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Can animals train to be noticeably stronger, faster, more agile... than other animals of the same species?
Humans have a huge variation in physical ability because of exercise differences. Olympic athletes are a number of times stronger than average people on the street. It seems that variation in animals is very small, but I am wondering if one could force an animal to follow a specific program and eat specific food to get a lot stronger, agile, etc. than an average animal of the same species.

When I visited the Cheetah Outreach Center in South Africa, the guides there told us that their captive cheetahs couldn't run nearly as fast as wild ones, and that wild ones were much more muscular than the ones in the center; their point was that actually having to run full-out or starve caused much more rigorous training than occasionally jogging after a fake rabbit on a string. That's supported by this article:

The cheetahs being studied didn’t come close to the speeds reported for wild cheetahs — the zoo animals reached 38 mph (61 kph), while the greyhounds topped out at 43 mph (68 kph).
The researchers said this was probably because the captive-born cheetahs have never really gotten the chance to let loose in the wild and run full throttle.
"They have lived in a zoo for several generations and have never had to run to catch food. They have probably never learned to run, particularly," Wilson said.

Cheetah Speed Attributed To Animal’s Ability To ‘Switch Gears’ While Running

In other words, animals in the wild are training like they are Olympic athletes,

@ArcanistLupus It's almost like they trained as hard as if their lives depended on it... :)

I once visited a zoo that had a large enclosure for cheetahs, and “feeding” the cheetah entailed hooking meat on to a zip wire running across the enclosure’s longest side. The meat hook was then propelled at high speed along the zip wire and the cheetahs had to “chase” it in order to eat. The idea was to simulate hunting to provide physical exercise.

Related question https://biology.stackexchange.com/questions/40367/how-do-crocodiles-stay-fit

Can animals train to be noticeably stronger, faster, more agile.. than other animals of the same species?

Yes, of course!
Humans are animals, so yes! But even in non-human animals. You can look for example in a tutorial on how to train a dog (or a horse) for specific skills (speed, high jump, long jump, etc...).

It seems that variation in animals is very small

Such a general statement can only be wrong. Consider dogs as an example. The fastest dogs go at 72 km/h (~45 mph) while many dog breeds barely reach 5 km/h (~3 mph; and they're all considered as the same species). So, there is a lot of genetic variation among dogs.
Now when it comes to variation caused by training it is a little harder to estimate. Consider having a look at Guy and Snow (1977), McKeever et al. (1987), Evans and Rose (1987) and Rivero and Piercy (2008). For what it is worth, note for example that trained racing horse can go up to 70km/h while most horses can go only up to 40-45 km/h. There are a number of studies showing the effect of training on horses.

I don't think that dog breeds are a great example. Clearly, breeds differ substantially due to genetic differences. It doesn't take much thought to understand that certain anatomical features would be better suited for fast running, say. However, the OP is looking for differences due to training/exercise/diet. It doesn't matter that they are in the same species, the differences are still due to non-training related causes. Therefore, I think that it would be better to use an example of variation within a breed (Although, even this could be partly due to genetic differences)-

@Eff Highly agreed! If you want to use dogs as an example then take two same sex pups from the same litter and provide a life of luxury to one but take the other on for police K-9 training and five years later let them play and I am positive you will notice great differences.

@Eff The claim I was responding to was It seems that variation in animals is very small. I indeed considered a case where a fair part of the variance is likely genetic. I never meant that the observed difference between a chihuahua and a greyhound is caused by training. But I very much agree that this is a confusing phrasing, so I clarified that I talked about genetic variance and added a paragraph with papers on the effect of training in horses. Thanks for your comment!

@Remi.b Okay, there is no disagreement then. And yes, your edits clarify things a lot.

Definitely when it comes to horses. They are selectively bred for generations to work in different sports: dressage, show jumping, endurance, racing and so on. As one example: to train a horse for olympic level dressage takes ten years or more in order to build muscles and coordination.
Some example of horse sports, several of them describes how horses are trained:
https://en.wikipedia.org/wiki/List_of_equestrian_sports#Olympic_disciplines

Welcome to Biology.SE! Thank you for answering the question. I'm not sure, though, what the link to a list of horse sports does to help support or add to your answer.

Even our ordinary trail-riding horses will be out of shape in the early spring, and will get tired doing rides that they can easily handle later in the year.

Wild animals may have less variation in traits such as speed of running, if they predominantly eat similar diets, and if the slow ones are regularly getting eaten and failing to breed. Wild animals likely run at around the optimal speed for their environment.
The process of training implies some level of domestication - humans protecting the animals, perhaps modifying their diet, and expecting them to perform a service in return.  In this situation, the animal's day-to-day activities would likely change, together with the change in diet.  Animals' physiology tends to be able to change substantially in response to these kinds of environmental and behavioural changes (phenotypic plasticity).
So I guess the answer is yes to whether animals can be trained to perform differently, but the question of whether they would want to is maybe open.

One could argue that it isn't a matter of wild animals having "less variation" but rather that the variation is harder to observe because the weaker ones are so much less likely to survive.

There are actually two questions here:

Can animals train to be noticeably stronger, faster, more agile...
than other animals of the same species?'

As a couple of others have stated, yes.  This is, in fact, evident in horse racing, dog racing, dog agility course competitions, and a few other similar competitions.  If animals couldn't be trained to become stronger/faster then those sports would not exist as they are.

Is there natural variation in strength/agility/speed/etc in animals they way there is in humans?

This question is implied by your statement "It seems that variation in animals is very small..."  In fact, statistical analysis asserts that virtually every measurable difference between organisms falls on a Normal Distribution (see also Bell Curve).  However, this only works if we compare like populations, or "apples with apples".  For example, I certainly would not compare a bull dog's running speed with that of a whippet (racing dog similar to a greyhound, and a cool Devo song).  But if I compared all whippets then they would be normally distributed.  Now, if I had a trained whippet vs a non-trained whippet then we are again going to run into problems (see point 1).
Here is the thing with the normal distribution though, 68% of the population lies within 1 standard deviation of the average.  This means that over 2/3 of the population is pretty close to average.  Further, 95% of the population lies within 2 standard deviations of the average.
Here is a slightly more realistic example of this:  The average height of men worldwide is roughly 5'10" and the standard deviation is roughly 3".  Thus 68% of men worldwide are between 5'7" and 6'1" tall.  (Yes, I'm rounding these numbers a bit but you get the point.)  You can do something similar with weight, strength, etc, though certain attributes are difficult to measure.
What does this really mean?  Well, the natural speed of say a cheetah in the wild is normally distributed.  That is, if we could measure them all.  However, in the wild, not all cheetahs survive.  As part of survival, only the fastest and strongest survive so what we actually have is a much smaller set.  This is why animals might appear to have less variation.
If you look then you can see the variations in nature.  Go to a park and stop and look at the pigeons.  Some are actually quite fat while others are not.


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What are these four large snails doing?
Hiking in some hills near Taipei after a rain, I saw lots of large snails out and about. Here "large" means the shells are say 8 cm long, and the snail itself fully stretched out 10 to 15 cm perhaps.
At one point I saw a cluster of four snails stuck together in a confusing way. The one on the right was slowly climbing uphill, pulling the other three along.
What is going on here? I see some connections between some of the snails, but I can't really understand most of what I'm looking at here, nor why four snails would be stuck together sideways like this.

The middle two, at least, are having sex with their love dart.

@vkehayas ouch!

thumb up for snails love

These are probably giant African snails, Achatina fulica, an invasive species of land snails. The two snails in the middle are mating using love darts. The other two may be waiting for their turn.
See also: Wikipedia - Achatina fulica

Yikes again! A top 100 invasive species, spreads human disease, and a delicacy according to Wikipedia.

These snails, Achatina fulica, belong to a family of land snails called Achatinidae. They are invasive and while being agricultural pests, can also be vectors of pathogens. The two snails in the middle are actually mating through a reciprocal simultaneous exchange of gametes through the sexual organs that are clearly visible. These species of land snails do not use love darts as suggested by Dr. Evenor.

Please provide citations or other forms of evidence to support your answer.

As @theforestecologist indicates - for species ID answers we expect an image from a credible source that shows the IDd species and additional evidence is necessary, such as proof that the species indeed inhabits the region where it was spotted. etc.

source: Stack Exchange

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Methods of investigating the occurrence of non-standard bases in nucleic acids
Recently the popular scientific press gave considerable publicity to three publications in Science (30th April 2021 — see below) relating to the substitution of the nucleic acid base, 2-amino adenine, for adenine in certain bacterial viruses (bacteriophages). For example Quantum Magazine:

DNA Has Four Bases. Some Viruses Swap in a Fifth.
A few decades ago, researchers found viruses that had swapped one of the four bases in their DNA for a novel fifth one. Now, in a trio of papers published in Science in April, three teams have identified dozens of other viruses that make this substitution, as well as the mechanisms that make it possible. The discoveries raise the thought-provoking possibility that this kind of fundamental genomic change could be much more widespread and important in biology than anyone imagined.

I am interested in (and my question is) how this was established experimentally, and how widespread it is in nature, but find the original papers too technical for the non-specialist. Is it possible to provide a summary explaining this, and in general terms how one would search for nucleic acid analogues in organisms?
Original Science Papers
These are listed below, with an extract from the summary of each, where I have difficulty with the technical terminology.

A third purine biosynthetic pathway encoded by aminoadenine-based viral DNA genomes “We show that S-2L and Vibrio phage PhiVC8 encode a third purine pathway catalyzed by PurZ, a distant paralog of succinoadenylate synthase (PurA), the enzyme condensing aspartate and inosylate in the adenine pathway.”
A widespread pathway for substitution of adenine by diaminopurine in phage genomes “We identified dozens of globally widespread phages harboring such enzymes, and we further verified the Z genome in one of these phages, Acinetobacter phage SH-Ab 15497, by using liquid chromatography with ultraviolet and mass spectrometry.”
Noncanonical DNA polymerization by aminoadenine-based siphoviruses “Congruent phylogenetic clustering of the polymerases and biosynthesis enzymes suggests that aminoadenine has propagated in DNA alongside adenine since archaic stages of evolution.”

