfaces combine colour with a range of other desirable properties such as resistance to abrasion and bacterial degradation, water repellency (hydrophobicity) and photoprotection. All of these features are often desirable for artificial materials thus, materials scientists and engineers increasingly draw on the diverse structural variation in nature to inspire new technologies and provide blueprints for materials design [6–11].

Synthetic photonic structures were produced well before they were discovered in nature [2] but have now been characterized in numerous species spanning a broad range of animal groups (particularly birds, beetles, butterflies, cephalophods and fishes) as well as single-celled organisms (diatoms) and plants. Natural photonic structures have already inspired development of many coloured materials including pigment-free (i.e. structurally coloured) cosmetics, textiles, paints, various optical coatings, security labelling or anti-counterfeiting technologies (e.g. metallic holograms on credit cards and banknotes), optical devices that focus or polarize light, various sensors and technologies to improve the efficiency of solar cells [8,11]. Perhaps most famously, the structural properties of the iridescent blue wings of Morpho butterflies have been mimicked in the development of pigment-free cosmetics and iridescent blue ‘Morphotex®’ fabric (figure 1a,b).

Figure 1. Examples of nature (a,c,e) and the mimicry it inspires (bottom). (a) Morpho butterfly and (b) dye-free Morphotex ® fabric (c) compound eye of the housefly and (d) the ‘bee-eye’ camera lens (e) cryptic camouflage of a nightjar and (f) a stealthy sniper. Image credits: (a) Wikimedia Commons (b) Donna Sgro (c) Thomas Shahan (d) John Rogers (e) Jolyon Troscianko (f) Realtree/Caters News.

The key parameters determining optical properties of photonic structures are the size, spacing and regularity of the optical elements, as well as the ratio of the refractive index of the structure's component materials (e.g. chitin, keratin or guanine versus intervening air or cytoplasm). Optical properties can also be influenced by external factors such as pH, temperature, humidity and electromagnetic fields [11]. Many animals that change colour do so in response to such external stimuli and these changes can involve structural colour [12]. This is important in the development of ‘smart materials’ (materials with properties that change in response to external stimuli) and various optical sensors, including humidity, thermal and chemical sensors. For example, the Hercules beetle (Dynastes hercules), which changes colour with varying humidity, has inspired the development of highly sensitive humidity sensors [13] and the quasi-ordered collagen arrays in turkey skin have inspired sensors that change colour in response to target chemicals [14]. These are just a couple of the rapidly growing number of examples of biomimetic or bioinspired technology based on ‘tuneable’ structural colour [9,15,16].

Nanophotonic structures produce a wide range of optical effects in addition to colourful, reflective surfaces. Moth and butterfly eyes have anti-reflective surfaces on their corneas, which reduce reflectivity by a factor of 10 and aid vision in low light conditions [6]. Similarly, various insects have transparent, anti-reflective wings, which enhance camouflage, and anti-reflective coatings have recently been discovered in deep-sea crustaceans [17]. These structures have inspired the design of coatings to improve anti-reflective properties of windows and lenses, and solar cells to increase energy capture and to expand the performance of light-emitting diodes [10]. The biomimetic potential of other optical properties of natural structures, including structurally-assisted blackness and ultra-whiteness, is now being explored [10,18,19]. Notably, many natural materials combine multiple optical elements into sophisticated structures to produce diverse optical effects. For example, many butterfly wings combine both one- and two-dimensional photonic crystals, as well as an element of irregularity or disorder, that increase the angle of scattering such that the colours are apparent from a broader range of viewing angles [5,20].

