What are the hairs/spikes on the edges of these leaves for?

I believe the hairs are known as trichomes. They can be uni- or multicellular. Depending on the plant and type of hair, they can serve one or more of several purposes. They may interfere with feeding by small and/or large herbivores, depending on how annoying to the palate they are. Some plants use hairs to keep frost away from the surface of the leaf. They can serve as nucleation points for water droplets in areas where the plant's primary source of water is fog. On the other hand, they can also help reduce transpiration in windy areas by breaking up the flow of air across the leaf. Finally, in hot/dry areas, they can reflect some sunlight to protect the leaf's tissues.

So, the function really depends on the type of plant and its habitat. I'm not a botanist, so I can't confirm whether or not your guess of Sempervivum is correct, but if it is, then the hairs would likely help reduce transpiration in hot, dry, windy areas, and possibly block some sunlight.


Oxytocin is produced by cleavage of the protein of the oxytocin/neurophysin I prepropeptide gene. The precursor peptide is cleaved by Proprotein-Convertase 1
. Mice lacking the gene which encodes for this enzyme have reduced levels of oxytocin. The final step in the biosynthesis of oxytocin is carried out by Peptidyl glycine alpha-amidating mono-oxygenase.


Why do tattoos persist if body cells are regularly renewed?

First, tattoo pigment isn't injected into cells. If you were to puncture a cell with something the size of a tattoo needle, it would die - full stop. Many cells are destroyed in the process though, mostly by tearing, which initiates the wound healing process.

So what actually happens is the particles lodge in between the cells of the dermis (the layer below the epidermis, or outer layer of skin) and new cells crowd around it as damaged cells are replaced.

Since the particles in good tattoo ink are too big to be carried off by macrophages, they just sit there. That doesn't stop them from trying, though. Macrophages take up the pigment but are unable to escape with their garbage. Fibroblasts envelope the particles, both intracellularly and within the extracellular matrix they generate. At the end of a fibroblast's life, its contents are taken up by the same process - still too big to remove.

Smaller particles will be carried off by macrophages capable of both consuming the particles and migrating into the lyphatic system, which is why some ink fades more than other kinds. Ink composed of fine particles would be expected to fade severely. New tattoos are also sharper because some of the ink that was injected is lodged in the epidermis, which is the layer that grows out and is shed over time.

In this biopsy of a tattooed mouse, you can see how the epidermis has carried some of the pigment out of the skin while much of the dermal layer's pigment has been either removed lymphatically or enveloped:

Source: Tattooing of skin results in transportation and light-induced decomposition of tattoo pigments--a first quantification in vivo using a mouse model.

Thus, over time the pigment will be moved around a bit by this cellular activity, in fact deeper into the dermal layer on the whole.

The intent of using laser light to remove tattoos is to break those particles down into smaller pieces burst any cells containing them - again initiating the wound healing process. However, unlike in previous cases, when macrophages reach the site they can now sweep the remaining particles away to the lymph nodes.

Sources

General - Tattoos and tattooing. Part II: Gross pathology, histopathology, medical complications, and applications.
Process - Cutaneous Wound Healing

Secondary sources:

Fate of tattoo pigments in skin (pdf)
How Laser Tattoo Removal Works - Smarter Every Day


Why is Portuguese man o' war considered a colony?

Physalia and Siphonophorans in general are multicellular Metazoans.

But the whole discussion is about modularity on the level of individuals: Siphonophorans are colonial organisms, which means they are composed of multiple individual polyps and medusae. This is in fact quite common among Hydrozoa, but in Siphonophora the degree of integrity and function division among the components is of extraordinary level.


Can forensic DNA analysis be used to generate a visual approximation of a suspect?

In theory it's possible to have an approximation, but not to know with certainty. Identical twins have the same genomes and look very much alike. Whether it can be done in practice depends on how well we can model the relationship between genes and looks and on how much information is necessary for a judge to permit arresting and questioning a suspect.

Scientists know relatively little about how genes influence physical appearance yet. The height of the suspect is controlled by hundreds of genes with complicated interplay between them, so I don't think it's possible to estimate it just yet. Eye color is more simple: it's controlled by only 3 genes. We know weight is partially controlled by genetics but exactly which genes are responsible is not clear. Age is impossible to tell by DNA alone. Skin color should be predictable, since it's caused by melanin production, and we know which genes are responsible.

So to sum up, DNA analysis can tell the gender, skin color, and eye color of the suspect, but very little about height and weight, and virtually nothing about age. That's not enough information to identify a suspect, although perhaps someone with legal knowledge could comment on this.

But let's say in the future we know enough to determine all these traits. Then DNA analysis would be helpful but never enough to identify a suspect. The problem is that different cells in your body undergo different mutations in their DNA with time. That's how one gets cancer. Let's say there's a mutation in the eye color gene in skill cells from a murderer found on a victim's body. It won't affect the murderer's eye color but it will affect the forensic analysis. So it's impossible to know for sure what the suspect's appearance will be.


Can a certain part of human dna can be replaced with other animals dna?

Yes. They're identical. When we eat animals or plants we digest their DNA to use to make our own DNA.


Why does crying lead to a running nose and reddened nose tip?

When you cry, you produce tears, which come out of your tear ducts. These are not only open to the eyes but also have a connection to your nose, see the image below:

A part of your tears runs through this connection and mixes with the mucus which is present in your nasal system making it thinner and allow it to flow more easily. If the tear flow is prolonged, the nose will produce more mucus and make your nose running for a longer time. The nose appears redder because the blood flow is increased. This is partly due to the production of more mucus and also because you repeatedly touch the nose when using a handkerchief.


First, pentoses aren't a major source of nutrition, at least for humans. That said, pentose absorption works the same way a lot of nutrient absorption works: the "magic" of metabolism, with respect to diffusion.

Pentoses leave the intestinal lumen, entering the intestinal cells, where their concentration is lower. From there, they again travel via facilitated diffusion into the bloodstream, again because their concentration is lower in the bloodstream.

From there, we can expect one of two outcomes: either an equilibrium will eventually be reached(i.e., lumen==intestine==blood), or the bloodstream pentoses need to be metabolized into something else. Indeed, certain pentoses (specifically D-ribose; I'm not sure if others can end up in this pathway as well but it is a very common pentose) can be metabolized in the pentose phosphate pathway for anabolic purposes. Others may end up in proteoglycans.

Regardless of the metabolic pathway, the effect on the process you are wondering about is the same: the metabolites no longer "count" in terms of concentrations for diffusion. Because membranes are not permeable to everything, if they are not permeable to the products of metabolism there is no way for those products to "diffuse backwards."


There are many articles in health literature debating on the question. Everytime the experimental setup seem to me quite basic and I am affraid that one cannot infer many things from these experimental designs. I guess the ethics is limiting much of the medical experimentation (which is good!). Usually it is just the report of observations of what happen to the global health of a patient when one amino acid is missing in their food. Therefore, these articles does not explain much about the metabolism reasons of these needs (which was your question) but only try to define what are the needs. Moreover statistics seem sometimes a bit fuzzy (or absent) to me.

Anyway here is a review of these results and there is a whole paragraph on the question of histidine. The best is that you read it yourself. To make it short: Histidine doesn't seem to be more important to the children than other amino acid. Moreover there is big storage of histidine in our body suggesting that one that is histidine deprived for a while might use these stored histidines.


Modern reference for Kropotkin's lazy bees

The quote refers to 'robber' bees, but in today's terminology, there are actually three separate phenomena. "Cheating" in bees and other social animals refers to the exploitation of a social contract for one's own benefit. Example: bee workers lay their own eggs rather than tending those of the queen. "Laziness" or "inactivity" of bee or other social insect workers is incredibly widespread, but it is not clear that it is selfish: it may be a side-effect of imperfect task allocation, or those individuals may be a reserve work force. "Robbing" in bees usually refers to removal of nectar or pollen from flowers without pollinating them.

"Cheating" associated with illicit reproduction is widespread in social insects, including in bees, and there's a broad literature on it (search terms "anarchist" "queenright", "policing") but it sounds like your question concerns differential effort and environmental resources specifically.

Differential effort in labor ("laziness vs. busynesss") has been seen in many social animals. The way you frame the question seems to be in terms of:

  "how many lazy individuals can a society tolerate given environmental
  conditions?"

Most observational/experimental studies seem to have approached the question in terms of:

  "how can what appears to be cheating actually be adaptive?"

For instance, Kukuk et al. suggest that in Halictine bees, lazy bees who avoid the high-mortality-risk foraging tasks are actually acting as caretakers and orphan-rearers for the brood of the foraging busy bees. It's also been proposed that apparently lazy insects act as a "defensive reserve" for the nest, although at least in Bombus impatiens, experiments show no evidence that lazy bees defend any more than busy bees (Jandt et al.)

Lazy individuals could also be acting a labor reserve ("substitute helpers"), in case of food or colony depletion. To me, this scenario is the closest to what you mention – the idea that lazy individuals become busier, either voluntarily or through coercion, in time of need. Baglione et al. show that this is the case for carrion crows, and quantify it to some degree along the terms you suggest. On the other hand, Cartar (cited in Jandt and Dornhaus) shows that for a number of bumblebee species, it was more likely that busy bees would work harder or switch tasks than it was that the lazy bees would become busy!

In sum, what you/Kropotkin suggest exists in all social insects, although the mechanisms of sociality and of laziness are diverse and various among species.