If posted an answer now. It's not short, but I've tried to make it intelligible and to address the points in the question. However I have not attempted to explain the sentences word by word. The language is technical and I thought it better to indicate what each paper claimed to have achieved and the evidence for the claims.

General approach to identifying non-standard bases in organisms

Purify from source material with standard separation methods
Identify using chemical methods and comparison with known compounds
Establish the biochemical pathway for synthesis etc. — the specific reaction(s) required to produce (and handle) the compound and the enzymes responsible for catalysing these reactions.
Identify the genes for any new enzymes identified
Search the Genbank nucleic acid database for similar groups of genes in other organisms.

Notes
1 and 2. Modern methods can detect molecules in small quantities in impure mixtures
3 and 4. Often done in concert. Genes in a small viral genomes may suggest possibilities.
5. If one wishes to work on a different organism, it is then necessary to establish that the genes do encode enzymes that catalyse the synthesis of the base.
In general, a knowledge of chemistry is much more important than biology in being able to carry out this sort of work.
SPECIFIC EXAMPLE FOR BACTERIOPHAGES SUBSTITUTING 2-AMINOADENINE FOR ADENINE
1. Purification
In this case purification is relatively easy. One can physically separate the phage particles on the basis of size etc., and then extract the DNA from the protein using standard chemical separations and break it up (hydrolyse) into individual components including bases. This was first reported in 1977 in Nature by Kirnos et al..

Cyanophage S-2L was isolated from water samples taken in the outskirts
of Leningrad. It can lyse blue-green algae Synechococcus sp. 698 and
S. eloniatus strains 58 and 6907 … The phage was grown on S. sp. 698
and concentrated by chromatography on DEAE-cellulose (Whatman DE-32)
and purified by centrifugation in CsCl gradient.

2. Identification
Classically a chemist would analyse the atomic constituents and their ratio in an unknown molecule, perform partial degradation to produce known constituents, deduce a possible structure and attempt to synthesize to confirm this. The ease of identifying unknown molecules has increased over the years as the number of already identified compounds with which one can compare has increased (there had been much work done on minor bases found in transfer RNA) and the methods available have grown and become more discriminating. It is interesting that the cyanophage work was done in the former Soviet Union, where biological sciences were low in prestige and funding. Standard equipment for examining the spectral properties of compounds (the light or other electromagnetic radiation emitted or absorbed on excitation of particular chemical bonds) would be available, however. The conclusion that an unknown base was present in the DNA of this phage was almost certainly serendipitous, resulting from standard analysis of the purity of the DNA by simple spectrophotometry. (Protein contamination results in absorption at 260nm.)
There were unusual features in the spectrophotometric properties, and even more marked changes when analysis was performed by the method of circular dichroism. As 2-aminoadenine was among the base analogues that had already been described and characterized, establishing that this was the base in the phage DNA that was present instead of adenine was possible by comparison of their physical chemical behaviour.
I find it ironic, in the context of the recent publicity, that this report (which was accompanied by a more extensive paper in the journal, Virology) received little attention in the subsequent 43 years.
3. and 4. Biochemical Pathway and Genes
The first of the triplet of recent Science papers established the pathway for the synthesis of the dZTP (where Z is 2-aminoadenine) that is the precursor for DNA synthesis, the DNA polymerase enzyme that was needed to handle this modified base, and an enzyme dATPase that removed the normal DNA precursor, dATP.

It also established that four of the genes that encoded these proteins are encoded by the phage genome. The strategy by which this was accomplished is worth presenting as it has been used in other circumstances to identify the genes for particular reactions. The general logic is:

Enzymes to perform reactions not carried out by the host are likely
to be coded by the phage.
We expect a new phage enzyme to arise from the acquisition of a host
enzyme that performs the required reaction, but on a different
substrate (reacting molecule) which we know can quite easily mutate
to bind a different molecule and hence give a different product.
(Change its substrate specificity.)
Families of enzymes that catalyse the same reaction share
recognizable structural features, so we can identify candidates in
the phage genome for the reaction of interest by conceptual
translation into protein.
We can then attempt to test our putative candidate by expression and
biochemical assay and by observing the effects of deletion or other
genetic manipulation.

The summary sentence for the first paper indicates that in this case they found a gene in the phage related in this way to host gene purA. The host gene catalysed a reaction of the same chemical type as the one required, but reacted with normal purines (hence the Pur) in standard pathway, and they were subsequently able to establish that the product of the phage gene  (which they named purZ) catalysed the reaction in the pathway above. A comparison of the chemistry is shown below.

5. Identification in other organisms
One could, of course, search for 2-aminoadenine by purifying DNA from other phages (in 1977 this would have been the only option) and the authors of the recent paper did this in one case (the summary of their second paper) but they also employed the much faster
general strategy of searching the phage genome sequences deposited in Genbank for genes similar to purZ (and the other three mentioned). This is aided by the grouping (clustering) of the genes of interest — an additional indication that they work together. This clustering is not always the same, but the diagram below shows the similarities between several phages and how this gives one confidence of the presence of the pathway in phages other than S-2L.

How ancient is this evolutionarily?
The last paper is concerned with the question of when this base change occurred in evolutionary time. The general strategy is to consider a phylogenetic tree of phages — which is generally assumed to reflect the phylogeny of their host bacteria. The diagram shows an imaginary simplified phylogenetic relationship. 1. Indicates the current species at the right, with their divergence from each other at various periods in the past on the left. 2. Represents the identification of phages in which the base changes are currently found by red balls, so that in 3. by colouring the branches in red we can deduce at what point in the past the enzyme system for producing and using the modified base arose.

The third paper, in effect does this sort of thing and finds that this indicates that the 2-aminoadenine:

…has been used as an information carrier among siphoviruses since the
evolutionary divergence of actinobacteria, cyanobacteria, and
proteobacteria ~3.5 billion years ago.

Does this occur in bacteria?
This cluster of genes has not been reported in any bacteria (and you can be sure that the authors of the three Science papers looked), although one cannot exclude that this change has happened in some unstudied bacteria. However it is unlikely to be occur in known bacteria because of the rationale for its existence in phages. Bacteria have a system to combat phages called the restriction/modification system. They encode specific restriction endonucleases that cleave at specific sites in the DNA (generally 4-6 base pseudo-palindromes) and protect their own DNA by methylating bases in these sites. It was established in the 1980s that the substitution of 2-aminoadenine for adenine in phage S-2L renders its DNA resistant to many restriction endonucleases — i.e. this is a viral response to the bacterial defence system.

+1 I am relieved to see that I will (with some effort) be able to understand this thorough answer. Thanks!

I know comments aren't meant for this kind of thing, but thank you David for yet another fantastic and informative answer

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Animals with substantial five-fold symmetry besides starfish? Any land animals?
Animals with four, six and eight legs are widespread while the concept of seven legs (fictitious Heptapods) are the makings of amazing scifi short stories and blockbuster movies.
Are starfish the only types of animals currently (or ever) with five mostly equal sized appendages and substantial five-fold symmetry? Are there theories why five is unusual on land but common in the sea?
update: There is an interesting subtlety here. This answer points out that a sea star's legs are the little things under the five appendages, so I've adjusted the question to address instead five-fold symmetry and five appendages.

below: "Ophiopetra lithographica from the Lower Hienheim Beds (Lower Tithonian,Upper Jurassic) near Regensburg, Germany" from here.

below: "A green brittle star - Ophiarachna incrassata" from here.

below: "Une ophiure superbe (Ophiolepis superba) à la Réunion." from here.

I suggest that you will find it very interesting if you knew that actually there is a land animal with five limbs. If you are interested check here . I didn't want to post it as an answer because I thought it does not fully answers your question ;) . I forgot to mention that the land-animal I mentioned doesn't show symmetry to the fifth "limb".

@The_Mad_Fish I was a little hesitant to click your link until I saw it was the NewScientist. I clicked and then a big Aha! yep, well done :)

hahaha I hope that I covered you lol ;)

Many (if not most) of the Echinoderms (to which starfish belong as well) have five-fold symmetry, such as many sea liliy (Crinoidea) and sea urchin (Echinodea) species.
Five-fold symmetrical sea lilly:

Sand dollar (type of sea urchin):

Maybe you could add that they are, however, *Bilaterians (as opposed to Radiata), as their larvae, representing the ancestral state in the group, have bilateral symmetry.

I should have recalled sand dollars, thanks. OK so there are diverse members of an entire phylum, that's great! Echinoderms are also the largest phylum that has no freshwater or terrestrial (land-based) representatives so that settles it.

@AlexDeLarge that's an interesting feat.

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Is O4I2 sufficient to reprogram cells (ie induce pluripotency)?
Is exposure to the chemical O4I2 (ethyl 2-((4-chlorophenyl)amino)-thiazole-4-carboxylate) sufficient to reprogram an adult cell back to pluripotency?
They sell this chemical online for pretty cheap. My question is, if I wanted to start a colony of induced pluripotent stem (iPS) cells, would I only need to buy this or are other reprogramming materials required?

No, the chemical O4I2 (thats a name, not a chemical formula btw) only helps to induce production of the Oct-4 transcription factor. Even if just this chemical is sufficient to express Oct-4 (which it might not be, I'm not really sure about that), you still need to induce transcription of other genes (usually Sox, cMyc & Klf4) to obtain iPS cells.