In addition to optical properties, it is important to contemplate other properties of materials, such as their stability, durability, mechanical and thermal properties. This requires consideration of multiple components of the solar spectrum including ultraviolet (280–400 nm), visible light (400–700 nm) and near-infrared (700–2600 nm) radiation. Ultraviolet radiation causes chemical reactions that damage biological (eyes, skin, etc.) and synthetic materials, and visible and near-infrared reflectance are both important to surface heat gain because approximately 50% of direct solar radiation falls within each of these wavelength bands. Development of nanophotonic-enabled smart materials to control environmental energy flow, including solar radiation, is burgeoning. For example, ‘cool coatings’ for roofs and buildings can be used to mitigate the ‘urban heat island’ effect and reduce energy use [21]. Such materials reflect a higher proportion of near-infrared radiation than similarly coloured ‘standard’ coatings. The biomimetic potential for manipulating both visible and near-infrared reflectance is significant (although yet unrealized) because in plants and animals, visible and near-infrared reflectance and the relationship between them can vary substantially [22]. Living organisms have already solved design challenges associated with colour and heat in myriad ways over millions of years of evolution, providing rich opportunities for development of biomimetic and bioinspired materials.

3. Perception

As with biomimetic colour production, the number of applications inspired by animal visual perception has proliferated in the past decade.

(a) Cameras and sensors

Studying diverse animal visual systems has provided engineers with new solutions for the design of better imaging technology and artificial sensors. The typical digital camera, which houses a photosensitive chip (e.g. a CCD or a CMOS sensor) behind a lens with a single aperture, was modelled on the human visual system [23]. Our eyes use a lens to focus the light on the retina, where rods and cones then convert the image into electrical impulses, triggering a cascade of visual processing. Conventional digital cameras can be powerfully applied to many imaging tasks, but they are often bulky, computationally costly and constrained in their field of view. For these reasons, interest in non-human eye designs—especially the compound eyes of arthropods—has exploded [23,24].

Compared with simple vertebrate eyes, compound eyes are compact and lightweight, providing a wide field of view with high temporal resolution, given their tiny packaging [25]. Mimicking these properties in cameras and sensors is giving way to a new generation of imaging technology. Recently, we have seen the invention of a ‘bee-eye’ camera with a 280-degree field of view (figure 1c,d [26]), a miniature curved artificial compound eye [25], a digital camera covered with 180 artificial ommatidia, inspired by eyes of fire ants Solenopsis fugax and bark beetles Hylastes nigrinus [27], and the development of hyperacute visual sensors based on retinal micro-movements in flies [28]. This new fleet of imaging technology has important consequences for surveillance, medical endoscopy, smart clothing, robotics and drones [24,25,29].

As biomimetic efforts in imaging and sensing continue, we expect to see increased emphasis on colour processing and colour discrimination—which will require detailed knowledge of colour vision systems across animal taxa. Consider nocturnal helmet geckos Tarentola chazaliae, which possess large colour cones that are 350 times more sensitive than those of humans at the colour vision threshold [30], or the mantis shrimp Haptosquilla trispinosa. Despite the shrimp having 12 different photoreceptor types, they appear to be deficient in fine colour discrimination [31] and may in fact scan objects to rapidly recognize basic colours, though this idea needs further testing. It is only a matter of time before new camera systems exploit increased colour sensitivity, as in geckos, and rapid colour processing, as in mantis shrimps.

Breakthroughs in night vision technologies are also on the horizon. How are so many nocturnal insects able to see colour, identify visual landmarks, orient using celestial cues and detect faint movements, all in low light? A recent hypothesis [32] is that insects achieve this through a process called neural summation, in which the light received by groups of neighbouring ommatidia is summed up, greatly improving the signal-to-noise ratio in low light. A night vision computer algorithm designed to mimic neural summation successfully recovered colour and brightness detail from videos filmed at night [32]. Algorithms like this may soon be incorporated into night vision technology, which has extensive military, monitoring and navigation applications. In addition, a new artificial fish eye, designed to mimic the light-focusing crystalline microstructures in the elephantnose fish Gnathonemus petersii retina is capable of resolving images in very low light [33].