 Baglione V, Canestrari D, Chiarati E, Vera R, Marcos JM. 2010. Lazy group members are substitute helpers in carrion crows. Proc Biol Sci 277: 3275–3282. (free)
Cartar RV. 1992. Adjustment of foraging effort and task switching in energy-manipulated wild bumblebee colonies. Animal Behaviour. (full text not online?)
Jandt JM, Robins NS, Moore RE, Dornhaus A. 2012. Individual bumblebees vary in response to disturbance: a test of the defensive reserve hypothesis. Insectes sociaux. (behind paywall, buy Jandt kindly has uploaded for free on her site)
 Jandt, Dornhaus. 2009. Spatial organization and division of labour in the bumblebee Bombus impatiens. Animal Behaviour 77: 11–11. (behind paywall, but also free on Jandt's site)
Kukuk PF, Ward SA, Jozwiak A. 1998. Mutualistic benefits generate an unequal distribution of risky activities among unrelated group members. Naturwissenschaften. (Behind paywall, but this free article by Forbes et al. reports similar information)

Also see:
Jandt JM, Dornhaus A 2011 ‘Competition and cooperation: bumblebee spatial organization and division of labor may affect worker reproduction late in life’, Behavioral Ecology and Sociobiology 65: 2341-2349.
- shows that selfishness/cheating may actually play a role

Dornhaus A, Holley J-A, Pook VG, Worswick G, Franks NR 2008 'Why do not all workers work? Colony size and workload during emigrations in the ant Temnothorax albipennis' Behavioral Ecology and Sociobiology 63: 43-51
- this paper reviews other literature about how many bees/ants in a colony are lazy; up to 75% or even more at a time!


Where do plants obtain the metal ions needed for biological processes?

Many ions are absorbed by the plants via the action of bacterias. Fe or B for example require chelating action from microbes. P and S need to be oxidised to enter the plant as well.
Source: Le sol, la Terre et les Champs - http://www.sangdelaterre.fr/index_135_151.html


For cells to become infected with bacteria, some bacteria will still be present in the blood. These are still engulfed by phagocytes in the same fashion. However once engulfed the antigens on the surface of the Bacteria are placed on the surface of the phagocyte, this is known as an antigen presenting cell (APC). Specialized lymphocytes known as Th Cells bind to these antigens and then divide. These then stimulate Cytotoxic T cells which secrete a chemical known as perforin. The perforin makes holes on the membrane of 'non-phagocyte' infected cells allowing water to enter. This essentially causes the cell and the bacteria to explode, known as cell lysis.

So basically the infected cell is simply destroyed unless hydrolytic enzymes break down the Bacteria.


Why do spiders have a leaf at the bottom of a piece of web?

As far as I know, it has a practical effect. Spiders hunt for small insect and don't like when bigger animals damage their webs. So that they make the web visible for mammals, but in the way which doesn't prevent the prey from being caught.

I don't have reference for this, my colleague (entomologist) told me so.


Identification of proteins in this animation of a ribosome translating mRNA

The protein involved in "pushing" the tRNA and mRNA is the elongation factor EF-G. The protein involved in "transporting" the tRNA is the elongation factor EF-Tu.

Quoted from the Wikipedia articles:

EF-G:

  When it binds to the ribosome A-site, EF-G causes the tRNA previously occupying that site to occupy an intermediate A/P position (bound to the A site of the small ribosomal subunit and to the P site of the large subunit), and the tRNA in the P site is shifted to a P/E hybrid state. EF-G hydrolysis of GTP causes a conformation change that forces the A/P tRNA to fully occupy the P site, the P/E tRNA to fully occupy the E site (and exit the ribosome complex), and the mRNA to shift three nucleotides down relative to the ribosome due to its association with these tRNA molecules. The GDP-bound EF-G molecule then dissociates from the complex, leaving another free A-site where the elongation cycle can start again

EF-Tu:

  The tRNA anticodon domain associates with the mRNA codon domain in the ribosomal A site. If the codon-anticodon pairing is correct, EF-Tu hydrolyzes guanosine triphosphate (GTP) into guanosine diphosphate (GDP) and inorganic phosphate. This creates a conformational change in EF-Tu that causes EF-Tu to dissociate from the tRNA of the ternary complex (and therefore leave the ribosome). The aminoacyl-tRNA then fully enters the A site, where its amino acid is brought near the P site's polypeptide and the ribosome catalyzes the covalent transfer of the polypeptide onto the amino acid . The tRNA on the P site (without peptide) moves to the E site and is then released.


Is there any strong factor against human edible plants being widespread and easy to gather?

Define "easily available to human", lots of fruit are perfectly edible to humans. Human have only become widespread in the last few million years so there is not enough time to see things specialized in humans via natural selection. Especially since we  are both generalists and for most of the world completely new factors in the environment.

But there are plants that have evolved to be eaten by humans. Wheat, rice, and, maize have done amazingly well by having the right factors to be useful to humans, they are also some of the most common plants on earth now thanks to us.
Artificial selection is still evolution, it's just not natural selection. Humans are generalists and its hard for natural selection to push things to specialize in edible symbiosis with a generalist, especially in as short a time as humans have been around, but artificial selection can do it just fine becasue it is faster, provided the plant in question survives us long enough.

Being useful to humans is also a bit of a mixed bag sometimes it means we spread you over the whole world, such as wheat and dogs, but sometime is means harvesting to extinction like Silphium. Then you have things like avocado which almost went extinct becasue humans killed off their parter animals and almost nothing else could eat them, then we invented farming and decided we liked them and brought them back from the brink. Human intelligence and cultural information sharing means capabilities and technology change so much faster than the speeds natural selection tends to work at, most things just have not had the time to really adapt to how fast we changed the world,  unless we take an interest in forcing them to.


Can some colours be processed faster/more accurately than others?

The answer is yes and yes. Firstly, motion cannot be processed at equiluminance. In other words if you have clubs that are equally as bright as their background you will not be able to see them move even though they are clearly visible because of a different color. It's a remarkable effect (demo link below), as you become in effect motion-blind. Obviously you notice after a while that things moved, but you don't see them move smoothly as you are used to. This is similar to what people with akinetopsia experience (had lesions to brain areas involved in motion processing). So have clubs that have clear luminance contrast to the background (very dark, or very bright).

Then there are known difference in processing latencies for different colors. More specifically yellow is processed faster than blue. And black is processed faster than white (if you consider them colors). These effect are massive, a few hundreds msec in some cases which is very long. There is also a known relationship between stimulus intensity (here color contrast) and response time, called Piéron's law. However that effect saturates at fairly low contrast so as long as you can see the clubs clearly it's unlikely there will be a difference in response time for more contrasted colors.

Finally there are discrimination differences for colors. For example yellow and orange are more easily discriminable than blue. But that's only true if you have to perceive a low contrast color difference (a yellow club on a yellow background). Here again as long as you see your clubs very clearly, it's unlikely the specific color of the clubs will make a difference.

So overall I would recommend to use clubs as contrasted as possible to the background (which is common sense). Then prefers darks to lights colors, and prefers yellows to blues. The ideal color is brown, which is in facts a dark yellow.

http://visionlab.harvard.edu/Members/Patrick/Demos/index.html

http://www.michaelbach.de/ot/col-flicker/index.html

Komban, S. J., Alonso, J. M., & Zaidi, Q. (2011). Darks are processed faster than lights. Journal of Neuroscience, 31(23), 8654-8658.

Wool, L. E., Komban, S. J., Kremkow, J., Jansen, M., Li, X., Alonso, J. M., & Zaidi, Q. (2015). Salience of unique hues and implications for color theory. Journal of vision, 15(2), 10-10.

Witzel, C., & Gegenfurtner, K. R. (2013). Categorical sensitivity to color differences. Journal of vision, 13(7), 1-1.


Can you get enough water by eating only fish?

If you have a man in a box scenario where you only look at numbers, the answer is, no, he won't last 14 days.[1]

The difficulty with this question for me is that the body doesn't always behave the way it's supposed to. The 3-3-3 rule (3 minutes without air, 3 days without water, three weeks without food) and the "100 hour rule" (4.166 days) aren't absolutes.[2] Some people die in hours, some 10 days. The variables are too great.

Guinness World Records puts the record for survival without water at 18 days[3] by an 18 year old male forgotten in a cell by the police. But he was in a cool basement, and licked the walls which had a small amount of moisture on them. Had he been sweating or 2 decades older, he probably wouldn't have lasted as long.

Water requirement under extreme circumstances varies. How much clothes is your male wearing? Does he have shade? Where in the ocean is he? How inactive can he be? Can he oil his skin with fish oil? But mostly, does he have a still suit (j/k)? These things all matter.

Eating protein without water isn't wise. Carbs are better, but your guy doesn't have them. The better thing for your guy, who can certainly live for 14 days without food, is to suck the water out of the fish, and what he can't suck out, wring out at the end. If he has access to the whole fish, the eyeballs and the spine also have water in them.* The body has all kinds of homeostatic mechanisms to preserve fluids, including continuous secretion of ADH (Anti-Diuretic Hormone), osmoreceptors and baroreceptors to regulate fluid volume and how much water is lost from the kidneys.[4] He'll suffer terribly; fluid will be sucked out of his joints and cells and his blood urea nitrogen will go up and his kidneys will be damaged, he'll hallucinate, he'll need hospitalization, but might he live? If he is young, healthy and hydrated going in, and other factors (a tarp for shade, etc.) mitigate his water loss, I think the answer is yes, he might.

*In 1953, a French physician and sea survival expert, Alain Bombard, set sail in a Zodiac inflatable dinghy with the only food and water officially sealed to discourage himself from using it. He started immediately with drinking small amounts of seawater, and would suck water from fish, and, if he had any fresh rain water, would eat raw fish. He sailed from Minorca to Barbados, eating supplied food and water only once. His rival survivalist, another physician, Hannes Lindemann, contested Bombard's claims, but did well at sea as well.
[1] The Biology of Human Survival : Life and Death in Extreme Environments
[2] Dehydration
[3] Andreas Mihavecz
[4] Fluid Physiology, Ch. 5, 6


I found the explanation given below here (my emphasis). It may not be authoritative, but it makes sense to me.

You can determine the approximate shape of your visual field by looking straight ahead, and holding a hand out to each side and noticing where you can no longer see them. Do the same for above and below, and you'll see that your peripheral vision probably extends to about 180 degrees (or a little less) left and right, and about 100 degrees up and down. Your brow, nose, and cheeks narrow the vertical angle.
So your visual field has a ratio of about 1 to 1.8.
Interestingly, and not entirely coincidentally, ordinary films and wide-screen TVs have a ratio of 1.78 (16:9).

Another way to see this effect is to look at someone's head in profile and from directly above. In the former  case you have a clear view of their eyes, in the latter you don't. (Tested on a small sample - one 3 year old male, playing with an iPad).