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Where does the extra blood in arterial circulation when exercising come from?
When exercising more blood is in our arterial circulation.
Where did this blood come from and how did it get there ?

http://health.howstuffworks.com/wellness/diet-fitness/exercise/sports-physiology8.htm

Please do some googling before asking here.

Contraction of muscles presses on the veins and increases venous pressure, which increases blood return to the heart and therefore increases cardiac output via the Frank-Starling mechanism.
Importantly, the total volume of blood in the body does not change by this mechanism, though the amount in the arteries can increase because there is less blood in the veins.
That part of the story is just a minor contributor, though. The more substantial circulatory adaptations to exercise involve the flow rate to muscles. More blood gets to the muscles because heart rate increases, vessels in the active muscles dilate, and vessels in the gut constrict. None of these mechanisms change the amount of blood in circulation, they only change the flow rate in the muscles.

The splanchnic circulation serves as a reservoir for blood.  The splanchnic circulation consists of visceral and digestive organs.  Blood can be mobilized from these organs out to the muscles in time of need.
from http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1943356

I think of this as blood's regular job, helping move nutrients around, dropping them off in the liver.  Peacetime work.  When it is time to mobilize, blood moves out of these organs and into the periphery where the muscles can get it.
same source

The Splanchnic Blood Reservoir Normovolemic healthy male adults have a
  blood volume of approximately 70 ml/kg body weight. Splanchnic organs
  constitute 10% of the body weight, but they contain 25% of the total
  blood volume. 1,6 Nearly two thirds of the splanchnic blood (i.e.  , >
  800 ml) can be autotransfused into the systemic circulation within
  seconds (table 2). The liver and intestines each provide between 300
  and 400 ml of the blood; the spleen only contributes approximately 100
  ml, but the hematocrit of this blood often approaches 75%. Therefore,
  the splanchnic vasculature serves as an important blood reservoir for
  the circulatory system.

Other animals can mobilize more from their splanchnic beds.  Humans do mobilize blood from the spleen but dogs have contractile spleens that can actually squeeze blood out into the circulation when the muscles need it.

I sure don't understand the down vote.  Isn't this a good answer for the bio stack?

Not the down voter. Asking for reasons for down votes is unlikely to get you any answers for two reasons: 1) people are reluctant to give explanations for them and 2) even worse, when someone (like me) comes along and explains why it might have happened, they get blamed for the down vote and nasty comments ensue. Two reasons are enough, but there are more.


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Do organisms have a mechanism to control how fast mutations occur?
Sometimes the environment and other species can change rapidly (climate changes, changes in terrains from erosion, new river paths, etc), and it seems like a regular slow mutation rate would be bad, and faster-mutating species would thrive. On the other hand, this fast mutation rate seems wasteful and inefficient when the environment is changing slowly, thus slower mutating species thrive with less waste in this situation.
Organisms capable of responding to the pace of environmental change would seemingly do well in both situations. Does such ability to modulate the rate of mutation/evolution exist in nature?

The ability of a population to respond to environmental change through evolution occurs over generations, and so the generation time of an organism has to be less than the time scale of the environmental change for such an increase in mutation rate to be beneficial.
For bacteria at least, the answer to your question is yes. Bacterial stress responses involve upregulation of error prone polymerases and thus lead to an increased mutation rate. Check out this paper (links and emphasis added):
Foster PL. 2005. Stress responses and genetic variation in bacteria. Mutat Res 569(1-2):3-11.

Under stressful conditions mechanisms that increase genetic variation can bestow a selective advantage. Bacteria have several stress responses that provide ways in which mutation rates can be increased. These include the SOS response, the general stress response, the heat-shock response, and the stringent response, all of which impact the regulation of error-prone polymerases. Adaptive mutation appears to be [a] process by which cells can respond to selective pressure specifically by producing mutations. In Escherichia coli strain FC40 adaptive mutation involves the following inducible components: (i) a recombination pathway that generates mutations; (ii) a DNA polymerase that synthesizes error-containing DNA; and (iii) stress responses that regulate cellular processes. In addition, a subpopulation of cells enters into a state of hypermutation, giving rise to about 10% of the single mutants and virtually all of the mutants with multiple mutations. These bacterial responses have implications for the development of cancer and other genetic disorders in higher organisms.

This mechanism may be involved in the evolution of antibiotic resistance, for example (emphasis added):
Cirz RT, Chin JK, Andes DR, de Crecy-Lagard V, Craig WA, Romesberg FE. 2005. Inhibition of Mutation and Combating the Evolution of Antibiotic Resistance. PLoS Biol 3(6):e176.

The emergence of drug-resistant bacteria poses a serious threat to human health. In the case of several antibiotics, including those of the quinolone and rifamycin classes, bacteria rapidly acquire resistance through mutation of chromosomal genes during therapy. In this work, we show that preventing induction of the SOS response by interfering with the activity of the protease LexA renders pathogenic Escherichia coli unable to evolve resistance in vivo to ciprofloxacin or rifampicin, important quinolone and rifamycin antibiotics. We show in vitro that LexA cleavage is induced during RecBC-mediated repair of ciprofloxacin-mediated DNA damage and that this results in the derepression of the SOS-regulated polymerases Pol II, Pol IV and Pol V, which collaborate to induce resistance-conferring mutations. Our findings indicate that the inhibition of mutation could serve as a novel therapeutic strategy to combat the evolution of antibiotic resistance.

To expand on the first point in this answer, that's a big reason why "diversity" both in an ecosystem and within a species is important to conservationists in the face of changing climates, etc. Low populations or genetically isolated groups are less likely to have the diversity necessary to survive changes in the environment, because for many animals there just isn't enough time to respond with new mutations when the environment changes, the diversity has to already be there.


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Can I train my non-dominant hand and make it dominant?
Are our dominant limbs decided on birth or is there some way in which I can train my non-dominant hand and make it as coordinated as my dominant?

You can find science studies and less thorough reading material on that from google, including for becoming ambidextrous. i.e. scientific american suggests that: It is possible to train your nondominant hand to become more proficient. A concert pianist demonstrates superb skill with both hands, but this mastery is complementary rather than competitive. My maths teacher was obliged to write right handed since he was in school, even though he was left handed. We agreed he was the least legible of our teachers.

Of course you can train yourself and make your non-dominant hand to be equal or even greater than your actual dominant handedness. Handedness is directly wired to the right/left hemisphere of your brain, so by training, you will actually re-wire your brain and acquire new pathways. It's a hard process in terms of breaking habits, otherwise, it's non-invasive and non-painfull, where most humans tend to give up before acquiring this skill justifying it as an unnecessary/low priority goal.
Handedness is not decided upon birth. It's gained in the earlier process (while a child is still in mother's womb) based on personal/individual preference (expressed by sucking a finger btw) toward right-handedness (90%) or left-handedness (9%), cross-dominance/ambidexterity (1%).

https://youtu.be/DU3OdTLuHf0
https://en.wikipedia.org/wiki/Handedness
https://ghr.nlm.nih.gov/primer/traits/handedness


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Why do sperm have centrioles and do female eggs cells even have centrioles?
I was just wondering why it is that sperm have centrioles underneath the acrosome, but that also prompted a thought as to whether eggs have them too?

Oocytes do not have centrioles. During fertilization, the centrioles of the sperm become the centrioles of the zygote. Only one pair is needed, as there is only one cell (i.e. zygote) right after fertilization.

Please add a link, summary, and/or citation for a source to back up your claims.

During fertilization the centrosme inter the ooplasm with the sperm nucleus,  if the oocyte still keep its centrosme there will result 2 centrosme in zygote with 4 centriole. Each one will migrate to pole of cell and produce 4 poles not two and the 4 daughter cells of one division will have one centriole in this case through mitosis will shut off.

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text:
What's this insect (Oregon, USA)?
Any ideas? This was taken in July on the beach of Bandon, OR, in the USA.

Your picture most likely shows Lichnanthe rathvoni of the family Glaphyridae.

The older answer is almost certainly not correct in any of its guesses; all of the possibilities listed are Palaearctic (see the sites https://fr.wikipedia.org/wiki/Epicometis_hirta, https://en.wikipedia.org/wiki/Tropinota_squalida, and http://www.coleo-net.de/coleo/texte/oxythyrea.htm for confirmation; the first and third will need translating for those not fluent in French and German, respectively).
Referring to Part V of M. H. Hatch, The Beetles of the Pacific Northwest (1971) (which covers the states of Idaho, Oregon, and Washington, and the province of British Columbia, in their entirety, and the western part of the state of Montana), and assuming the subfamily Cetoniinae is correct, I had thought this was Trichiotinus assimilis Kirby; there are inconsistencies between this photo and those provided by bugguide.net (see http://bugguide.net/node/view/22486); specifically, the elytra here are well-separated apically, and the coloration is quite different.  A review of Volume 2 of American Beetles showed me my error: the insect is a member of the family Glaphyridae (formerly a subfamily of Scarabaeidae), and the genus Lichnanthe; returning to Hatch, 1971 shows only L. rathvoni LeConte from the covered area; photos of that species in bugguide.net (see  http://bugguide.net/node/view/115846) show some variation in markings from the photo here (which is to be expected), but are structurally fairly close.
The genus Lichnanthe was most recently revised in the following paper:
Carlson, David C..  1980.  Taxonomic revision of Lichnanthe Burmeister (Coleoptera: Scarabaeidae).  Coleopterists Bulletin, 34(2):177-208.
which is available through JSTOR (a subscription, one-time payment, or access through a university will be needed).

This question already has an accepted answer. Given that your answer suggests the question refers to a different species than the one in the accepted answer, you should provide further evidence to why you think your answer is the correct one (at least a picture and a contrasting discussion what features match your ID but not the suggested one), otherwise your answer will probably be down-voted. Thanks!