(b) Liquid crystal displays and optical devices

Polarization transformation, or the act of converting linear polarized light to circular polarized light and vice versa, is essential to the design and operation of LCD displays, optical storage (CDs, DVDs and Blu-ray Discs) and even three-dimensional movie technology. Usually polarization transformation is performed by an optical device called a waveplate. The discovery that a special class of photoreceptor in the peacock mantis shrimp Odontodactylus scyllarus can efficiently convert polarized light has major implications for the optical device industry. These photoreceptors, called R8 cells, detect polarized light and then shift the plane of polarization, turning circular polarized light into linear polarized light. The shift occurs because R8 cells contain arrays of small folds called microvilli, the membranes of which are birefringent (e.g. their refractive index depends on the direction of polarization of light). The arrangement and structure of the microvilli causes the R8 cell to act as an achromatic waveplate over a wide range of wavelengths [34]. Inspired by the R8 cells, a team used thin films to fabricate a multilayered, birefringent structure which functions as an achromatic waveplate over a broad spectrum [35]. The result, an artificial waveplate with highly desirable optical properties, could transform the optical device industry. The artificial waveplate is an advance because, unlike most synthetic waveplates, its performance does not depend on wavelength.

(c) Computer vision and robotics

Principles of animal vision—especially human vision—have been a driving force behind computer vision and machine learning. The deep synergies between biological and computer vision have been reviewed recently [36,37]. Here, we briefly highlight two developments in the active field of bioinspired computer vision. First, a central goal of computer vision is to extract salient features from a scene historically, algorithms have used intensity-based (achromatic) descriptors only. However, colour is now being incorporated into many computer vision models [38,39], with a focus on fundamental aspects of human colour vision, including colour opponency [40] and colour constancy [41].

In addition, there appears to be a steady shift toward studying non-human visual systems in the context of computer vision, largely motivated by the desire to build robots that can navigate in ways and in environments that humans cannot. Honeybees, for example, have become a model system for the study of visually guided flight [42]. When a bee flies through a narrow passage, it balances the speed of image motion detected by the two eyes this keeps the bee from colliding with either side of the passage. Similar novel algorithms are being used to program autonomous terrestrial and aerial vehicles [42]. Desert ants Cataglyphis spp. have also influenced new navigation solutions. Capable of finding their way back to nests after foraging hundreds of metres away in the desert, these ants rely on polarized light to return home. Recently, a research team designed a robot which effectively navigates using an ant-like polarization sensor [43]. Finally, new infrared sensors, inspired by specialized IR-sensing structures in fire-loving Melanophila beetles, have been developed [44] and could be used in robots trained to survey dangerous fire zones. These advances underscore the continued importance of studying diverse visual (and, in the case of IR, thermomechanical) systems in the context of robotic navigation.

(d) Biomedicine

One of the most exciting advances in applied colour vision involves bionic devices, which are designed to restore some visual perception to blind patients. Based on the retina of the human eye, the Argus® II Retinal Prosthesis System (Second Sight, Sylmar, CA) is an implant that electrically stimulates the retina, inducing visual perception. The device consists of a 60-electrode ‘retina’, which is surgically implanted, plus a camera worn on glasses and a small video processing unit (VPU). The camera captures the visual field and sends the information to the VPU, which translates the scene to a series of electric pulses on the 6 × 10 ‘retina’ array. Remarkably, blind patients fitted with the Argus II showed considerable improvement in spatio-motor tasks [45] and a small improvement in colour perception [46].

4. Functional considerations

As this themed issue will show, coloration has multiple consequences for both non-humans and humans, and the latter extend into recreational activities, aspects of culture, the realm of defence and even conservation of biodiversity.

(a) Competitive sports

Parallel areas of research bear on the issue of external coloration in competitive sports. First, in a handful of non-human primates, red signals social status, as in male gelada Theropithecus gelada [47], drills Mandrillus leocophaeus [48] and mandrills Mandrillus sphinx [49]. Second, in humans, facial redness is associated with anger in some populations (blushing aside [50]). Furthermore, human subjects perceive themselves as being more dominant or aggressive when they choose to wear red clothes [51] and the heart rate of red dressers is elevated in the context of physical combat [52]. Interestingly, men but not women perceive red subjects as more dominant [53].