The vascular system is different in monocots and dicots. In dicots the vascular tissues are arranged in concentric circles; one of these rings is meristematic cells (undifferentiated cells that can differentiate into any cell type). This ring of meristem tissue is called the vascular cambium and is where secondary growth occurs - xylem grows inwards and phloem grows outwards.

Whereas:

  Monocots have a distinctive arrangement of vascular tissue known as an
  atactostele in which the vascular tissue is scattered rather than
  arranged in concentric rings. Many monocots are herbaceous and do not
  have the ability to increase the width of a stem (secondary growth)
  via the same kind of vascular cambium found in non-monocot woody
  plants. However, some monocots do have secondary growth, and because
  it does not arise from a single vascular cambium producing xylem
  inwards and phloem outwards, it is termed "anomalous secondary
  growth". (Wikipedia)

For palms specifically:

  Palm trees increase their trunk diameter due to division and
  enlargement of parenchyma cells, which is termed diffuse secondary
  growth. (Wikipedia)

Parenchyma cells are type of cells found in plant ground tissue, which makes up the bulk of plant mass.


Identifying a spider from my childhood memory

This may be what you are searching for:

It's actually a male purseweb spider (Atypus affinis), the color fades to black, eventually.

Source: http://www.spiderzrule.com/purseweb2.htm


Peterchev et al. (2010) reports

  The current amplitude is [... ] held fixed at the device maximum (e.g., 800 mA or 900 mA)...

and that

  [constant-voltage devices are] now obsolete

The total stimulus duration as I understand is a pulse train of a few seconds (Peterchev, 2010). The duration of total treatment is about 20 minutes in the treatment room and up to an hour including recovery (source: Hopkins Hospital).

Note that the total stimulus duration depends on the total amount of injected charge. This in turn depends on stimulus frequency, stimulus shape, frequency and so forth (Fig. 1). For an excellent overview see (Peterchev et al., 2010).

Fig. 1. Sample ECT waveforms: (a) sine wave, (b) biphasic pulses with indicated parameter definitions, and (c) monophasic pulses (Peterchev et al., 2010)

Reference
- Peterchev et al., J ECT (2010); 26(3): 159–74


How does someone with red-green colorblindness see yellow on a monitor/television?

Normal people see color due to the bellow mentioned combination of red, green and blue:

But due to genetic factors, The graph Distorts:

Now,If consider the normal Color code for yellow:

Yellow = R(255) + G(255) + B(0)

Or in other words

Max. Red + Max. Green + no Blue = Yellow

That means even if you can see a little of Red and Green, you can still a little deeper or lighter shade of yellow.

So Summing it up in the images:

Normal

Red ColorBlind

Green ColorBlind

Blue ColorBlind

Source:

Coblis — Color Blindness Simulator

A quick introduction to colorblindness


Does the plant cell vacuole form by the invagination of the cell membrane?

Yes, in part, but the complete answer is way more complicated than that.

Endosomes (the vesicles formed by "invagination" of the cell membrane, as you said) are responsible for (part) of the biomembrane of the cell vacuole. However, some biomembrane comes from the Golgi-ER system, and almost all proteins come from ER (having passed by the Golgi apparatus).

Have a look at this image (Marty, 1999):

Its legend says:

  Seven basic pathways are used for the biogenesis, maintenance, and supplying of vacuoles. Pathway 1: entry and transport in the early secretory pathway (from ER to late Golgi compartments). Pathway 2: sorting of vacuolar proteins in the trans-Golgi network (TGN) to a pre/provacuolar compartment (PVC) via an early biosynthetic vacuolar pathway. Pathway 3: transport from PVC to vacuole via the late biosynthetic vacuolar pathway. Pathway 4: transport from early secretory steps (ER to Golgi complex; pathway 1) to the vacuole via an alternative route with possible material accretion from Golgi (indicated by the asterisk). Pathway 5: endocytotic pathway from the cell surface to the vacuole via endosomes. Pathway 6: cytoplasm to vacuole through autophagy by degradative or biosynthetic pathways. Pathway 7: transport of ions and solutes across the tonoplast. AV, autophagic vacuole; E, early endosome; ER, endoplasmic reticulum; PVC, pre/provacuolar compartment; TGN, trans-Golgi network.

According to the same paper (Marty, 1999):

  Experimental evidence suggests that material within the vacuolar system in plants derives confluently from both an intracellular biosynthetic pathway and a coordinated endocytotic pathway. (emphases mine)

Source: Marty, F. (1999). Plant Vacuoles. THE PLANT CELL ONLINE, 11(4), pp.587-600.


Certainly ants evolved from insects that could fly.  All the earliest wasps (ants are specialized wasps) could fly.

Building and maintaining wings is expensive in terms of energy.  That's an obvious evolutionary advantage to not having wings.  So if there's insufficient benefit from having wings then there's selective pressure against having wings.


I think your question is interesting, though the use of "expression" is misleading in context of your rabbit example.

Examples of environmentally influenced gene-expression in humans?
...
That is, a phenotype which requires BOTH a certain genetic background and particular environmental influences in order to be expressed?

In the example you give, the color-changing phenotype is not due to changes in gene expression but rather a conformational change in a tyrosinase variant at low temperatures that leads to decoupling of an inhibitor from the enzyme.  This is not to say that there aren't any changes in expression with changes in temperature -- only that the phenomenon you describe is ultimately a change in enzyme activity and not the induction of a specific allele.  See Kidson and Fabian, 1981 [1] --

It is proposed that at the normal body temperature of 37 degree C, tyrosinase from Himalayan skin is strongly bound to an inhibitor. At lower body temperatures, the affinity of the enzyme for the inhibitor decreases, thus allowing the synthesis of melanin to increase. This change in affinity of the enzyme for the inhibitor could be regulated by temperature-induced conformational changes in either the enzyme or the inhibitor or both.

Note that this study was conducted in "Himalayan" mice, not rabbits, though the authors do reference an earlier rabbit study [2] --

These results are in support of Danneel's visual observations ('41) that "ferment" activity of Himalayan rabbit skin is absent at temperatures above 25 degree C.

the full text of which can be found, in German, on Google Books.

Concerning a human example of allele-environment interactions, look no further! The same temperature-sensitive tyrosinase mutation has been reported in people with oculocutaneous albinism (OCA) [3], albeit with a slightly different phenotype.  From the abstract:

In this paper, we report a new type of OCA that results from a tyrosinase allele producing a temperature-sensitive enzyme. The proband had white hair in the warmer areas (scalp and axilla) and progressively darker hair in the cooler areas (extremities) of her body. Melanocyte and melanosome architecture were normal. Quantitative hairbulb tyrosinase (dopa oxidase) assay demonstrated a loss of activity above 35-37 degrees C. Plasma pheomelanin and urine eumelanin intermediates were reduced and correlated with hair melanin content. This is the first temperature-sensitive tyrosinase mutation to be reported in humans and is analogous to the Siamese mutation in the cat and the Himalayan mutation in the mouse.

References

Kidson SH, Fabian BC. The effect of temperature on tyrosinase activity in Himalayan mouse skin. J Exp Zool. 1981 Jan;215(1):91-7.
Frisch KV, Goldschmidt R, Ruhland W, Winterstein H. Ergebnisse der Biologie. Eighteenth Volume.
King RA, Townsend D, Oetting W, et al. Temperature-sensitive tyrosinase associated with peripheral pigmentation in oculocutaneous albinism. J Clin Invest. 1991;87(3):1046-1053.


This is a Cattle Egret (Bubulcus ibis), which is a heron in its breeding plumage. When not breeding, the bird is white. See the images for comparision:

Breeding cattle egret with colored feathers.

Nonbreeding cattle egret, completely white.


Can concentration of a protein be determined from a gel quantitatively (rough estimation)?

Yes, you can use SDS-PAGE as a semiquantitative estimate of protein concentration. You need to create a standard curve with a protein of known concentration to compare against. Quantification is done by densitometry. It's a quick and easy process, but keep in mind some limitations:

Band intensity depends not only on the amount of protein but also on the amino acid composition of the proteins and the dye used
The unknown protein and standard should be run on the same gel to remove variations in gels, electrophoresis, staining, destaining and imaging
Densitometry can be quite qualitative depending on how it's done

I'm not sure if you're looking for a protocol, but it's relatively straight forward. I usually load 2, 4, 6, 8 and 10 uL of 100 ng/uL BSA as a standard and 2, 4 and 6 uL of the protein of interest (based on past experience with my proteins and their purification). The gel is stained with Coomassie and the band intensity estimated with a program called ImageJ. A standard curve is created by plotting intensity as a function of mass, from which the concentration of the unknown can be found.


What insect is this? (Black body two orange lines in its back and six legs)

It's a larvae from a ladybird (or ladybug).  Judging by the stripe pattern it is a Common Spotted Ladybird (wiki: Harmonia conformis) and from the body shape & size I'd also say 3rd instar.

The one you have photographed, and the one on flickr, are larval forms of the ladybug, just like when a catepillar becomes a butterfly, the ladybugs also have a larval stage in their life cycle which crawl around and look very different to the adult form.


Identification of an alpine blueberry type

Possibly Vaccinium gaultherioides (sometimes considered a subspecies of Vaccinium uliginosum), which are present throughout the Alps.

For example, see InfoFlora*:

 Vaccinium gaultherioides Bigelow, © Konrad Lauber – Flora Helvetica – 2012 Haupt Bern

You can see the prevelance of this species throughout the Swiss alps in the below range map (also from InfoFlora):

______________________________________enter preformatted text here
* the national data center for the Swiss flora

I don't know the flora of the Alps personally and I feel you post lacks enough detail for me to confidently pick and choose among many Vaccinium candidates. From those I've examined, this species seems most visually similar to yours.


As the definition of biological age is very ambiguous, I propose that to generate an algorithm, you first need to create a quantifiable definition. I submit:

  Biological age is a measure indicating what portion of one's calculated life expectancy is already expended, adjusted proportionately for the average life expectancy of their major demographic.

Wow, that's a mouthful! So, let's break it down.