In addition to my comment under the previous answer, see figure 103.34 (page 69) in the reference I cite there (the elytral markings differ from those in the photograph, but those can vary from one individual to another).  Figures 101.34 and 104.34 illustrate two of the other three Pacific Northwest genera (and the genus that is missing is most frequently encountered with ants).

After considerable delay I finally obtained a copy of Carlson 1980; that work reinforces the identification given above (the new species named by Carlson were not found in Oregon at the time of description).

Awesome, I already up-voted after your last edits, so my +1 still holds. :-)

I'm pretty sure it is in the Cetoniinae (flower beetle) family. Off-hand I would put it in the genus, Tropinota. It may be a subspecies or relative of Tropinota squalida or Tropinosa hirta. But it could also be closer to the genus Oxythrea.

The two (three? I'm assuming that either "Tropinota" or "Tropinosa" is a misspelling) genera given here do not appear in Arnett, et al., 2002, American Beetles volume 2 (pages 67 to 71).


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Why does size decrease across the sequence of human chromosomes?
The following graph shows a decrease in the number of base pairs per chromosome across the sequential set of human chromosomes:

Is this because chromosomes were originally numbered by their size on the karyotype?

You nailed it!
Nomenclature
Autosomal chromosomes
Chromosomes are numbered based on their size (in base pairs).
Sexual chromosomes
Sexual chromosomes (when they exist) are defined as the largest number regardless of their length. Note that the definition of a sex chromosome can sometimes be a little bit troublesome (see this book).
Exceptions
It sometimes happens that the first approximation of the length of a chromosome is inaccurate and that chromosomes are therefore numbered wrongly. In such case, when we realize the mistake, we just keep numbering the chromosomes the same way we did before even if it doesn't follow the standard nomenclature! This is, for example, the case of chromosomes 19 and 20 in Homo sapiens as you can see on your barplot. Chromosome 20 is actually a little bit longer (by about 4.5 Mb) than the chromosome 19. There are many other types of exceptions as well. Thanks to @Dexter  pointing out int he comments that in Drosophila melanogaster (model organism) the sex chromosome is numbered before the automosomes (autosome = non-sexual chromosome).

Sometimes people use sex chromosomes at starting and then autosomes (e.g: Drosophila melanogaster )


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Why do small organisms make faster movements than big organisms?
I hesitated to ask this question because it seems so obvious and intuitive. However, I am not able to explain this tendency.
Background
It seems to me that small organisms make faster movements than big organisms. I don't mean that they are able to travel at higher speed (the cheetah is a big animal and is the fastest terrestrial species) but I mean that their movement are fast, quick and their members undergo high acceleration.
Examples
I would guess for example that the legs of a tiger beetle (clade of fast sprinter beetles) (see movie) undergo much higher acceleration than the legs of a cheetah (fastest terrestrial organism on earth) (see movie). To avoid taking the extreme, I would think that the legs of a Drosophila (see movie) undergo higher acceleration than the legs of a dog (see movie). The organism that is able to create the fastest acceleration is the mantis shrimp. Wikipedia says:

Both types (smashers and spearers) strike by rapidly unfolding and swinging their raptorial claws at the prey, and are capable of inflicting serious damage on victims significantly greater in size than themselves. In smashers, these two weapons are employed with blinding quickness, with an acceleration of 10,400 g (102,000 m/s2 or 335,000 ft/s2) and speeds of 23 m/s from a standing start. Because they strike so rapidly, they generate cavitation bubbles between the appendage and the striking surface. The collapse of these cavitation bubbles produces measurable forces on their prey in addition to the instantaneous forces of 1,500 newtons that are caused by the impact of the appendage against the striking surface, which means that the prey is hit twice by a single strike; first by the claw and then by the collapsing cavitation bubbles that immediately follow. Even if the initial strike misses the prey, the resulting shock wave can be enough to stun or kill the prey.

Finally, note that Gabel and Berg (2003) show that the flagella can rotates up to 270 Hz.
Questions

Am I right to think that small organisms tend to make faster movements than big organisms?
If yes: Why do small creatures make faster movements?

Does it has to do with time for chemical diffusion?
Does it has to do with mechanics? ($F=ma$... But muscles are smaller as well).
Does it has to do with the resistence of biological tissues?
...

This might be explainable with physics, force = mass * acceleration, so acceleration = force divided by mass. If the mass is small enough, then it won't take much force to get large accelerations. While smaller muscles won't generate as much force as the larger muscles, their reduced mass may still allow greater acceleration.

Muscles are much smaller as well so that it is not totally intuitive to me why acceleration is higher in small organisms.

Right, but I'm not sure how mass and force scale with muscle size. Mass should scale linearly with muscle volume, assuming constant density, but force generation might not scale the same way. If smaller muscles can produce more newtons/gram, they could produce higher accelerations.

Yes, indeed! I'd be curious to get some more info to see if this is a plausible explanation.

I think this might have something to do with Kleiber's law which is approximately true. It basically states that larger animals have slower metabolisms than smaller animals. http://equation-of-the-month.blogspot.co.uk/2012/06/kleiber-law.html
If Kleiber's law is true then smaller animals would have more disposable energy per unit mass compared to larger animals which would allow them to have relatively large kinetic energies.

It's a general phenomenon that the time scale correlates with the size scale of complex systems.
Energy consumption is the main concern dealing with the speed for biological organizations.
In the absolute sense, a turtle has a higher speed than a small bug. But based on their sizes, the bug seems much quicker and faster. So we need to normalize the speed with the size scale which we can temporarily call 'fastness".
Here is the relationship between the fastness and the mass:

Where u is speed of the organism, M is mass, alpha is a constant which we assume that the metabolic energy is related to the body mass of the organism with a power law.
The final equation says that if alpha > 1.67 then the larger would be faster. But our observation tells us that the smaller the faster. Therefore, we know alpha < 1.67.
In fact Kleiber's law tells us that the alpha is about 0.75.
You can check some numbers related to some animals here

An increase in linear dimension by $x$ causes an increase of $x^3$ in volume and mass.  The force that a muscle can generate roughly scales with the cross-sectional area of the muscle, an increase of $x^2$ for a muscle scaled by a factor of $x$.
This means that larger animals need proportionally larger muscles (by a factor of $\sqrt {x}$) to achieve the force required to generate any given acceleration.  This becomes impractical fairly quickly, so we just make do with less acceleration.
If you consider a 1 cm ant scaled to human size with no other modifications (a 200-fold increase), it would be 8,000,000 times more massive but its muscles would only be 40,000 times stronger.  It may have started out about 50 times stronger than a human, mass-for-mass, but at human scale, it's only 1/4th as strong; it would barely be able to move at all.
There are other biomechanical factors that can influence speed that favor smaller creatures as well.  One example is the ability of mantis shrimp to store amounts of mechanical energy that are quite large on their scale in the curvature of their exoskeleton (like storing energy in a car's leaf spring.)  Similar energy storage on a human scale is just not practical.


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Is it worth to experiment with pro-biotics at home?
Let's assume that Joe has done some investigation on Internet and wants to see, if pro-biotics would help him. Now he goes to amazon.com and buys a pro-biotic product with excellent average rating. Note that not all of the reviews are from  "Amazon Verified Purchaser" for the specific product, but you got the point that it sound convincing that other people claim to benefit from the product.
So validity of Joe's pro-biotic experiment starts from pro-biotic supply chain. What are the steps in his pro-biotic experiment where experiment could go wrong; and what are the precautions he can take to make his experiment successful - either prove or disprove their benefits?
In the answer I seek something between lines (feel free to reuse these points to make your answer whole):

Joe should be confident that seller is selling the real thing and not  candies. Are there any regulations that ensure that there is no fraud going on at this step from Over-the-Counter seller? How common is such fraud by sellers? Have there been any studies?
The bacteria might die during shipping before Joe actually received his pro-biotics, for example, because of temperature changes. Obviously responsible seller should know how his merchandise should be shipped.
Joe should probably not take pro-biotics together with other drugs or even together with other pro-biotics, because they might kill each other.
There already could be some bacteria living in Joe's body that immediately kills "good bacteria" in pro-biotics without even making it.
And most important - The initial hypothesis found by Joe on Internet about "good bacteria" in pro-biotics was wrong in the first place. Is there a website that I can check with convincing research that has studied how each bacteria affects our body as a whole?

Also, would it be worth to grow culture of pro-biotics at home to make sure that there is bacteria in the first place? How hard that would be? We have microscope at home.
The reason I am asking this is because a person very close to me is super excited about pro-biotics so that it starts to affect my life. I just want to get opinion from people in the biology field on how skeptical they are about DIY people doing such pro-biotic experiments at home. I am not sure yet whether I should support this person or try to talk out of this. It seems that this person has been reading a lot on Internet about this subject so it is not easy for me to argue back.

The supplement market in the United States is regulated by the Food and Drug Administration, however, they are not required to prove that their products work as they are usually sold as a food supplement and not as a medicine. As such, their clinical studies, if done, come under little scrutiny. Also there is a very small number of the species that make up the human microbiome that can be cultured outside of the human GI tract. A healthy diet is likely a better solution, unless of course "Joe" has a medical condition such as IBD and can find a Doctor willing to perform a fecal transplant.

@AMR With "Also there is a very small number of the species that make up the human microbiome that can be cultured outside of the human GI tract." did you try to imply that it is impossible to make pro-biotic supplements in the first place, because most species of good-bacteria would die right away once packed in pro-biotic capsules? I.E. suggesting that pro-biotic suppelement claims for that kind of bacteria would be scam? Is there somewhere a catalog of bacteria that would identify these kind of bacteria that can't be transferred via capsules?

"Studies of Segmented Filamentous Bacteria biology have been hampered by the current absence of ex-vivo culture methods." -Ivanov II, Littman DR. Segmented filamentous bacteria take the stage. Mucosal Immunol. 2010;3(3):209-212 Nothing in science is ever impossible it is just a question of feasibility and whether someone has accomplished it. Obviously the ones in yogurt can be cultured, but many of the ones that they find genomes for in samples have not bet cultured, yet. The question of whether they can be ingested in capsule form and populate the colon is up for debate.