These issues likely have consequences for success in sports and indeed, a related body of work shows that red clothing has an incremental positive impact on contest outcome in one-on-one sports where opponents are evenly matched. These sports include boxing, tae kwon do, Greco-Roman wrestling and freestyle wrestling [54]. Moreover, in the lucrative professional soccer arena, in home games the team that wears red jerseys is more likely to win [55]. While some of these effects may be due to differential treatment of red-clad competitors by referees [56], the discovery that red goalkeepers save more penalties suggest players’ own perceptions are involved [57].

There seem to be a variety of responses to red clothing including aversion [58], reduction in speed of approach [59] and higher arousal [60], but the underlying mechanisms are opaque: red might signal health, blood oxygenation or flux, diet, or ability to mobilize testosterone. Certainly red appears to signal dominance in several vertebrate groups and is innately avoided in some taxa [61]. This is a field of enquiry that needs to be extended to other colours and across other team sports incorporating referee bias. The influence of clothing colour in sport is big business: there are huge financial implications because of betting and advertising revenue.

(b) Fashion

Colour is an integral part of both clothing and cosmetics. For example, some studies have demonstrated that Caucasian men find women wearing red to be more attractive than those wearing blue, and show a greater willingness to date them and spend money on them [62] others have shown that Caucasian women are aware that red makes them appear more attractive in that they alter facial expressions [63] and are more likely to wear red when looking for casual sex [64]. Yet other studies have shown that women perceive other women in red as being disreputable [65]. Thus far, research has mostly concentrated on red coloration with scant academic attention paid to other colours [66], although differences among individuals in perception of a blue dress has attracted much attention on social media [67].

Clothing has involved use of animal products starting from hides worn by archaic humans to silk produced by silkworms to women's hats made out of feathers, but recently there has been a surge of interest in biofabrication. For example, a dress has been constructed out of structural fibres similar to a Morpho's wings, and microbes are being harnessed to produce clothes constructed of cellulose. Companies include Bolt Threads, BioLoom, Modern Meadow, Biocouture, Pembient and BioFur. Practical examples aside, clothing fashions have yet to be seriously scrutinized using biological principles. Certainly, fashion changes very rapidly, suggesting a Fisherian runaway process but this may be only a superficial comparison and does little to explain how the colour of clothing is related to illumination (e.g. brighter clothes in the tropics), temperature (e.g. whiter clothes at lower latitudes), or a variety of cultural variables such as marriage practices.

Apart from clothing, cosmetics are another method of changing external appearances and principally involve four components: colouring the lips to perhaps highlight verbal communication and kissing decorating cheeks to make them appear redder, mimicking coloration associated with health and blood oxygenation and accentuating the size and shape of eyes. Eyebrow and eyelid make-up may enlarge the apparent distance to the eye and make the eyebrow more conspicuous, mimicking an eyebrow flash [68]. Women who use cosmetics are attractive to some men [69] and can influence people's behaviour, including tipping. Changing epidermal coloration is not limited to the face, however, as seen in tanning in some Western societies [70] and application of dyes and coloured soils in ceremonies in former and current non-Western societies. Information on altering skin colour is reasonably well documented in Caucasians, but comparative understanding geographically and historically across societies needs much more attention [71].

(c) Military

Military tactics demand deception (e.g. dazzle coloration and observation post trees), camouflage (e.g. clothing and netting covering equipment), concealed movement (e.g. at night and hugging features of the landscape) and decoys (e.g. constructing false vehicles and buildings) that have many parallels in animal external appearances and behaviour (figure 1e, f [72]). These analogies were not lost on the military and in the past century commanders reluctantly drew on biologists to inform some of their field operational techniques. Famously, Abbott Thayer developed countershading for submarines and ships, Norman Wilkinson and John Graham Kerr established dazzle coloration for shipping, and Hugh Cott constructed decoys in the North African desert. Yet a close inspection of their and others’ achievements reveals that they actually used their biological expertise in the form of intuition rather than deriving military tactics from first principles in biology [73], although they did use the scientific method to investigate forms of camouflage and deception.