Life expectancy is calculated :

Ascertain a person's major demographic (Geographic residence, Race, Gender and Generation).
Find the average life span of that demographic.

This is negligibly speculative as a living person's Generation has not yet fully perished
Statistical outliers, such as infant mortality, are generally excluded from this calculation

Adjust for known major factors that have accepted statistical impact.eg:

Lifestyle
Current medical conditions
medical history

Average Life expectancy of subject's demographic was calculated in #2 above.

So, now let's throw in some sample numbers.

Statistical Facts: (totally made up)

Caucasian males living in the France, born in the 1970s have an average life span of 72 years.
Exercising 30 minutes or more daily increases life expectancy 6 years
Smoking decreases life expectancy 7 years
Not smoking increases life expectancy 2 yearsHold on a second?! Wouldn't not smoking already be accounted for in the "Smoking..." section? Well, no, because our demographic sample are all "unknown" so having specific knowledge would statistically change the results in either direction
Heart Disease decreases life expectancy 8 years
Devout religious affiliation increases life expectancy 6 years.
Family history of diabetes decreases life expectancy 2 years.

Two subjects both Caucasian, french males born in 1974 (40 years old chronologically):Their mom's actually shared a labor and delivery room!

Beavis - known: Smoker with heart disease.
Butthead - known: Devout Buddhist, very athletic, non smoker with a family history of diabetes

Beavis' life expectancy is 57 (72-7-8)Butthead's life expectancy is 84 (72+6+2+6-2)

Beavis has expended 70.2% (40/57) of his life expectancyButthead has expended 47.6% (40/84) of his life expectancy

Despite sharing a birthday:Bevis' biological age is 50.5 years (.702*72)Butthead's biological age is 34.3 years (.476*72)

Note: It's almost 6 hours past my bedtime, so please excuse any stupid mistakes or miscalculations.  The general concepts are what is important


Why can't dopamine cross the blood brain barrier but l-dopa can?

Both L-Dopa and Dopamine are polar molecules and thus hydrophilic. They are solvable in water but not in lipids, so they are not able to cross the Blood-brain barrier on their own.

The difference is that L-Dopa has a transport protein (SLC7A5) that allows it to pass through the Blood-brain barrier, whereas dopamine doesn't.


Why does meiotic recombination disrupt the independent assortment of genes on the same chromosome?

Recombination does not make any two genes completely independent because there will not systematically be a recombination event between two given loci (=position on the chromosome).

Distance between loci

Consider two scenarios that describe the position of two loci on a chromosome.

Tightly linked loci

Consider two very closely linked loci. Let's say that a recombination event occurs somewhere in the chromosome. It is very likely for this recombination event to occur somewhere else than between these two loci. These two loci are essentially linked and do not segregate independently

Distant loci

Consider now two loci on the same chromosome. Each locus (=singular of loci) is found at one end of the chromosome. If a recombination event occurs, it is pretty sure that it will occurs between the two loci. As a consequence, the two loci will segregate (quasi) independently.

Conclusion

As a conclusion, recombination allows to break down the linkage between two loci but it does so at a given rate that depends on the physical distance between the two loci and on the per nucleotide recombination rate.


Where would Saccharomyces cerevisiae be found in highest concentrations in environment?

Here is a link to an interesting article which reports a survey of wild isolates of Saccharomyces cerevisiae in China.

  Wang, Qi-Ming, et al. (2012) Surprisingly diverged populations of Saccharomyces cerevisiae in natural environments remote from human activity. Mol Ecol 21: 5404-5417

A relevant quotation from the article:

  In addition to grapes and oak tree (Quercus spp.) bark, S. cerevisiae was successfully iso-lated from a variety of damaged fruit collected in orchards or markets in different provinces of China; from the bark of different deciduous trees; forest soil and rotten wood collected in primeval, original secondary and planted forests located in different regions covering temperate, subtropical and tropical climate zones from northern to southern China. Unexpectedly, the success rate of S. cerevisiae isolation from fruit samples (6.5%) was lower than that from tree bark (16.5%), soil (10.8%) and rotten wood (9.2%) samples. S. cerevisiae was more frequently isolated from forest soil samples (success rate 13.7%) than from orchard soil samples (success rate 9.1%). Among the fruits giving positive S. cerevisiae isolation, grape samples showed the lowest success rate.

Table S2 in the supplemental information records isolates as follows:

climatic zone    sites   isolates
__________________________________
tropical           5       20
subtropical        2       14
temperate          13      51

Superficially, from this it looks as if there would probably be little difference between New York state (humid, continental) and Florida (humid, subtropical).


ChIP-seq for histone modification not in agreement with RNA-seq for expression

It is difficult to draw any conclusion without further experimentation. There may be many other factors that prevent the expression of the gene including factors like post-transcriptional regulators. Some histone modifications like the ones you are mentioning are also a bit dicey and there can be bivalent modifications too. However, if there is a strong reason to speculate that these marks are associated with repression then you can try these:

You can verify how many genes are there whose expression is not in accordance with the histone marks. If this for a small number of genes then you can investigate them separately. Use a statistical test to verify the significance of your correlation between histone mark and expression. If the discordance is widespread, then I would suggest you to repeat the RNAseq (easier and cheaper than repeating ChIP-seq). BTW, how were the read qualities? Depending on that you can decide which experiment needs repetition. Repetition will help you to know if the observation is indeed correct (a biological replicate); possibly you may end also up concluding that these marks are actually dicey.
If a few genes show discordance, then just do Real-Time PCR for these genes. RT-PCR is more sensitive and another technique of quantification is anyways good. Use a few concordant genes also, in the experiment.


Can you knockout a gene specifically in the dorsal root ganglion in adult mammals?

It requires two genetic constructs to create a conditional KO organism. One parent with a transgene that expresses a DNA recombinase (such as Cre) after the promoter of a gene that is ONLY expressed in your tissue of interest. The other parent contains a modified gene of interest to be removed in the presence of said DNA recombinase but is fully functional otherwise.

Therefore, the ability to target a Knockout to a specific tissue is dependent on identifying a gene that is only expressed in the tissue of interest.

It is actually easier to create a whole animal KO, but because gene products can have different functions temporally in development and in different tissues, a whole animal KO may be lethal, whereas removing it in a specific tissue may not be and allows study of the effects of said removal.

Thus, if your gene of interest were lethal when removed from whole organism, AND you know of a gene that is only expressed in the DRG, you would have incentive to see if a CKO animal could be made.

A brief search on Cre Lox technology will bring up 1000's of images and articles.
Here is one and a nice illustration:


Why do we grow so much hair on our heads compared to our bodies?

Wheeler (1992; and previous) discusses the evolutionary loss of "non-functional" hair in hominids from the perspective of water balance.

Wheeler's hypothesis is that naked, bipedal hominids could have tolerated higher ambient temperatures as well as elevated metabolic heat production. Naked skin would confer higher levels of evaporative cooling, but would have entailed more water loss.

Wheeler argues that bipedalism necessarily would have preceded loss of hair, which seems to agree with Carrier's (1984) hypothesis that early hominids were distinguished not by large brains but by upright, bipedal postures with striding gaits. Humans are unique among similarly sized mammals in their capacity for endurance running.


Which complexes physically pump protons in photosynthesis?

General Approach

Although I am not an expert in this area, as an ex-chemist I find this topic one of the most fascinating and fundamental in chemical biology. I have constructed an answer starting from my copies of the 5th (available on line) and 6th editions of Berg et al. Biochemistry (2003 and 2007, respectively), and then searched the Protein Data Bank for structures of the cytochrome b6f complex, and worked from the papers associated with more recent entries.

Definitions

First, it is important to be clear on the following:

  What is meant by a proton pump (physical or otherwise)?

I think that the question — and the scientific community in general — probably assumes a pump to have some sort of channel or revolving door through which the protons are driven from one side of a membrane to the other. If one were able to tag an individual proton to follow it, one would find that it was physically translocated across the membrane. (A model for this might be the Na+/K+-ATPase. See also Berg et al. Biochemistry in Chapter 13 “Membrane Channels and Pumps” although this does not actually mention pumps in relation to either photosynthesis or oxidative respiration.)

This would be in contrast to the net translocation of protons across a membrane by chemical sleight of hand. A reaction at one side of the membrane would consume protons, and a reaction at the other side would emit protons. However no individual proton would pass through the membrane.

Both these processes would be working against a concentration gradient and require energy, in this case in the form of reducing power — not, of course, ATP.

This difference is illustrated in Berg et al. with respect to cytochrome c oxidase (Fig.18.21) in which both processes occur, where the authors refer to ‘pumped protons’ and ‘chemical protons’:

And the answer is…

That the situation in photosynthesis is similar to that for the oxidative electron transport chain:

  Net translocation of protons across the membrane is achieved both
  chemically (in photosystem II) and by ‘pumping’ (in cytochrome b6f).

So the ‘someone’ in the question was correct in saying that the chemical type of net translocation occurs in photosynthesis, but was incorrect in saying that this was at the cytochrome b6f stage.

Structural Evidence

The cartoons shown above (taken from Berg et al.) are based on a wealth of indirect experimental data. However some of us are never convinced until we have seen the stigmata. The structure of the cytochrome b6f complex was reported in Science in 2003 by William Cramer’s group, and in the diagram below (my modifications) there is a channel through which the passage of protons is indicated.

A more recent (2013) paper from the same group considers the proton transfer pathway in cytochrome b6f in more depth, and I reproduce below Fig. 1B from that paper to indicate the type of molecular detail.

Heavy reading, but wonderful stuff!


Under what conditions does the body burn fats, proteins and carbohydrates?

Introduction

The system that regulates body energy store consumption is hugely complicated, but is mainly a cooperation between hormones released by the pancreas (insulin - lowers blood sugar and glucagon - raises blood sugar) and the liver (as the bodies main glycogen store and factory for various energy related tasks).