If you look at my answer here http://biology.stackexchange.com/questions/41478/can-an-argument-be-made-that-humans-are-90-bacterial and here http://biology.stackexchange.com/questions/41415/do-intestinal-flora-have-the-same-dna-as-their-host/41429#41429 I have provided a lot of details about the microbiome and there are many references linked that you can research for yourself.

This is a list of the 539 journal articles that have been published as a result of the Human Microbiome Project. https://commonfund.nih.gov/publications?pid=16

Statistics-wise the sample size is too ridiculous to call this an experiment, because you can't control any random effects if your sample consists of a single person.

I agree with Eli, unless you have a lab and a moderate amount of microbiological training/skill, you're not going to know the answer to any of those questions.  When it fails, you'd have no way of knowing where.


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Which is better adapted for global warming: deciduous or evergreen trees?
Evergreen photosynthesise for longer and don't lose their leaves all at once, whereas deciduous plants do and enter periods of hibernation during winter, among other differences (correct me if I am wrong).
Is there any significance in these differences considering the future impact of global warming on trees?

Please edit your question so it takes into account rules of thiw site http://biology.stackexchange.com/help/dont-ask there is no actual problem to be solved: “I’m curious if other people feel like I do.”

Which kind of tree do you see as you move towards the equator? That should give you a pretty good idea of what matters in warmer climates.


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What is the difference between stomata in evergreen broadleaf trees and deciduous broadleaf trees?
They must have some difference in their stomatal density /whether they are hypostomatous or amphistomatous/whatever, mustn't they?

@Christiaan - Evergreen have needles. Broadleaf have broader leaves, which are generally larger than needles. It is not unreasonable that two trees of similar size need a similar number of stomata. So the question is how do the stomata of the two types of leaf differ? Do needles have a higher density? My first thought would be that evergreen trees must have more needles than broadleaf trees have leaves.


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new DNA sequencing technologies?
Last year I did my thesis in the field of a new method for DNA analysis.
Which I think is very interesting although I cannot seem to find any new methods in this field especially the SMRT sequencing method.
Do you maybe know a new method(s) which are introduced for DNA research in the area of SMRT sequencing ?

You mean new sequencing technologies introduced since last year?

I think you expect the development of new technologies by far to fast. I am not even sure if new experimental ideas have been developed in this time, let alone made commercial.

This question is broad. Nobody knows what you have done in your thesis. Please explicitly mention what kind of analysis you are interested in. Research is always happening and there is always some development. Unless you provide specifics, your question may be put on hold.

@WYSIWYG I already have my answer :)

Yes, there's a new technique called Sanger sequencing. Have you heard of that? In other words, if you don't tell us what you know, how can we tell what you don't know?

Community edits to clarify, and votes to reopen, I'm too new on this particular site to help rep wise, but I think from the comments that the accepted answer is conformed by the O'P'er to be excellent, the O'P'ers meaning seems therefore to be now understood sufficiently.

I don't know, which technique you worked on, but there are the so-called 'Next Generation Sequencing' methods. I think the oldest of that is a pyrosequencing technique called 454 sequencing (I think it is provided by Roche). However, this method is too expensive compared to even newer methods and the support will be stopped within the next months, as far as I know.
Furthermore, there are the Illumina and the ion torrent technique. Finally, there is SMRT sequencing of which some people say that this is even third generation sequencing. I think, this paper provides a nice overview. And if you're interested in further reading, yet you know what to search for.

thanks for you comment, so there aren't any new techniques at the moment. I didn't work with them but i know every one of them and how they work. I worked on a new nanohole based single molecule sequencing technique

I'd recommend working on your question @pwghost even though it may well not get reopened.

@alan2here edited it :)

Sorry for being vague with my comment, I've found this frustrating enough myself so I do apologise for doing it as well. I think it's the word "new", could you narrow that down, perhaps to this and last for example?


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Cellular respiration — How is the water expelled?
The equation of cellular respiration is as follows:
6 O2 (g)  +  C6H12O6 (aq) $\rightarrow$ 6 CO2 (aq)  +  6 H2O (aq)  +  ATP
How is the water produced expelled from the body (of course, after some of it is used)? Is it expelled in urine? Or is the water vapour we breath out actually the by-product of respiration? Or, is it expelled in both methods/ways?

Homework is an appropriate tag for this question. Take a look at this to learn what fall under homework.

Sure. I misconstrued homework questions to be relating to questions that come in your assignments/projects/etc. Good that I read it. Thanks.

there is complex interchange of substance between different metabolic pathways.

@SanjuktaGhosh. As one who taught this for 24 years, I doubt this is a homework question, I think it's curiosity.

It appeared trivial to me because the water produced as byproduct in a reaction becomes part of the cytoplasm's water and it can be used up either in any other metabolisms where it is needed or by simple diffusion end up in blood from where it might get excreted out or recycled back to the cells. The water can even be excreted as sweat or end up in any other body secretions. As such though it is curiosity but is eligible for homework tag. @bpedit

Edited: I was wrong, the balance varies quite a bit by species. Reptiles and birds are far more water efficient than large mammals becasue they do not lose water through sweat or urine. There are animals that are metabolically water neutral, but humans are not one of them. In humans the water produced metabolically does far exceed the water used metabolically. I should have realized that reptile also produce less water. source 1source 2
In humans there are three main ways water is take in, drinking, injection (food), and a net metabolic production. There are four major losses, urine, sweat, respiration, and feces. so it is through one of these four methods.

This doesn't sound right. Metabolically, the human body is a net producer of water, as the respiration equation suggests. We require water because of respiration, sweat and urination, but this is a matter of using ingested water as a solvent to "flush out" other waste products. Water is not consumed by the body for metabolic purposes.

it can't be only urine and sweat , becasue organisms that use uric acid and don't sweat still need to drink.

I did a major edit, I am so used to dealing with birds and reptiles I hadn't considered how much it might vary.


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Please help Identify these algae
Found this algae in a small stony stream that feeds a medium sized river. I can not identify either of the filamentous algae in this photo

@GerardoFurtado sorry, just uploaded

Please add a location and the relative length /width. (and add a scale/let us know the magnification) . Thanks.

@theforestecologist, I do not know the relative size, but that is 40x magnification. I apologize all i have access to is my high school science lab

@theforestecologist This sample was from green algae growing on large granite rocks in a stream feeding the Dan river in North Carolina

@northcarolinaalgae you could mention that in the question.


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Can bacteria be reservoirs for animal viruses?
When people talk about reservoirs, they usually talk about bats, dogs, deer, etc. All animals. But can bacteria be reservoirs for animal viruses? Any examples?
I know that bacterial viruses can at least infect bacteria (bacteriophage). But can animal viruses also hide in bacteria for extended periods and come out at "will" by commandeering bacterial machinery?
I know that bacteria have different polymerases and ribosomes than animals, but is this at least a theoretical possibility?

https://en.wikipedia.org/wiki/Prophage

I have assumed that the you mean animal viruses when you refer to viruses (otherwise your question does not make sense) and have altered the question to make this explicit. If I am incorrect, please reframe the question clearly.

Does this answer your question? Can viruses that normally infect eukaryotic cells also infect bacteria?

The Answer is No
There are no examples of animal viruses infecting bacteria or incorporating themselves into bacterial genomes. Nor is it a theoretical possibility, given our knowledge of bacteria, eukaryotes, eukaryotic viruses and bacteriophages.
Why is it not a possibility?
As the questioner admits, the replication, transcription and translational systems of eukaryotes and prokaryotes are quite different. None of the known viral genomes could replicate and their genes be expressed in cells of the other kingdom. Why, the questioner may ask, could not a virus evolve to have signals recognized in both types of cell — at least in theory. Perhaps it could, but there is another factor to be considered, and this is the question of how viruses interact with the cells they infect. This is relevant to how other species can harbour human viruses and why there would be nothing driving a virus to acquire the means to replicated and be expressed in both system.
Receptors for Viruses on Host Cells
The point the question fails to take into account is that entry of both eukaryotic and bacterial viruses is a specific process involving interaction between protein or carbohydrate components of the virus and those in the membrane of the host cell. The host components are called virus receptors, and generally differ for different viruses. There are many reviews of this topic in the literature, so I cite a couple of examples freely available on the internet: Grove and Marsh on animal viruses and Rakhuba et al. on bacteriophages.
Viruses evolve to exploit one particular host species, and tend to be specific to that species because, although there may be a functionally similar protein in other species, differences in amino acids in the proteins (or sugars in carbohydrates) preclude recognition. When viruses cross the species barrier, this is due to mutations that allow recognition of the receptor protein in another species. If the change still permits recognition of the receptor in the original species then even if the virus is eliminated from the second (e.g. human species) it will still be present in the original species. Subsequent contact between humans and the species can therefore lead to a reappearance of the virus in humans.
This is how the original species acts as a reservoir. There is no question of a virus ‘hiding’ in bats by some sort of evolutionary pressure to allow it to return later to humans. Understanding this you will see that:

The differences between the membranes of bacteria and humans are so great that there is little likelihood of an animal virus finding a receptor on a bacterial cell.
Even if it managed to do so, it would not be able to replicate in the bacterium.
There is no evolutionary pressure that would select for the series of mutations that could convey the ability for such replication.

Footnote: ‘Dormant’ Viruses
There is another quite different phenomenon in which certain bacterial or animal viruses ‘hide’ within the species they normally cause a lytic infection. This involves incorporation in the genome and later release. In bacteriophages it is called lysogeny and in animal viruses examples include retroviruses and herpes viruses. This has no relevance to the question.