A major problem for the military is that personnel and transport must often be moved and will thereby encounter different backgrounds, different weather and different lighting conditions, so there is often no single solution to remaining concealed. Form, shadow, texture, colour and movement all have to be taken into account when considering transport, stationary equipment and people (e.g. [74]). Nowadays, modern armies, navies and airforces are more open to working with scientists who bring new methods to describe camouflage patterns and coloration [75] and visual tracking [76] to the table.

Rapid contemporary changes in weaponry involving heat detection, night vision, new explosives and suicide bombing are driving the search for new defences including invisibility, uncovering explosive signatures at the molecular level, and in using the background to modulate colours of personnel and vehicles. The extent to which principles of animal coloration such as masquerade can be linked to military deception, disruptive coloration and background matching to uniforms, and dazzle coloration to transport, are open, interesting and important questions.

(d) Wildlife management and conservation

Policymakers, engineers and scientists involved in colour research are collaborating on solutions to reduce wildlife–human conflict. Here we mention two case studies. First, in the USA alone, bird collisions—many of which are with buildings—may be responsible for almost one billion bird deaths per annum [77]. However, the use of patterned glass with UV-reflecting components (visible to birds but not to humans) might reduce collisions by 60%, and these design features are making their way into construction [78]. Moving forward, UV-reflecting glass should account for variation in avian UV perception [79]. Second, sensory-based conservation could also help solve the problem of ‘polarized light pollution’ (PLP) [80]. PLP is created when sunlight reflects off man-made smooth, dark surfaces (such as buildings, asphalt roads, glass panes) and becomes linearly polarized. These human products resemble the surface of dark waters, which are the most common natural polarizer. As many animals have refined polarization vision, the rise of anthropogenic PLP will affect behaviour and ecology of many taxa. This is already happening: male dragonflies establish territories on cars and females lay their eggs there, waterbirds crash-land on asphalt parking lots (although the influence of PLP is contentious here) and aquatic insects such as caddisflies land on glass structures, only to be picked off by opportunistic birds [81]. The introduction of materials that reduce surface polarization (e.g. rougher, brighter asphalt) could dramatically reduce the negative impacts of PLP on animals in the urban environment.

As external appearances are an integral part of protective coloration and signalling, changes in lighting, background environment, or the medium through which colour signals are transmitted will likely lead to population changes in external appearances [82], which could be used as bio-indicators of pollution. The most famous historical example is melanism in the peppered moth Bison betularia [83] a more contemporary example is that melanism in several taxa may rise as global warming-induced fires increase (as in pygmy grasshoppers, Tetrix subulata [84]). Many other environmental changes are occurring. For example, as mangrove acreage declines with sea-level rise, changes in colour frequencies can be expected in Bornean gliding lizards Draco cornutus that match the colours of freshly fallen leaves in either mangroves or rainforest [85] and as snow cover declines with global warming, populations of Alpine rock ptarmigan Lagopus muta and snowshoe hares Lepus americanus will dwindle [86,87]. In aquatic environments, where particulate matter in water absorbs short wavelengths causing a shift towards orange and red, similar evolutionary colour changes can be expected. For example, turbidity driven by eutrophication interferes with mate choice in cichlids based on their coloration and promotes species hybridization [88], whereas turbidity brought on by phytoplankton blooms reduces nuptial coloration in sticklebacks Gasterosteus aculeatus affecting both scale coloration and honest signalling [89]. Colour shifts are conspicuous markers of subtle anthropogenic change.