Fed State

In the fed state (high blood glucose e.g. after a meal), the body produces a large amount of insulin.  When the ratio of insulin:glucagon is high (≈0.5):

Dietary glucose is absorbed by the liver when glucose concentrations are over 8mM.  This glucose is then either

used in respiration by the liver
converted to glycogen to be stored in the liver
converted into fatty acids which are then transported out to the periphery in very-low-density lipoproteins (VLDLs)

Adipose tissue (fat tissue) takes up glucose in the blood.  This glucose is then:

used in respiration by the adipose tissue
converted into fatty acids then tri-acyl-glycerols (TAGs) - fat.  VLDLs from the liver can also be absorbed by adipose cells to be used for this.

Skeletal Muscle again directly absorbs glucose from the blood

During contraction glucose is used directly in respiration to fuel the activity
In preparation for future contraction it is converted into glycogen and stored in the cell
Amino acids are incorporated into cellular proteins though if they are superfluous then they can be used in respiration

The brain directly absorbs glucose and uses it in respiration

Early Fasting State

Where the insulin:glucagon ratio has dropped to around 0.15

In the liver

Glycogenolysis is activated to release glucose from stored glycogen to compensate for falling plasma glucose levels (signalled by elevated glucagon)
Triglycerides in the liver are preferentially broken down for hepatic respiration - fatty acids are transported in from the blood to meet the livers own energy demands
The liver begins the process of gluconeogenesis - making glucose from non-carbohydrate precursors

Adipose tissue

Rapidly starts lipolysis - stored fats are broken down into free fatty acids and glycerol.
Some of the free fatty acids are used for the adipose tissues own respiratory demands
The majority is released to the periphery to be utilised by other tissues
The glycerol released can't be used by most tissues, but is taken up by the liver where it can be used to make glucose by gluconeogenesis

Skeletal Muscle

Uptake of glucose from the periphery is reduced to preserve glucose for cells that can't easily use other fuels - e.g. the brain or red blood cells
Free fatty acids become the main fuel for skeletal muscles to conserve the glucose for elsewhere
Unlike in the liver, glycogenolysis is not activated as there are no glucagon receptors in muscle tissue.  This means glucose is only produced from glycogen when muscles are actively contracting, as before.
At this point proteins can start to be broken down,  their skeletons used as an immediate source of energy and amino acids released to be taken up by the liver and used in gluconeogenesis

The brain directly absorbs glucose and uses it in respiration.  Fatty acids can not be used as these do not cross the blood brain barrier

Late Fasting State

If there has still been no glucose intake, the insluin:glucagon ratio falls even further, to around 0.05.

Liver

No further glucose has entered the liver and within 24h all hepatic glycogen stores have been depleted
Gluconeogenesis becomes the principle source of all plasma glucose - the liver creates new glucose from:

Amino acids - muscle & liver protein breakdown
Glycerol - from adipose tissue
Lactate - from red blood cells and muscles

High amounts of fatty acids are converted into Acetyl CoA to be used in respiration by the liver, but too much Acetyl-CoA is produced.  The remainder is converted into ketone bodies that are useless to the liver, so jettisoned to be used by other tissues (esp. the brain)

Adipose tissue

As the fast continues into a few days, adipose tissue adapts to producing large amounts of free fatty acids.  This becomes sufficient for most body tissues
These fatty acids are used preferentially by all tissues that can use them, conserving glucose for the brain

Skeletal Muscle

Fuelled almost entirely by fatty acids and ketone bodies from the liver and adipose tissue
Protein breakdown continues to release carbon skeletons and amino acids for gluconeogenesis - but this is inhibited in the presence of high levels of ketone bodies to prevent unnecessary muscle wastage (still allowing the human to hunt)
Amino acids are incorporated into cellular proteins though if they are superfluous then they can be used in respiration

The brain

Once ketone levels reach a critical level, they can cross the blood brain barrier to be used as a supplementary energy source
However, it is not sufficient alone, so a net source of glucose is needed from somewhere in the body

Progressing to starvation

This process can continue for a number of weeks, with the body eventually exhausting fatty acids in adipose tissue and being unable to produce ketone bodies in the liver, losing the inhibition of proteolysis causing a last ditch response of muscle breakdown for energy.  Death is usually from heart failure resulting from cardiac muscle breakdown.

Summary

This chart might be useful in summary, it shows where the glucose levels in the blood are coming from at various stages, the gluconeogenesis line indicating protein and fatty acid breakdown:

Exercise

Exercise has to be very intense to have any effect on this system in normal situations.

Resting Muscle metabolises stored fatty acids for its own energy.  Glycogen stores are replenished from glucose ready for more vigorous contraction.
Brisk Walking fatty acid metabolism again provides almost all the energy
Sprinting Glycogen stores are used, respiration is almost entirely anaerobic as blood vessels are constricted by the muscle activity and ventilation has not had time to increase.  Lactic acid is produced, which can be used by the liver for gluconeogenesis
Middle distance running: aerobic metabolism takes over as the body adjusts to the higher oxygen demand.  Lactate is still the major end product

One example of where this may be more noticeable is during a marathon.

0 Mins - Muscle is resting at the start line, as above.
10 mins - Muscle and liver glycogen released to power muscle contraction
2 Hours - A marathon requires roughly 700g of glycogen to complete, however the liver can only store around 500g.  This is largely depleted after roughly 20 miles.  Blood glucose levels fall rapidly and the body switches to fatty acid metabolism.  This only provides around 60% of the power output and pace falls off (known as hitting the wall).  At this point, virtually every reserve power source is being used simultaneously to keep the body going.
Finish - Muscle and liver glycogen are entirely depleted. If glucose levels haven't been maintained by other means, hypoglycaemia results causing confusion, hallucinations and even coma and death.


How do warm-blooded animals keep their temperatures constant?

Since there seems to be several distinct sub-topics in your question, I will answer them one-by-one:

1). There are a variety of mechanisms that allow endothermic animals to maintain thermal homeostasis in a cold environment. The main ones are:

a). The shivering response: When the core body temperature of a endotherm drops below a critical value (36.8C in humans), it causes the posterior hypothalamus to stimulate certain skeletal muscle groups (especially around vital organs) to start to "shiver" rapidly, generating heat.

b). Compared to ectotherms, endotherms have more mitochondria per cell, thus allowing them to have a higher metabolism. Since metabolism always generates heat, an [general] increase in cellular metabolism will cause an increase in body heat.

c). Many endotherms have layers of insulating matter, such as fur, blubber, feathers…etc, allowing them to preserve body heat. In addition, endotherms can also route blood away from  capillaries via vasoconstriction of arterioles, reducing the area in which heat can be lost.

d). As mentioned by Memming, brown adipose tissue also plays a role in temperature regulation. Thermoregulation-based metabolism in brown fat causes the P+ in the electron transport chain to go through thermogenin instead of ATP synthase. This process generates heat, but no ATP.

e). Some endotherms, such as penguins and arctic wolves have countercurrent exchange in their capillaries. This is when warm arterial blood "passes" some of its heat to cooler veinous blood. This feature allows some of the heat normally "wasted" into the air to be recycled back into the body.

Note: Though it is true that endotherms are able to keep their body temperature constant irrespective of their surroundings (ignoring extremes), they do this at a cost of requiring significant amounts sustenance. Most endotherms require much more sustenance than ectotherms.

2). Your second sub-question is very interesting. Though it is true that generating heat will require substantial amounts of carbohydrates/fats/...etc, it does not necessarily mean that the net consumption of sustenance in cold environments is greater than that in normal environments. In most cases, endotherms in cold environments will have exhibit significantly less activity than when in an optimal environment. The decrease in activity when in a cold environment will likely balance out the increase in thermo-regulation based metabolism. This likely explains why people tend to drink equal or slightly less amounts of water when in cold environments. One more thing: some reactions heat-generating reactions (like the alternate ETC pathway) do not require water. Glycolysis and Krebs actually generates water (not to say that there is a net gain in the body :))

3). In truth, nothing "prevents" ectotherms from generate heat. They simply do not have the cellular "machinery". Ectotherms metabolize in ways very similar to other organisms, using molecules like ATP, glucose, fat…etc. Unlike endotherms however, they spend very little of their energy on temperature regulation. As a consequence, their overall metabolic rates are dependent on the external temperature. The point is this: A substantial portion of endotherm sustenance is used to generate heat. Only a small (if any) portion of ectotherm sustenance is used to regulate heat. As a result, endotherms require much more nourishment than ectotherms.

4). I am not entirely certain what you mean by "evolutionary path", but I will just say this: In many ways, endotherms and ectotherms are organisms that have found different ways to the same problem; how to regulate body heat for maximal survival and reproduction. Basically,

ectotherm- more dependent on environmental temperature, requires less sustenance

endotherm- less dependent on environmental temperature, requires more sustenance

5). You are quite correct. The cellular and genetic components are very similar. Some morphological aspects seem to be shared as well.

  Sources:

  Cambell & Reece (2010) Biology (9th ed)

  Swan, K. G.; R. E. Henshaw (March 1973), "Lumbar sympathectomy and
  cold acclimatization by the arctic wolf", Analysis of Surgery 177 (3):
  286–292,

  Guyton & Hall (2006) Textbook of Medical Physiology. (11th ed)

  Romanovsky AA. (2007). Thermoregulation: some concepts have changed.
  Functional architecture of the thermoregulatory system. Am J Physiol
  Regul Integr Comp Physiol. 292(1):R37-46.


How does 'phosphorylation of glucose' maintain concentration gradient in membrane transport (facilitated diffusion)?

Sort of a "magic trick" that biology does.

With facilitated transport, the movement is passive. That is, you have a protein that certain molecules/ions can pass through, but you aren't doing any pumping or using energy to move molecules. That means that the molecules are free to move in either direction, according to concentration (and electrical) gradients.

Therefore, assuming no influence of electrical gradients, the highest concentration a passively transported molecule can reach is equal concentration inside and out.

Chemically, phosphorylated glucose is not glucose. It is phosphorylated glucose. If you phosphorylate every glucose molecule that comes in, your internal concentration of glucose would stay at zero. If phosphorylated glucose can't leave via the same facilitated diffusion pathway, then glucose will effectively only come in via that pathway, it can't go back out. The result is that, although glucose inside can never be higher than glucose outside, the sum total of phosphorylated glucose + glucose inside can continue to rise above the concentration of glucose outside.

Of course, this step isn't exactly free, because it costs the energy of phosphorylation.