I have greatly extended my answer, explaining why the answer is no, as I thought it important to talk about the role of virus receptors in viral infection and species specificity. The confusion of ideas about viruses 'hiding' also needed to be addressed.


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Explanation of the results of Warburg's Flashing Light experiment?
Between 1919 and 1920† Warburg obtained a higher rate of photosynthesis in Chlorella, exposed to rapid alternating periods of light and darkness, than when exposed to constant illumination.  I would expect the opposite — that continuous illumination would generate more ATP and $\ce{NADPH}+ \ce{H+}$ in the light reaction, and thus give a higher rate of photosynthesis. In the light of what we now know about photosynthesis, is there any obvious explanation for Warburg’s results?
†Cited by Emerson, Robert and Arnold, William (1932)

Can you pls put a link to his paper?

I cannot comment so I write here. Besides details that I let to people with better knowledge than me, it seems you compare or "equate" amount of product and rate. That is not correct. Think of a sprinter (that actually stop, breath and eventually restart) and a marathon runner. Who is going faster and who is covering the longer distance? Indeed I suspect that a kind of fatigue is at play, like inhibition, saturation of some path. However this latter is just me speculating. I wanted to point out the difference above. It might help.

Your justification was indeed a help.  I read this logic somewhere, but want to know precisely what the inhibitory factor is. Besides it may seem that I'm confusing rate and yield, due to my last line, but actually I'm talking about rate and not yield..

I have taken the liberty to gut this question of the references to a possible effect of the light on the 'dark' reactions of photosynthesis as the poster provided no reason or logic to make such a connection and there is no reason to make such a connection. Warburg was not in a position to deduce anything much from the original experiment, but I think it is still of interest (5 votes) to ask if his observations can be rationalized in terms of today's knowledge of photosynthesis. So I have recast it with that single focus. There seems to be literature out there discussing it.


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Difference between imputing and typing in GWAS studies?
In genome-wide association studies (GWAS), what is the difference between imputing and typing? Are they the same?

'Typing' is an SNV-typing. It is an explicit SNV detection using Affymetrix GeneChip arrays, Illumina BeadArray.
'Imputing' is an imputation. It is a statistical inferring from existing genotype data using haplotype estimation. It is useful because different genotyping arrays genotype a slightly different set of SNVs and they can't detect all variants as whole genome sequencing is still pricey.

No, they are different altogether.
Typing in GWAS is genotyping individuals from a selected population to know say the genetic variation of SNP's (single nucleotide polymorphisms) among them via chips like Illumina Core-Exome etc.
Imputing is the statistical process of imputation of SNP's of an individual from a reference source like the HapMap reference panel. The process is a bit complex and typical tools like IMPUTE2/BEAGLE4/MINIMAC2 rely on HMM (Hidden Markov Models) to fill in the SNP's.
So, in essence within a GWAS study first, we genotype individuals (as it's cheaper than sequencing all SNP's) and get 300-500k SNP's via the chips as above, then impute the remaining variants using an established Human Genome Reference panel using the above software.
Edit:
An excellent resource for understanding imputation is Yun Li's 2009 paper.

Please add some references to your response.

I have added one here, but I usually don't see references in the answers from most of the people in this forum !!!


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Can Oxaloacetate cross the outer mitochondrial membrane?
I am aware of the Malate–Aspartate Shuttle, but something is not clear to me and different sources seem to contradict each other. Some show oxaloacetate (OAA) being reduced to malate in the mitochondrial inter-membrane space (IMS), whereas others show the reduction happening in the cytosol.
Where does the OAA → malate reduction happen? i.e., can OAA cross the outer mitochondrial membrane (from the cytosol into the IMS) so that it can be reduced in the IMS, or must it be reduced in the cytosol before crossing either of the two mitochondrial membranes?

I've edited your question a little. I defined the abbreviations you used. This makes the question clearer and I mention it in the hope that it will help you in formulating future questions. (It is not necessary to abbreviate malate to mal to save three characters, so I spelled this out in full.)

In general the outer mitochondrial membrane is thought to be basically permeable (through porins) to small molecules such as OAA. As is typical in biology, the situation may actually be more complex -- see for example this paper. But I think the default assumption is that metabolites freely cross the mitochondrial outer membrane.
You might also ask whether either the mitochondrial MDH or the cytoplasmic MDH enzyme is likely to be found or be active inside the intermembrane space.

Good point about considering which enzyme is active. Thank you for the concise answer.

Oxaloacetate (OAA) cannot cross the inner mitochondrial membrane.
The process of oxidative phosphorylation and the electron transport system (ETS) occur in the mitochondrion, whereas $\ce{NADH}$ generated by the reduction of $\ce{NAD+}$ in glycolysis is in the cytoplasm. The problem is that the inner mitochondrial membrane is not permeable to $\ce{NADH}$ , so a shuttle system is required for the transport of the reducing equivalents through the mitochondrial membrane. There are two of these, one of which is the ‘Malate–Aspertate’ shuttle.

In the process (see above) oxaloacetate (OAA) takes up the reducing equivalents from $\ce{NADH}$ to form malate in a reaction catalysed by malate dehydrogenase. The inner mitochondrial membrane is permeable to malate, which passes through carrier proteins (Malate-$\alpha$-ketogluterate transporter) into the mitochondrial matrix where it is converted back to OAA. As this happens the concentration of OAA decreases in the inter-membrane space, and as OAA cannot pass directly through the inner mitochondrial membrane it is converted into aspartate in the mitochondrial matrix by reacting with glutamate to produce $\alpha$-ketoglutarate and aspartate. The aspartate then travels  to the inter-membrane space through specific carriers(Glutamate-aspartate Transporter). In the inter membrane space the aspartate combines with $\alpha$-ketoglutarate to form glutamate and OAA (the reverse of  what happened in the mitochondrial matrix). Thus the concentration of OAA is maintained in the inter-membrane space, and the reaction continues.
Conclusion
OAA is converted into malate in the inter-membrane space. In the mitochondrial matrix malate is converted back to OAA, as illustrated in the illustration below.

Image source : Malate–Aspartate Shuttle, Wikipedia

I have edited your answer extensively. Although what you wrote about OAA and malate seems reasonable, your remarks about reduction were incorrect (reduction is the addition of an electron, not an electron and a proton) and there is no such molecule as NADH+. Further an illustration in Wikipedia cannot prove a 'fact'. A fact is a fact, and is established by experiment.

Thank You for the edit. But I have one question, addition of an electron is definitely reduction, but can't I say the addition of an hydrogen as addition of an electron and proton, in that case it is also reduction. I am not arguing ( and definitely it was my fault) but it can be said like that. And about the 'fact' - some people prefer such sources , they think that an answer is incomplete without a citation from a notable site or book and they don't even judge whether the answer is reasonable or not.

This is the textbook answer, but there are also studies suggesting that oxaloacetate can cross the inner mitochondrial membrane, see for example http://www.sciencedirect.com/science/article/pii/0003986177900200
It might be that this is cell type and/or condition dependent. Or perhaps the transport rate for oxaloacetate is too slow.

In reply to your response to my comment. 1. On the reduction reaction. First, it is not necessary to discuss it in answering this question, which doesn't even mention it. It is, of course, relevant to explain that the problem is the transfer of NADH into the mitochondrion and NAD+ out. But, as I wrote, there is no such molecule as NADH+, so this mistake detracted from the virtues of the answer. Indeed the figures you reproduce show NADH. As for your question, there is no addition of a proton, but of two hydrogen atoms, and the balanced equation is: NAD+ + 2H ⇋  NADH + H+.

In reply to the second point in your comment. Of course, it is expected that you quote sources in support of your answer, and Wikipedia is useful because it is free to access. In fact your figure wasn't support for your argument, but an aid to the reader in understanding it. The fact that someone had gone to a some trouble drawing it lends authority to your point of view, but many of us are rather suspicious of Wikipedia entries (any one can edit them) and so are unhappy about statements that they support facts. (I realize that it is also a question of facility in English and experience.)

jyoti: Thank you for your detailed explanation. However, it does not directly answer my question and I tried to show I was already assuming this information by staying "I am aware of the Malate-Aspartate Shuttle". My interest in whether OAA can cross the /outer/ mitochondrial membrane. You seem to have deliberately avoided addressing this, mentioning how NADH must be imported then suddenly you speak about OAA already being in the IMS (without mentioning how it got there).

(continued) I find it interesting that you picked two illustrations that both show OAA in the IMS, when most of the other diagrams I saw through Google do not depict the IMS at all and rather show the OAA reduction occuring in the cytosol. Either way, I think we may be beyond textbook illustrations as they may not have been created with the subtleties of this issue in mind. Namely, how does OAA cross the outer mitochondrial membrane (if it does at all)? Is the outer membrane somehow more "leaky" than the inner? Could this be related to the endosymbiont origin of the mitochondrion?

There are porin channels in the outer membrane which make it more permeable than the inner one


text:
Difference between Category, Rank and Taxon
Is there any differences between the terms Category, Rank and Taxon or they all are same?
I remember an explanation which goes on like this:
Category and Rank are the same and are the categories of taxonomic heirarchy whereas taxons are the organisms present in those.
Is this correct?

Maybe adding some example context would help answer. Anyway, a taxon is not an organism, but rather any level and grouping one can distinguiah, the last smallest one being a species (a group of individuals). Of the other two, no idea to be honest.