A separate issue is that conservation donor support and political interest often hinge on flagship species. Many of these species are conspicuously coloured, such as the golden toad Incilius periglenes. Since brightly coloured species are arresting and memorable, these seemingly insignificant factors can tip the balance in garnering the necessary political will to set up protected areas such as Lake Nakuru National Park for flamingoes Phoenicopterus roseus and P. minor in Kenya, the El Rosario monarch butterfly Danaus plexippus sanctuary in Mexico, and Wolong National Natural Reserve for giant pandas Ailuropoda melanoleuca in China. Coloration is an unrecognized factor in shaping conservation policy.

5. Conclusion

By highlighting numerous applications of animal coloration research, we hope to underscore its broader importance and impact. Exploiting the potential of animal coloration for biomimetic and bioinspired applications entails many components. These include characterizing the complex structures producing various colours and modelling their optical effects characterizing the neurophysiology of colour vision developing methods to reproduce biological structures and systems (e.g. top-down construction, self-assembly, cell culture) and developing ways to mass-produce technologies efficiently and cost-effectively. This is a truly multidisciplinary exercise, requiring collaboration between biologists, physicists, materials scientists, chemists and engineers. Understanding the function and evolution of animal coloration also has implications for a broad range of societal issues from sport and fashion to military camouflage and wildlife management, necessitating conversations between biologists and social and political scientists. For biologists, the goal is to unravel the fundamental biology underlying colour production, perception, function and evolution, whatever its application. It is around these themes that this special issue is organized.

Competing interests

The authors have no competing interests.


No funding has been received for this article.

How belly fat differs from thigh fat -- and why it matters

Researchers discover that the genes active in a person's belly fat are significantly different from those in his or her thigh fat, a finding that could shift the way we approach unwanted belly fat -- from banishing it to relocating it

Sanford-Burnham Prebys Medical Discovery Institute

IMAGE: Steven Smith, M.D., directs the Florida Hospital -- Sanford-Burnham Translational Research Institute for Metabolism and Diabetes. view more

Credit: Sanford-Burnham Medical Research Institute

ORLANDO, Fla., January 11, 2013 - Men tend to store fat in the abdominal area, but don't usually have much in the way of hips or thighs. Women, on the other hand, are more often pear-shaped--storing more fat on their hips and thighs than in the belly. Why are women and men shaped differently? The answer still isn't clear, but it's an issue worth investigating, says Steven R. Smith, M.D., director of the Florida Hospital - Sanford-Burnham Translational Research Institute for Metabolism and Diabetes. That's because belly fat is associated with higher risks of heart disease and diabetes. On the other hand, hip and thigh fat don't seem to play a special role in these conditions.

In a study published in the Journal of Clinical Endocrinology and Metabolism, Smith and colleagues help explain this discrepancy by determining how belly and thigh fat differ genetically. This research might shift common thinking about fat--rather than focusing on how to banish belly fat, perhaps we need tip the balance in favor of heart-friendly fat in the lower body. In that case, the study also provides a first step toward aiming treatments at specific regions of the body, especially those that contribute most to the complications of obesity.

Belly fat genes vs. thigh fat genes

Smith and colleagues first took fat samples from men and women. Then they compared the genes most active in belly fat to those most active in thigh fat.

Here's what they found: The genes operating in a person's thigh fat are hugely different from those in his or her belly fat. For men, 125 genes are expressed differently in the belly than in the thighs. For women, it's 218 genes (most are unique to women, but 59 genes are the same as those that varied in male fat).

The most notable genes that differed are known as homeobox genes. These genes are known for their role in helping shape a developing embryo--determining which cells and organs go where. Many homeobox genes are influenced by hormones such as estrogen.

Why are these homeobox genes important for fat? "We believe these genes actually program those fat cells to respond differently to different hormones and other signals," Smith says.

Stem cells show fat is preprogrammed for its location

In the course of their work, Smith and his team also isolated stem cells from belly and thigh fat and grew them in laboratory dishes. This was a nice control because fat cells in a dish aren't influenced by nerves, hormones, or other outside signals.