This Sequence Data (DNA) has very few Methionin-starts. How is that possible?

If anyone stumbles across this question, I found out what the problem was in the end:
contrarily to my assumption that the DNA sequences where all in proper 5'3'-direction, it turned out that we found the exact ORF on the complementary strand in the other direction and who knows where else. Luckily, the MMETSP-Data also featured a /pep directory, in which the needed sequences where found in a clean version.
Thanks for reading and good Luck.


What does "Origin" mean in NCBI GenBank?

The ORIGIN may be left blank, may appear as "Unreported," or may give a local pointer to the sequence start, usually involving an experimentally determined restriction cleavage site or the genetic locus (if available). This information is present only in older records.
The sequence data begin on the line immediately below ORIGIN.

[source]
Given that it's left blank in your file, it doesn't signify anything other than the end of the annotation and beginning of the raw sequence.


Double Digestion with Restriction Enzymes Using Different Buffers

NEB double digest planner is suggesting to use 2.1 buffer for your combination of restriction enzymes (XmaI 50% and KpnI 75% activity). I would be more worried about the star activity of KpnI in CutSmart buffer than the lower activity. The latter can be overcomed by prolonging reaction time or using more enzyme.


Why don't warts caused by HPV spread to the whole body?

Plantar warts grow deep into the skin and slowly [1]. It is a common thing for warts to multiply [1], but because of the slow growth speed, their symptoms [2] and the self clear-up [1] they can't end up by covering the entire skin surface of a previously healthy person.

There are cases of generalized warts in patients with immune deficiency like hypogammaglobulinaemia, impairment of cell mediated immunity [3]. The immune system plays an important role in limiting warts. There is also a case of generalized facial warts in a patient with no other known medical condition [4].

References:

American College of Foot and Ankle Surgeons, Plantar Wart (Verruca Plantaris)
MAYO Clinic, Diseases and Conditions - Plantar warts.
Reid TM, Fraser NG, Kernohan IR. Generalized warts and immune deficiency. Br. J. Dermatol. 1976 Nov;95(5):559-64. PubMed PMID: 1086679.
Semon H. Papillomatosis: Generalized Facial Warts. Proc. R. Soc. Med. 1935 Dec;29(2):90. PubMed PMID: 19990539.


Do single nucleotides spontaneously bind to ss DNA?

I am no expert on the topic, but single stranded DNA is commonly found during DNA replication, when DNA helicase splits apart the DNA strands so that the DNA can be replicated. When this occurs, the two DNA strands naturally have a high affinity for each other, bearing complementary base pair sequences, and another molecule must be present in order to prevent the two DNA strands from re-binding. These are single-stranded binding proteins, and they bind to ssDNA to prevent re-binding from occurring. As this prevents the DNA from binding to the antiparallel strand, I would imagine it has a role in preventing single DNA nucleotides from binding to the DNA strand as well.


Blood pressure difference while seated and laid down

I can't offer specific advice as to your personal readings, but it is normal to expect a difference in blood pressure between sitting & supine (lying down) positions.
I have taken this quote from the Department of Health Care Sciences at Wayne State University website.

Effects of body position on blood pressure
Blood pressure is commonly measured in the seated or supine position; however, the two positions give different measurement values. With that in mind, any time a value is recorded, body position should also be recorded. It is widely accepted that diastolic pressures while sitting are higher than when a patient is supine by as much as 5 mmHg. When the arm is at the level of the heart, systolic pressure can be 8 mmHg higher, such as when a patient is in the supine position rather than sitting. A patient supporting their own arm (isometric exercise) may increase the pressure readings. If the patient’s back is not supported (i.e., when a patient is seated on an exam table instead of a chair) the diastolic pressure may be increased by 6 mmHg. Crossing the legs also may raise systolic pressure by 2-8 mmHg. Arm position plays a dramatic role in value errors as well. If the arm is below the level of the heart, values will be too high; if the arm is above the level of the heart, values will be underestimated. For every inch the arm is above or below the level of the heart, a 2 mmHg difference will be found (Pickering et al. Circ 2005;111:697-716).

So if you are comparing your own blood pressure day-to-day, make sure you keep a consistent position.
Additionally, if you are reading guidelines for healthy/risk blood pressures, make sure you take this into account.


What's the use of DNA sequencing results?

It's just a "string" where nucleotides encode something but I have no idea what they encode specifically.

It sounds like you are describing a computer program, represented by a string of bytes on the hard drive.

Unfortunately, the analogy breaks down very quickly because DNA is vastly more complex and a lot of aspects are still poorly understood.

But the basis is the same: a string of symbols encodes information. In the case of DNA, different parts encode different things in a different manner.

The elephant in the room are of course coding sequences: stretches of DNA, contained in so-called “genes” – which code for proteins and other stuff.

Coding sequences use a fairly simple encoding schema that’s known as the genetic code, decoded in 1961. The genetic code has the nice property of being (almost) universal across all species, and easy enough for a child to understand:

Three consecutive DNA base pairs form a codon. Each codon stands for one amino acid (except for a special “stop codon”). Amino acids form so-called polypeptide chains – proteins. There are codon tables, just as you have manuals for assembly mnemonics in computing:

Unfortunately, it’s not trivial to know where genes are on the genome. Just by eyeballing the sequence there is nothing to distinguish one stretch of DNA from its surrounding. But there are certain recognisable stretches of DNA (“motifs”) which we can use to locate genes and other interesting regions.

Grossly simplified, a gene is preceded by a promoter region which is highly conserved between species (but gene-specific). Once you’ve identified one species’ promoter, you know it for other species. Furthermore, all promoters share highly similar elements, for instance the TATA box – literally the occurrence of “TATA” in the genome.

Of course, just looking for occurrences of “TATA” would yield vastly more spurious hits than actual promoters but combined with other information you get a gene model – a statistical machine which can tell you with high confidence where on a genome the genes are located.

Once you have found the genes in a sequence which you can trivially translate to amino acid sequences, you can try to form inferences about the function of the proteins (a protein’s function is an almost-direct consequence of its sequence). Unfortunately, discovering the function of a protein from its sequence alone isn’t possible but we do know the functions of many proteins.

When we now look at a genome and find a mutation in a protein-coding gene we can infer that the function of this protein is probably modified. Most mutations are so-called deleterious mutations (e.g. by deleting a single nucleotide you get a frame shift in the codons, and all the subsequent codons no longer make sense), meaning that they destroy the protein’s function.

Other, much rarer, mutations modify the protein’s function, making it more or less efficient, or giving it another function altogether.

In the simplest case (but these are rare), a single such mutation can explain a complex phenotype. This is known as a Mendelian trait and can be used to explain a phenotypes such as eye colour, but also hereditary diseases.

Usually, though, it is merely one of many adjusting screws which skew your susceptibility to a certain phenotype in one direction. For instance, you might be slightly more susceptible to breast cancer or diabetes.

This is one use of the DNA sequence, there are many more; in the last decade, we have realised that regulation of gene activity plays a much larger role than anticipated, and most research today looks at regulatory patterns on the DNA level. This is also done with sequence data, but there doesn’t appear to be a simple schema analogous to the genetic code to understand regulation. Instead, it’s a complex interplay of many completely unrelated mechanisms.


Whole Genome Sequencing vs Whole Exome Sequencing

WES, almost certainly. First of all, the vast majority of phenotype-causing variants are found in exons. For most analyses that are looking into disease causing mutations, WGS is pointless. It only makes your analysis harder and doesn't actually add anything useful.
If you know you're interested in CNVs, that's different. CNV detection is hard in general but is particularly hard from WES data. Detecting CNVs in WGS data is much less error prone. However, you really should bear in mind that there are currently no 'good' methods to detect CNVs. This is a non-trivial problem and still in its infancy. While there are various methods that can detect CNVs, none of them find all (or even close to all). In fact, this is such a problem in the field that the currently accepted wisdom is that you should use multiple methods and combine the results. In fact, many recent CNV detectors do exactly that. And they still don't find all of them (especially not in WES data). Basically, CNV detection is not for the fainthearted and is certainly not for the non-expert.
The good news is that if you do have a disease causing mutation, it is very unlikely to be a CNV. It is far likelier that you're just looking for SNPs. Which brings us to the next issue. I'm afraid the algorithm you linked to, from what I can tell, won't help you at all. You're not trying to compare your gene to a list of healthy and unhealthy ones and figure out which group is most similar to what you have. First of all, because there are many differences (mutations) that don't actually have any effect whatsoever. These so-called synonymous mutations would still be counted by your algorithm but should be ignored. Second, because tiny differences can be enormously important. There are specific tools for what you want to do; don't try and apply broad, general mathematical approaches. You need algorithms that are specifically designed to deal with biological data and which take the underlying biology into consideration.
So, what you're looking for are programs called "Variant Callers". Two of the most popular ones are GATK and FreeBayes. These will read an input genome and compare it to a reference genome and give you a list of "variants", sites where the input differs from the reference. You then want to use resources like ClinVar or MutationTaster to check whether those variants are considered pathogenic. This is a bit of shameless self-promotion since I work for the company which created it, but VarSome, "The Human Genomic Variant Search Engine" is a new variant search engine that combines information from many different sources in a centralized and easy to search repository. I recommend it highly (and it is free).
However, before you get to finding your variants, you will need to align your genome to the reference. Basically, modern sequencing methods work by cutting the genome into many, many small pieces, copying each piece multiple times and then sequencing each piece. So the output of a sequencing run is a text file that looks like this:
@SN956:1934:H55WMBBXX:2:1101:0:15733 1:N:0:NTTACTCG
NCCCCAAGGAGACTTGCTGAGACCTTGAACAAGTGACACAATGTGAGCAGAACTTGTCTTGACAGAAAATGCTTTG
+
#AAAFJJJJJJJJJFFJJJJJJJJJJJJJJJJJJJJJJJJJJFJJJJJJJJJJJJJJJJJAJJJJFAJJJJJFJJ7
@SN956:1934:H55WMBBXX:2:1101:0:15743 1:N:0:NTTACTCG
NCTTCCTCACTAAAGTCCCATTTAGTGCTGATTGTGCTTTGGCTACTTCTCCTCTTGCCATTTTCCTGAACCCACG
+
#AAFFJJJJJJJJJJJJJJJJJJJJJJJJJFJJJJJJJJJJJJJJJJJJJJJJJJJFJJJJJJJJJJJJJJJJJJF

This is usually several gigabytes (something like ~2-3G for WES and >80G for WGS). Therefore, the alignment of these sequences needs a powerful machine and you don't even want to try to align WGS sequences on your laptop. It will take weeks and will probably fail. Another reason why you should prefer WES over WGS for this. In my work, I routinely align WGS data to the reference genome and that can easily take >100GB of RAM.
The bottom line and what this rambling answer is trying to get across is that:

WES is better than WGS when searching for disease causing mutations. It is far easier to analyze the data and 99% of the cases you want are in exons. It is also much, much cheaper.
This isn't simple. You seem to think you can sort of waltz in and do it yourself. You can, but it is very far from trivial. It is also not cheap.