A taxon (plural taxa) is any taxonomic unit. For example, the class Mammalia is a taxon which includes all mammalian species. Similarly, a species is a taxon, Panthera tigris being the tiger. This taxon contains lower taxa, which are sub-species, such as Panthera tigris tigris (Bengal tiger) or Panthera tigris sumatrae (Sumatran tiger).
Rank is simply the level of a taxon in the taxonomic heirarchy. For example, the taxa Mammalia and Aves both have the same rank since they are both classes. Panthera tigris sumatrae is of a lower rank than Panthera tigris because the former is a sub-species and the latter a species. Use of the term rank is only truly meaningful when comparing two taxa.
Taxonomic category is usually – for better or worse – used interchangeably with the term taxonomic rank. A Dictionary of Biology (6 ed.) certainly indicates that the terms rank and category are equivalent. The major taxonomic categories are domain, kingdom, phylum, class, order, family, genus, and species. A category can contain one or more taxa.
Another example, to summarize:

Carnivora is a taxon, which contains many species including Vulpes
vulpes (red fox)
Carnivora is in the category of order
Carnivora (order) is a higher rank than Vulpes vulpes (species)

Welcome to Bio. Great answer, but adding a reference or two would be appreciated.

I am not sure if Reptilia is considered a taxon. It is most definitely not a clade.

@WYSIWYG Yes, it was a bad example - I've changed it

@HarryVervet Please correct me if I am wrong -- you said "the taxa Mammalia and Aves both have the same rank since they are both classes"... which would that imply that class is the name of their shared rank, and thus kingdom, phylum, etc refer to taxonomy ranks, and are not taxons themselves


text:
How do inward rectifier potassium channels work in the heart?
Apparently in cardiomyocytes, there is an inward rectifying potassium channel that operates during phase 4 of the cardiomyocyte action potential.  I have heard that despite this potassium channel being referred to as an inward rectifying channel, that in vitro the channel in fact still transports potassium from the inside to the outside of the cell.  It appears that Wikipedia seems to suggest otherwise (?).
Can someone please explain what the inward rectifier potassium channel does and its role in phase 4 of the myocyte action potential?

According to Boron's medical physiology textbook:

"Although inward rectifying potassium channels pass current better in
  the inward than the outward direction, the membrane potential (Vm) is
  typically never more negative than Ek (equilibrium potential of potassium across the membrane). Thus,net inward K+ current does
  not occur physiologically. As a result, the activation of GIRK
  channels (G protein coupled inwardly rectifying potassium channel)
  hyperpolarizes cardiac cells by increasing K+ conductance or outward
  K+ current."


text:
Somatic Mutations in meristem tissue in plants
In angiosperm, in which layer of the meristem does a new mitotic mutation occurring has chance to be found in a pollen grain or in an ovule?
I also welcome some insights about non-angiosperm plants.

You can see the wikipedia article on meristem.
The apical meristem differentiates into floral meristem that gives rise to flowers.
From this the cells specifically expressing APETALA3 (AP3), PISTILLATA (PI), AGAMOUS (AG) and SEPALLATA (SEP) would give rise to the stamen [ref].
CRC gene is essential for female development and plants lacking this will not produce pistils. So cells expressing this gene will give rise to female parts[ref].
Nonetheless mutation happening at any stage of the development of floral meristem can be transmitted to the pollens/ovules if the mutated cells stochastically give rise to that lineage.

Thanks. Do you know approximatively, how many cells are in the apical meristem?

Oh I don't have much idea. I didn't study much botany. I'll look up and let you know..


text:
Definition of Sexual Selection?
How do you define Sexual Selection (SS)?
(One might want to subdivide SS into intra- and inter- SS to answer)

Is SS clearly different from Natural Selection (NS)?
Is SS nested within NS or are NS and SS two different and (anti- or not) parallel processes?
Is the evolutionary processes due to sexual conflict are SS processes?

Sexual conflict arises when the reproductive interests of males and females are not aligned, generating sex-specific selection on shared traits such as mating rate (from this article)

(One may want to subdivise sexual conflict into intralocus and interloci conlict to answer)

Are the evolutionary processes of sexually antagonist genes SS processes?

Sexually antagonist genes are those genes where one allele is favored in females while another allele is favored in males (my own definition)

Can SS be accurately defined or is there a continuum of kinds or processes from complete SS processes to complete NS processes?

Stated differently, is SS defined as the color orange (it is a continum) or like a square and a rtiangle (no continuum)
(I talk here about kinds of processes, not about the relative importance of SS and NS in explaining the evolutionary dynamic of a trait or a locus)

If you define SS based on some other concepts that might be subject to various definition, please define this other concept. For example, if one says "SS occurs on a trait whenever this trait undergoes directional selection due to sexual competition", he will necessarily need to define "sexual competition" as well.

Below is a list of scenarios where you can answer by yes or no whether SS is involved in the evolution of some feature. In all of these scenarios, we'll consider cases where the males have to find a mate…

The males need good ears to find the females before other males. Is SS involved in the adaptation of ears abilities?
The males need good flying abilities (supposing we talk about flying animals) to have access to females before another male. Is SS  involved in the adaptation to good flying abilities?
The males need good flying abilities  to have access to females although there is not much between male competition because the vast majority of females won't never be fertilized. Is SS is involved in the adaptation to good flying abilities?
The males need good flying abilities to be able to fly a long time without spending to much energy otherwise they will die before finding a female. Is SS is involved in the adaptation to good flying abilities?
The males need good flying abilities to be able to fly a long time without spending to much energy otherwise they will die before finding a female. There are quite a few females but there the competition is so rough to find a female that is still unmated Is SS is involved in the adaptation to good flying abilities?
The males need good camouflage because when they fly to find a mate they may get eaten by a predator and die before reproducing. Is SS is involved in the adaptation to good flying abilities?
The males need good camouflage because when they fly to find a mate they may get eaten by a predator and die before reproducing. Here the difference is that the predators are attracted to the spot if they can sense many males. So the presence of the other males influence the probability of finding a mate of a given male. Is SS is involved in the adaptation to good flying abilities?

It looks like there are a ton of questions in my post but they are so related to each other that it would be stupid to ask them separately. All these questions basically sums up to the first question: How do you define SS? I welcome some references to papers that offers interesting definitions of SS.

hey.. check this article out.. came just yesterday..

Is SS clearly different from Natural Selection (NS)?
Is SS nested within NS or are NS and SS two different and (anti- or not) parallel processes?

Darwin, in The Descent of Man, and Selection in Relation to Sex defined sexual selection as a type of selection that "depends on the advantage which certain individuals have over other individuals of the same sex and species, in exclusive relation to reproduction." Throughout, he distinguishes between natural and sexual selection. This suggests to me that Darwin thought of them as different processes.  A spot check of various evolutionary texts show the authors all using some variation of Darwin's definition.
In my opinion, the two are are clearly different but not necessarily separate. Both NS and SS affect fitness, a major component of the evolutionary process.  I tend to think of SS as nested within NS. NS affects fitness indirectly. Beneficial traits increase survivorship.  The longer individuals survive, the more reproductive opportunities they will have and fitness will, on average, increase. But, survivorship does not guarantee reproduction. Thus, I think natural selection acts indirectly on reproductive success.
SS operates directly on reproductive success because males selected by females will reproduce, increasing their fitness. Sex is, after all, a natural process. In my view, female choice is the "environment" of the male (as far as reproduction) so variation of male traits in the female choice "environment" differentially affects the fitness of the males. That is natural selection.

Is the evolutionary processes due to sexual conflict are SS processes?

Absolutely. Sexual selection ultimately arises because of a difference between genders of energy investment in gametes. Males produce lots of gametes and relatively little energetic cost. Females produce relatively few gametes with lots of energetic cost (think of tiny sperm vs large, yolk-filled eggs). It benefits males to mate with as many females as possible because, even if a mating produces no offspring, he lost very little of his energy investment. Females will be choosier because they can't afford to waste gametes. Thus, there is an inherent conflict of interest between males and females.

Are the evolutionary processes of sexually antagonist genes SS processes?
Sexually antagonist genes are those genes where one allele is favored in females while another allele is favored in males (my own definition)

Are these genes related exclusively to reproduction?  If so, then that would be consistent with the original concept of SS. However, sexually antagonistic genes are not necessarily the result of or a cause of SS.  For example, Rice (1992) argued that sexually antagonistic genes may explain the evolutionary reduction of recombination between primitive sex chromosomes.
Rice, W.R. 1992. Sexually antagonistic genes: Experimental evidence. Science 256: 1436-1439.

Can SS be accurately defined or is there a continuum of kinds or processes from complete SS processes to complete NS processes?

I think SS is accurately defined, but whether is is a type of NS or not is (I think) open for debate. As I described above, I think of SS as a particular type of NS, one that operates directly on reproductive success rather than indirectly.

Below is a list of scenarios where you can answer by yes or no whether SS is involved in the evolution of some feature. In all of these scenarios, we'll consider cases where the males have to find a mate…
The males need good ears to find the females before other males. Is SS involved in the adaptation of ears abilities?

Depends. Do males and females also use their ears for other purposes, such as detecting prey or predators?  Is hearing ability much greater in males than in females? Darwin specifically addresses such a scenario. (Last sentence of page 256, first part of page 257.)
I think these ideas play out for most of your scenarios. It depends on if the traits differ between the sexes (not specified in your scenarios) and the traits lead directly to increased male reproductive success. But I will address one more.

The males need good camouflage because when they fly to find a mate they may get eaten by a predator and die before reproducing. Here the difference is that the predators are attracted to the spot if they can sense many males. So the presence of the other males influence the probability of finding a mate of a given male. Is SS is involved in the adaptation to good flying abilities?