Yet the researchers still saw the same location-specific differences in gene activity in the fat that developed from these stem cells. That result told them that the cells are preprogrammed. In other words, belly fat and thigh fat are genetically destined for their final location during development. It's not a difference that's acquired over time, as a result of diet or environmental exposure.

A new way of thinking about fat

Medically speaking, says Smith, it's important to understand these differences and how they arise. "Even though many women hate having large hips and thighs, that pear shape actually reduces their risk of heart disease and diabetes. In fact, women who have heart attacks tend to have more belly fat than thigh fat."

This research marks a new way of thinking. "Most people want to stop belly fat. But the problem is not just the fat--it's the location. Belly fat is just a marker of the problem. The real issue is in inability to store that fat on the hips and thighs," he continues.

Smith hopes that future studies aimed at understanding the fundamental differences in these fat depots could lead to specific treatments aimed at the regions that contribute most to the complications of obesity.

This research was funded by the U.S. National Institutes of Health (National Institute for Diabetes and Digestive and Kidney Diseases grants DK072476, R24DK087669, and P30DK46200), the Society for Women's Health Research Interdisciplinary Studies on Sex Differences (ISIS) Network on Metabolism, the Evans Center for Interdisciplinary Biomedical Research Affinity Research Collaborative on Sex Differences in Adipose Tissue at Boston University School of Medicine, the Genomics Core Facility at the Pennington Biomedical Research Center, and the Geriatric Research Education Clinical Center, Baltimore Veterans Affairs Medical Center.

The study was co-authored by Kalypso Karastergiou, Boston University Susan K. Fried, Boston University Hui Xie, Sanford-Burnham Medical Research Institute and the Translational Research Institute for Metabolism and Diabetes Mi-Jeong Lee, Boston University Adeline Divoux, Sanford-Burnham Medical Research Institute and the Translational Research Institute for Metabolism and Diabetes Marcus A. Rosencrantz, University of California, San Diego R. Jeffrey Chang, University of California, San Diego and Steven R. Smith, Sanford-Burnham Medical Research Institute and the Translational Research Institute for Metabolism and Diabetes.

About Sanford-Burnham Medical Research Institute

Sanford-Burnham Medical Research Institute is dedicated to discovering the fundamental molecular causes of disease and devising the innovative therapies of tomorrow. The Institute consistently ranks among the top five organizations worldwide for its scientific impact in the fields of biology and biochemistry (defined by citations per publication) and currently ranks third in the nation in NIH funding among all laboratory-based research institutes. Sanford-Burnham utilizes a unique, collaborative approach to medical research and has established major research programs in cancer, neurodegeneration, diabetes, and infectious, inflammatory, and childhood diseases. The Institute is especially known for its world-class capabilities in stem cell research and drug discovery technologies. Sanford-Burnham is a U.S.-based, non-profit public benefit corporation, with operations in San Diego (La Jolla), California and Orlando (Lake Nona), Florida. For more information, news, and events, please visit us at

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

Why Does DNA Need to Replicate?

DNA replicates to make copies of itself. This is an indispensable process that allows cells to divide for a living organism to grow or reproduce. Each new cell needs a DNA copy, which serves as instructions on how to function as a cell.

DNA replicates before a cell divides. The replication process is semi-conservative, which means that when DNA creates a copy, half of the old strand is retained in the new strand to reduce the number of copy errors. DNA contains the code for building an organism and making sure that the organism functions properly. For this reason, DNA is often called the blueprint of life. Its function is comparable to a builder using a blueprint to make a house. The blueprint contains all of the necessary plans and instructions for the organism. It brings the information for making a cell’s proteins, which are responsible for implementing the functions of an organism and determining the organism’s characteristics. After reproducing, the cell passes this crucial information to the daughter cells. DNA replication occurs in the nucleus of eukaryotes and the cytoplasm of prokaryotes. The replicating process is the same, regardless of where it takes place. Various kinds of cells replicate their DNA at different rates. Some undergo several rounds of cell division, such as those in a human’s heart and brain, while other cells constantly divide, like those in the fingernails and hair.