So, if you do actually have the money to pay for a WGS analysis (this costs several thousand euros/dollars, in case you didn't know), which is very surprising if you're just a private individual, instead of spending it on WGS, get a WES and spend your money on getting an expert to analyze your data for you. Seriously, this is what I do for a living, you really don't seem to have grasped quite how complicated it is. And no, I am not suggesting you hire me :). There are, however, companies that offer this sort of service. Use them, don't reinvent the wheel.
References
Useful review articles for CNV detection:

Zhao et al. BMC Bioinformatics, 2013, 14(Suppl 11):S1 (DOI: 10.1186/1471-2105-14-S11-S1, link)
Tattini L, D’Aurizio R and Magi A
Front. Bioeng. Biotechnol, 2015. 3:92. (DOI: 10.3389/fbioe.2015.00092, link)


I found the answer to this question and some more interesting details that people who stumble upon this might also need. First look at this paper, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191340/ and especially this figure, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191340/figure/F3/. The MSER is a ratio of the fraction of discovered peaks to the fraction of the sampled reads to recapitulate them, so if you are able to return all of the peaks with a small sample of reads then you have excellent coverage. Now even though you have great and well defined peaks you need another sample to confirm that they are indeed significant, and you can do this with the IDR, see this website - https://sites.google.com/site/anshulkundaje/projects/idr. The IDR is laid out pretty well in the supplemental material for this ENCODE paper, http://www.nature.com/nature/journal/v489/n7414/full/nature11245.html. Beautiful!!


How to manufacture different sized micelles in nano -scale?

A key factor that determines the radii of a micelle is the critical micelle concentration. The other is the the hydrophobicity of the micelles which can be measured using the contact angle. A lipid nanoparticle has a minimum size on the order of 50 nm due to the surface tension of the lipid bilayer. However, micelles can be much smaller.

As for the creation of uniform nanoparticles, I am going to claim that what I say next can be in no way a reasonable answer to a HW problem. Why? Because the information is hidden in some obscure PLoS paper (Stapleton and Swartz) with 7 citations using IVC. Typically, micelles created for emulsion-PCR are created by vigorous mixing and followed by an extrusion step. However, this creates a polydisperse droplets. Alternatively, if you were to use a microfluidic device, then more monodispersed droplets can be formed. The control of droplet size can be achieved by varying the flow rates of the aqueous phase and the oil phase as well as changing the surfactant.


Chlamydomanas are present in Kingdom Protista or Plantae?

It is generally accepted now that Chlorophyta are Plantae (see here). They are more closely related to plants than any other group of organism. Protist is a kind of basket term for any eukaryotic unicellular organism that is not an animal, fungi or a plant which is a rather exclusionary definition.

Personally, I think the kingdoms are pretty 'macro' oriented and do not really capture the diversity well of unicellular organisms. If you want to see a bunch of elderly scientist shout at each other over what appear to be arbitrary distinctions, I highly recommend attending the taxonomy session of any unicellular conference


Blood group antigens are either sugars or proteins found attached to the red blood cell membrane. ABO blood group antigens are the most clinically important antigens because they are the most immunogenic. As red blood cell antigens are inherited traits, they are usually not altered throughout the life of an individual. There have been occasional case reports of ABO blood group antigen change in malignant conditions,ABO antigen alteration associated with acute myeloid leukemia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5242122/

https://www.ncbi.nlm.nih.gov/pubmed/15135601 ( B to O change)

https://www.ncbi.nlm.nih.gov/pubmed/22270426 (New laboratory procedures and Rh blood type changes in a pregnant woman.)

A bone marrow transplant will replace the cells which make your blood cells with cells from the donor. Over about 3-4 months (life span of a red cell), your blood will become your donors type.


What caused the Mesozoic-Cenozoic radiation?

There is no real start to a radiation event.

First there are many mass extinctions and many radiation events, what you are referring to are just the most notable ones. also the big five do not occur after the odrivian the first occurs directly before.  Radiation events happen after every mass extinction even minor ones, the amount of radiation corresponds well with the severity of the extinction. The big five and the big three are just the ones we find the most interesting, not the largest, note graph below). The ordovician radiation event happened directly after the cambrian–ordovician extinction event for instance. And there was a massive diversification after the P_T extinction, it just does not get as much press because almost all the major players become extinct in later extinction events and becasue there are  fewer fossils from that time period. Every extinction event is followed by a radiation event. the Mesozoic-Cenozoic radiation is a large radiation because of the KT mass extinction otherwise it would just be the normal background biodiversity turnover.

Essentially radiations are always happening, there is always some radiation going one in some clades.  But if you suddenly wipe out a large number of species and organisms, many of those what survive will be the ones that were radiating simple becasue they were small fast breeding generalists which is also the group that radiate a lot. Small fast breeding generalists are what what best survive mass extinctions and a group that does a lot of radiating. There is also a large anthropomorphic component to this, if you take the tree of life and make a radom slice across it anywhere it sill look like many of the groups that survive are radiating becasue all the other radiation events are cut off, while we ignore stable groups becasue they are stable. You can even notice that the radiation of different groups start at different times but then explode after the event. Almost as if our artificial lines between groups is not a great predictor of diversification events. Radiation events are not one off occurrences with clear cut beginnings and ends but a prolonged uptick in an ongoing system with a lot of variation. there is no clear cut start to radiation events imagine trying to pick the exact second summer or winter begins using nothing but temperature data, there is just to much noise due to local and daily condition to make any such point anything but arbitrary.

So the large scale radiations is still caused by the extinction event, it however will almost always look like it was happening earlier becasue on a small scale it never really stops, and where we draw the lines for groups does not correlate well with radiation events, yet we still use it to decide which "groups" are radiating.

Sources

If you look at this paper and its graph you can see this effect in angiosperms. The group originates and begins to diversify before the KT but a massive upswing in diversity happens after (actually fairly long after, once the climate/extinction has stabilized)


Half-life and production rate of ion channels

The rate varies with channels and channel subunits, and you can also distinguish between membrane half-life and degradation half-life, because channels can be cycled bidirectionally between the plasma membrane and internal membranes like the ER. For many (most likely all??) channels these processes are under the control of phosphorylation and/or ubiquination.

For a rough estimate of magnitude though, the relevant time window is hours to days. I'll include a couple references below to support this time frame.

References

Bedford, F. K., Kittler, J. T., Muller, E., Thomas, P., Uren, J. M., Merlo, D., ... & Moss, S. J. (2001). GABAA receptor cell surface number and subunit stability are regulated by the ubiquitin-like protein Plic-1. Nature neuroscience, 4(9), 908-916.

Colley, B. S., Biju, K. C., Visegrady, A., Campbell, S., & Fadool, D. A. (2007). Neurotrophin B receptor kinase increases Kv subfamily member 1.3 (Kv1. 3) ion channel half-life and surface expression. Neuroscience, 144(2), 531-546.

Huh, K. H., & Wenthold, R. J. (1999). Turnover analysis of glutamate receptors identifies a rapidly degraded pool of the N-methyl-D-aspartate receptor subunit, NR1, in cultured cerebellar granule cells. Journal of Biological Chemistry, 274(1), 151-157.


Why does sexual selection evolve beautiful features?

I think I can expand on the answer by @boo2060.

The evolution of female mate choice depends on females achieving higher fitness by choosing certain males over others. At the broadest scale, there are two mechanisms by which this can occur, direct benefits, and indirect benefits.

Direct benefits
These are material things that (surprise) directly benefit the female. This might be the provision of food by the preferred male, access to a good territory or shelter that is under the control of the preferred male, protection by the preferred male, that sort of thing. Females will accordingly favour male traits that advertise potential direct benefits. These might include male size/condition/colouration, or even built structures like those of the bowerbirds. Basically, these traits show that the male knows how to look after himself, and by extension, he knows how to look after her (as males in good condition generally inhabit the best habitats and will offer the best protection and parenting).

Indirect benefits
These don't do much for the female, but they increase the genetic quality (and thus potential fitness) of her offspring. This is a much more complicated area of mate choice, and can be split into a bunch of (non-exclusive) hypotheses (below). And of course, attractive males may well offer both direct and indirect benefits.

Sensory bias: Males may, by chance, possess a trait that holds intrinsic appeal for a female. The best explanation might be that it mimics the colour or shape of a food source (e.g. fruit) that the animal eats, and thus the animal has pre-evolved preference for that colour or shape (e.g. red patches). From that point, males with more of that trait, whatever it is, will tend to be more attractive, for no rational reason. This hypothesis is sound, but is currently lacking good empirical evidence.

Fisherian sexy sons: This can in fact lead on from an initial sensory bias. Females may choose males that they find 'sexy', because their offspring will also be sexy, and thus be successfull in reproduction. This can lead to 'runaway' selection for sexier and sexier sons, at considerable survival cost for males. In this case, natural selection and sexual selection work in opposing directions.

Indicator mechanisms: This is the handicap principle or 'good genes' principle. If a structure is costly to produce or maintain, or increases the risk of predation, and yet the male possessing it is still alive, he must have good genes to have withstood such a handicap. It may also advertise that the male is not infested with parasites. The extravagant plumes of birds may be largely explained by this one, but also sexy sons and sensory bias.

Genetic compatibility: Individuals seek partners that are genetically compatible. A certain proportion of the fitness of the offspring depends on the specific combination of genes (i.e. it's not additive), and individuals that can signal or detect signals in such a way that they can choose compatible partners will have an evolutionary advantage. The best example is scent (e.g. preference for dissimilar MHC immune genes - see the human t-shirt experiment).

These mechanisms are well known in theory, but not always well-supported by evidence (yet). This is probably the best reference.


DnaK: the recommended name is Chaperone protein DnaK; the alternative names are HSP70, Heat shock 70 kDa protein, and Heat shock protein 70 (source: UniProtKB); the name of the protein, DnaK, is derived from the name of the gene, dnaK (Yochem et al., 1978, Mol Gen Genet. 164: 9-14):

  We show that a collection of 93 E. coli mutations which map between
  thr and leu and which block phage lambda DNA replication define two
  closely linked cistrons. Work published in the accompanying paper
  shows that these mutations also affect host DNA replication, so we
  designate them dnaJ and dnaK; the gene order is thr--dnaK--dnaJ--leu.

To find the recommended and alternative names of GroS and GroL, search UniProtKB . . .


What is this flat dry stick-like leaf that rattles?

I believe this a seed-pod from an Inga or Delonix plant.

Inga are native to South America, while Delonix are native to Madagascar. But they've been introduced to other places and I've seen similar plants in the northern hemisphere. Inda and Delonix are both members of the subfamily Caesalpinioideae. I found the name by searching for "seed pod shaker". Sometimes you just need to know what terms to google.

Shown in the image below is pacay, or Inga feuillei.

But your pod could also be from the flame tree, Delonix regia.


If you have a dsDNA genome and replicate it by rolling circle like most bacteriophages and many plasmids do, an endonuclease is pretty much a necessity.


According to the Wikipedia section on bacterial capsules, they're made of the same thing:

  When the amorphous viscid secretion (that makes up the capsule) diffuses into the surrounding medium and remains as a loose undemarcated secretion, it is known as slime layer.

Todar's Online Textbook of Bacteriology synonymizes "slime layer" and "biofilm":

  A true capsule is a discrete detectable layer of polysaccharides deposited outside the cell wall. A less discrete structure or matrix which embeds the cells is a called a slime layer or a biofilm.

This makes sense with what I remember learning about slime walls--the main difference I saw was that the capsule was directly associated with/only protects a single bacterial cell, whereas the slime layer is associated with/protects multiple bacteria. I'm not sure that I'd call it a biofilm though, as those are notoriously difficult to remove; their removal in hospital and food processing sysyems is a current research topic.

Regarding your three points above, I might instead argue that the slime layer provides another layer of protection in addition to the bacterial capsule.


Why Can't the passage of acquired behavior be considered acquired inheritance?

Yes, a behaviour is definitely a phenotypic trait.

Some acquired trait (typically behavioural traits but not only) can indeed be transmitted to a few future generations. But make sure to understand the mechanism. I can think of 3 different mechanisms:

epigenetics
covariance between parent fitness and offspring fitness (within one genotype and one environment) typically due to to parental care.
Transmission of tradition (in the broad sense). A tradition is also sometimes called a meme.

One will need a link to the specific paper you are reading to know what mechanism is in play in the study you are reading.


... it kinda resembles a dragonfly ...

That's because it is a dragonfly! This is a female Tramea onusta, most commonly known as a "Red Saddlebag", which comes from the red coloration found at the lower regions of the dragonfly's hindwings.

  ... it had what looked like a stinger on the end of it's tail.

That's exactly correct! Female dragonflies have what look to be a stinger, however, they're used for laying eggs instead (and not as a weapon). (source, p.5)


Roughly speaking how stable are short sections of single-stranded RNA in exposed environments compared to double-stranded DNA?

The main difference in stability is due to the very high amounts of RNase in pretty much all fresh biological materials. Naked RNA is easily degraded by just touching it with skin. The first step in most RNA extractions is often to add an RNase inhibitor.

For example, from Wikipedia's Ribonuclease; RNase contamination during RNA  extraction:

  The extraction of RNA in molecular biology experiments is greatly complicated by the presence of ubiquitous and hardy ribonucleases that degrade RNA samples. Certain RNases can be extremely hardy and inactivating them is difficult compared to neutralizing DNases. In addition to the cellular RNases that are released, there are several RNases that are present in the environment. RNases have evolved to have many extracellular functions in various organisms.


The movement you observed serves two functions:

Imitation of leaves to protect against predators
Improved stereoscopic vision while scanning for their own prey

Imitation of leaves (mimesis)
Chameleons in the wild live in trees and are surrounded by leaves. In order to protect themselves from predators they move forth and back to blend with leaves moving in the wind.
Also note that their torso shape resembles a leaf:

Why do they move like this even when there is no wind and they are not sitting on a tree? I suppose they just follow their instincts. Evolution "did not prepare" them for sitting in a cage. The lack of ability to know when to move and when not was not a evolutionary disadvantage so there was not pressure to get rid of it.
Improved stereoscopic vision
Chameleons are predators that use their tongue to catch prey e.g. grasshoppers. While they are looking for their next target, they scan their surroundings with both eyes independently, i.e. one scans the left hemisphere, the other eye scans the right hemisphere, thus during this time they have no stereoscopic vision.
Moving forth and back helps alleviating this. They can estimate the distance to their distance better through the use of motion parallax (closer objects seem to move more than object further away when we move sideways). Once they found a target they turn in its direction and then use both eyes to focus on it, preparing to shoot out their tongue.
(Disclaimer: I am not a biologist. This is from my own reasoning and the German Wikipedia article about Chameleons)


Firstly, it is important to note that, while autophagy's primary role is to 'shut down' the cell in hopes that reduced function will aid its return to homoeostasis, there is evidence of it being used as a primary method of programmed cell death in certain animals, where periods of massive cell elimination are required (e.g. insect metamorphosis). Source (Nature Review)

Your question is somewhat difficult to answer, as there is fairly limited research in the area, to my knowledge. For extrapolation purposes, it's also necessary to establish what we should consider as autophagy and apoptosis in simple organisms - how similar do the mechanisms of the processes have to be in a rudimentary form in primitive organisms to qualify as such? There is evidence of an apoptosis-like process, as well as autophagy in a range of protozoan bacteria. PLOS article (Evolution of apoptosis-like programmed cell death in unicellular protozoan parasites, Kaczanowski et. al) (Metamorphoses of Malaria: The role of autophagy in parasite differentiation, Isabelle Coppens) Additionally, based on genomic investigations, macro-/micro- autophagy are likely to be present in all non-parasitic primitive eukaryotes. (Origin and Evolution of Self-Consumption: Autophagy
Timothy Hughes and Tor Erik Rusten)

Based on some reading I did during my first degree, it is likely that both apoptosis and autophagy both developed from a precursor process that was present in prokaryotes (some bacteria, such as Myxobacteria, undergo a type of programmed cell death). An older nature article extrapolates that, based on prior research, it is likely eukaryotes came to possess the rudimentary processes of apoptosis (and likely autophagy) through the absorption of multiple strains of bacterial genomes. (Origin and evolution of eukaryotic apoptosis: the bacterial connection, E V Koonin and L Aravind)

Ultimately, I feel it's difficult to state which developed first, if, indeed, they did so separately. Assuming they originated from the same initial mechanism, which seems likely, there is a distinct possibility of them developing alongside each other. If this is the case, it's a bit of a 'chicken and egg' situation - at which point would you consider apoptosis apoptosis? There is evidence of both occurring in yeasts, as well as protozoa, so assuming these processes are indeed precursors to what we observe in multicellular eukaryotes, simultaneous development seems most likely.

Please excuse me posting the names of some articles, rather than links - I have limited use of them at the moment.


How to deduce if RNA virus infection or DNA virus infection

If you mean simply by looking at symptoms, then there is no way, especially if in the context of a medical visit.  You're better off learning the usual suspects and figuring out the patients risk and likelihood for a given infection.  A good example is Hepatitis.  Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) have similar (enough) outward symptoms, but the former is a DNA virus and the latter an RNA virus.  In fact, looking at enWikipedia's list of acute causes, it's all over the place!

If you can actually assay for it in the lab, then of course.  Although...


Yes, this should in principle work, and a number of groups have shows that it works in cultured cells:

  We found that CRISPR/Cas9 introduced InDel mutations into exon 2 of the ICP0 gene profoundly reduced HSV-1 infectivity in permissive human cell culture models and protected permissive cells against HSV-1 infection.... Combined treatment of cells with CRISPR targeting ICP0 plus the immediate early viral proteins, ICP4 or ICP27, completely abrogated HSV-1 infection. We conclude that RNA-guided CRISPR/Cas9 can be used to develop a novel, specific and efficacious therapeutic and prophylactic platform for targeted viral genomic ablation to treat HSV-1 diseases.

--Inhibition of HSV-1 Replication by Gene Editing Strategy

There's also been at least one trial in an animal model:

  Using a hydrodynamics-HBV persistence mouse model, we further demonstrated that this system could cleave the intrahepatic HBV genome-containing plasmid and facilitate its clearance in vivo, resulting in reduction of serum surface antigen levels. These data suggest that the CRISPR/Cas9 system could disrupt the HBV-expressing templates both in vitro and in vivo, indicating its potential in eradicating persistent HBV infection.

--The CRISPR/Cas9 System Facilitates Clearance of the Intrahepatic HBV Templates In Vivo


For this answer, I'm going to assume that by "sleep" you mean that it maintains a circadian rhythm/photoperiod. Recent unpublished research indicates that even protoplasts maintain their circadian rhythm under UV lights so the UV light isn't the problem. In order for the plant to "sleep" like you mention, the photoperiod needs to be maintained. The UV light needs to be on during the day and off at night. If you leave the UV light on all the time you would actually perturb the plant's photoperiod and it would be very unhealthy. Plant metabolism and photosynthesis requires both dark and light reactions. In summary...yes, the plant will sleep but you must maintatain the photoperiod by switching the UV light off and on.