Are lab mice too cold? Why it matters for science

A typical mouse laboratory is kept between 20 and 26 degrees C, but if the mice had it their way, it would be a warm 30 degrees C. While the mice are still considered healthy at cooler temperatures, they expend more energy to maintain their core temperature, and evidence is mounting that even mild chronic cold stress is skewing results in studies of cancer, inflammation, and more. Researchers review the evidence April 19 in Trends in Cancer.

"Most people only look at results from experiments at standard lab temperatures," says Bonnie Hylander, an immunologist at the Roswell Park Cancer Institute. "They're not necessarily aware that if you repeat the experiments with mice at a different temperature, you might get a different outcome."

There are multiple reasons to keep a mouse lab cool. Researchers don gowns, gloves, and masks to work with the animals, which makes the lower temperature more comfortableand also cuts down on the smell. The National Research Council, which publishes guidelines for housing mice, gives the 20-26 degrees C range and recommends that the animals have nesting material. But when mice are constantly trying to generate enough heat to stay warm, the chill causes their heart rate and metabolism to change, and they eat more food to make up the energy.

A few years ago, Hylander and Elizabeth Repasky, an immunologist at the Roswell Park Cancer Institute, along with their colleagues, began investigating the effects of cold stress on the mouse immune system's ability to fight tumors. As the team revealed in 2013, lab mice do a better job of fighting cancer naturally when they're nice and warm. Tumors grew slower and were less likely to metastasize compared to mice kept at standard lab temperatures. The warmer mice also responded better to chemotherapies.

Concerned about the implications for drug research and selection, Hylander and Repasky started digging into a growing body of research on mouse housing temperature in other fields. Now, they're sounding the alarm.

Studies in fields ranging from obesity research to neurobiology have shown that housing temperature can alter study results in mice. "While animal physiologists have recognized the potential of this problem for some time, we were surprised that essentially no work was done on cancer models. We thought it was very important to highlight how many other areas of biomedical research, some related to cancer, are influenced by standard housing temperatures," says Repasky. "We're concerned that too many publications in which results differ, either between labs in various countries or within the same lab, may be due to environmental conditions."

But the answer isn't necessarily just turning up the thermostats. "Working at a thermoneutral temperature for mice isn't very pleasant for people," Hylander says. "It's hot, and it's hard for people to work very long when they're overheated."

As a first step, Hylander and Repasky recommend that researchers report the ambient temperature used in their colonies and simply be aware that the cage positions, the number of mice per cage, and the type of disease being modeled can influence the degree of cold stress.

For a more direct approach, Hylander suggests that researchers try pilot experiments at warmer temperatures to see how the difference affects experimental outcomes. This could be accomplished by either keeping mice in incubators or giving the animals more nesting material (in the wild, mice ward off cold temperatures by building nests).

"We're not saying one housing temperature is better than another," Repasky emphasizes. "The different temperatures are simply resulting in differences in experimental outcomes, which could be important. I think a lot more research is needed to optimize the use of mice for testing therapies that will be useful in people."

Trends in Cancer, Hylander and Repasky: "Thermoneutrality, Mice and Cancer: A Heated Opinion"

Trends in Cancer (@trendscancer), published by Cell Press, is a monthly review journal that presents and debates the latest opportunities, impasses, and potential impacts of basic, translational, and clinical sciences but also discusses emergent relevant issues in pharma oncology R&D, technology and innovation, ethics and society, and current cancer policy and funding models. Learn more: http://www. cell. com/ trends/ cancer/ home. To receive Cell Press media alerts, please contact [email protected]

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

Watch the video: How does Cell division Takes place. Biology. (July 2022).


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