In this case, I would say not SS. The camoflage is necessary for survival, not direct reproductive success. This is natural selection.  Increasing the probability of finding a mate is not the same as guaranteed reproduction.


text:
Why is the ribonucleoside derived from thymine, 5-Methyluridine, abbreviated m5U and not T?
The wikipedia article about Nucleosides presents a table in which there are three columns — Base, Ribonucleoside and Deoxyribonucleoside — and structures, names and abbreviations for the nucleosides corresponding to the five bases, adenine, guanine, thymine, uracil and cytosine.
The abbreviation pattern for the deoxyribonucleosides is quite regular — they are all termed dN, where N is the first letter of the name of the base and ‘d’ indicates ‘deoxy’ (i.e. dA, dG, dT, dU, dC).
In the case of ribonucleosides, apart from one exception, the pattern is similar — they are all termed N, where N is the first letter of the name of the base (i.e. A, G, U, C). The exception is the ribonucleoside related to the base, thymine, which is not abbreviated T — as one might expect, but as m5U, from its name 5-methyluridine.

What is the reason for this? Why does the abbreviation for ribonucleoside derived from thymine deviate from that for the other bases?
Do people distinguish between m5U and U when referring to RNA, or is the letter U used for both?

I have simplified your question and removed the reference to alphabet. We are just talking about abbreviations, which by their very nature are imprecise, but arise over time because they are convenient.  We are not talking about God creating animals and giving them all names. Think about it in relation to your knowledge of DNA and RNA.

The m5U isn't a common constituent of RNA, regardless of the nomenclature, and so this notation does not explain why uracil is used in RNA - the answer you linked at the beginning of your post already contains the best explanation for that along with the explanation for why thymidine is found in DNA: simply, it started out as uracil and replacement machinery to deal with thymidine RNA never evolved.

The question that is open, is not why is uracil used in RNA. The question is why is m5U/T not used in RNA? I will change my question to only focusing on the nomenclature.

Because it's a different base. You could ask why isn't a uracil used that is methylated at any other point, as well, it's a different compound, it wouldn't "fit" in the transcription/translation machinery.

@David I'm getting a bit confused about what the actual question the OP has here; after I re-read the latest comment the OP says "the question is..." what you changed the title to be, but then after that says "I will change my question to only focusing on the nomenclature" which is exactly the opposite. I think we need some clarification or this should probably be closed as unclear.

You say your question is why is T not used in RNA, and not primarily about abbreviations. You certainly fooled me! I have changed the title to reflect this. Have I understood you correctly? If so the question needs revising to say that. And please stop talking about alphabets. I can help you with this (and answer that question). If this is not your question please clarify. Do you understand the roles of the different RNAs in protein synthesis? Are you worried about the fact that the base thymine (5-methyl uracil) is found in some RNA? Do you know where it is found? What books have you read?

@BryanKrause Sorry, am away and was working on my phone so things got messed up. My comment above should clarify things I hope. The problem is the question is more a stream of consciousness submerging what appears to be the major concern expressed in his comment.

@David No worries, I think we are more or less on the same page of being a bit uncertain about OP's intentions while trying to sort things out. If the new title is indeed what the OP wants answered, then it is a pretty clear duplicate of this question.

@BryanKrause It may appear to be a duplicate, but the poster is right in saying all the answers answer a different question — why T not U in DNA. So I think we should persist and, eventually andif appropriate make two distinct questions, perhaps by editing the previous one.

@David Why did you change the title? I will change it back. The title perfectly fits the question. Just leave it like this. It is the first question that needs to be answered before it makes sens for me to asks "why is m5U/T not used in RNA". I would then open a new question. And why are you using words like "you fooled me"?

I changed the title because you said in a comment "The question that is open, is not why is uracil used in RNA. The question is why is m5U/T not used in RNA?". I know something about the subject and will be able to help you if I know what your question is. I asked you specific questitions to help clarify this and you ignored them. I repeat, is your question about biology — why one base is used in RNA, whereas another is used in DNA — or about nomenclature  — why in the rare cases in which thymine occurs in RNA it is described more specifically? "You fooled me", was as the question was unclear.

@David. Sorry for the confusion. I meant that in link "The question is why is m5U/T not used in RNA?" is still open. But before I will ask this question in a "new thread" I want to get  certainty about the nomenclature. So this question is only about the nomenclature.

I have been away and working on my phone. I did not look at the link to the Wikipedia article on nucleosides, partly because of the screen size, and partly because it is a rule that questions must stand alone and not depend on someone having to go to another site. I now see what you are talking about. I will edit your question to reflect this and then give an answer. I will remove your reference to the lack of occurrence of T in RNA as it is not relevant. Until the title of the existing question is modified I suggest it is better not to ask a new one as it will be flagged as a duplicate.

I have given notice of my intention to change the title of the old question on the employment of U in RNA. I'll give it 24 hours and then attempt to change it.

From the standpoint of modern molecular biology, one can say that the table in the Wikipedia article would be better if — in the first instance at least — it left blank the entries for the ribonucleoside corresponding to the base thymine and the deoxyribonucleotide corresponding to the base uracil. This is because the thymine ribonucleoside is not a normal constituent of RNA, and the uracil deoxyribonucleoside is not a constituent of DNA.
It would also be more honest if the article explained that the abbreviations used in DNA and RNA databases employ the single letter to represent a deoxyribonucleoside monophosphate residue or a ribonucleoside monophosphate residue, as the case may be, and that only the chemist or student of nucleotide metabolism is likely to be concerned with the abbreviations presented.
It is in metabolism (for which these were named) that the abbreviations make sense. ATP is adenosine triphosphate, so the ‘A’ has to represent the nucleoside, adenosine, and dTTP, deoxy-thymidine triphosphate, is the metabolite that is a DNA precursor used by DNA polymerase. The reason that dU justifies inclusion is that dUMP exists in cells — as a precursor of dTMP (which is then converted to dTTP).
So finally to your Q1 about 5-methyluridine. The answer is that, as far as I am aware, this does not occur in cells as the free nucleoside or the free related base or nucleotide. It can only be considered as occuring at a particular positions in certain transfer RNAs (and ribosomal RNAs) where it is produced by the enzymic modification of the uracil ring by a 5-methyluridine methyltransferase. So in the metabolic era, before the detailed chemical analysis of minor bases in structural RNAs, there was never any reason for biochemists to refer to 5-methyluridine and consider its abbreviation.
You may or may not be aware that there are many minor bases of this type in different tRNAs, all produced by enzymic modification of the four bases occuring in an initial RNA transcript synthesised by RNA polymerase. There are over half a dozen different modifications of uracil, so it was far more meaningful for the scientists working on them to distinguish them with abbreviations that indicated their chemistry, rather than assigning arbitrary single letters to them. The fact that one could logically employ T as an abbreviation for 5-methyluridine would have been of no practical use, and, because of the association of thymine with DNA, could well have led to confusion. Hence, the committee standardizing nomenclature would have been faced with a fait accompli. In such circumstances realism prevails over idealism. (And in any case the names of the bases are a mess — how many students have been confused by adenine/adenosine but cytosine/cytidine.)
Regarding your second question: people don’t talk very much about m5U and U, but when they do they naturally distinguish between them because they are different molecules. Specifically, the databases for tRNA structures will distinguish clearly the different modified bases.

I think this sentence is unfortunate: "So finally to your Q1 about 5-methyluridine. The answer is that, as far as I am aware, this does not exist as such in cells, and only occurs at a particular position in certain tRNAs".
tRNA occurs in cells, ergo m5U occurs in cells. I read here, that it also appears in rRNA.

"Your second question doesn’t seem to make sense..." It is a simple question and you provided a clear good answer for it: "the databases for tRNA structures will distinguish clearly the different modified bases." No need to be more verbose as necessary.

@newandlost Ok about the second question. I'll remove the remark.

@newandlost — Regarding m5U and its occurrence in cells, I'll rephrase the sentence when I have a moment. The "as such" was meant to imply that there is no free ribonucleoside, m5U, or the related base, or any related nucleotide mono-, di- or tri- phosphate in cells. So these molecules are never encountered within cells, and for biologists (rather than chemists) are not discussed and naming is of little concern.m5U can only be considered as part of some tRNAs (and rRNAs) where it is the base that is of interest (rather than the nucleoside or nucleotide residues) as that is what is modified.

@newandlost — I've made the changes now. I could also add references to the discovery history of the identification of m5U in tRNA and rRNA, and examples of how it is designated in databases, if you really think this would be useful.

Good answer. Just a minor point --- RNA can also be broken down to the constituent ribonucleotides, as part of continuous RNA turnover. Wouldn't that release free 5-methyluridine then? (in very small amounts)

@Roland — It certainly must do initially, although it may be rapidly degraded as it is unlikely to be recognized by salvage pathway enzymes.


text:
Do fishes die from old age?
I was watching sea birds eating fishes and wondered whether any fishes died from old age or whether they are all eaten before this can happen?
I imagine that some big predator fishes must be able to live long enough to die from their age. However, do any fishes that are lower in the food chain reach an age such that they die naturally, or are they all destined to end their lives as food for a bird or another fish?

Salmon are famous for their spectacular natural/intrinsic death after spawning.

Yes, at least some fishes have intrinsic lifespans and deaths that are related to their own life-history and not to external forces such as predation or disease.

Fishes show three types of senescence. Lampreys, eels and pacific
  salmon exhibit rapid senescence and sudden death at first spawning.
  The guppy, red panchax, medaka, platyfish, Indian murrel and many
  other teleosts undergo gradual senescence, as observed in most of the
  vertebrates. A number of fishes (e.g. sturgeons, paddlefish, female
  plaice, flatfish, rockfish) show indeterminate growth, the occurrence
  of senescence in them is supposed to be very slow or negligible.

Patnaik BK, N Mahapatro, and BS Jena. 1994. 'Ageing in fishes' Gerontology 40:113-32

Fish do not die from old age, nor do any other animals. Rather, the older the animal gets the weaker it becomes which means that it is an easier target for predators or can easily succumb to disease.

Any citations for this?

interesting way of looking at it but I am not buying it.

@Oreotrephes  I agree with Humza Zaidi that aging itself is not a disease, but an accumulation of biological damage that makes an organism susceptible to eventually lethal diseases. This is discussed in this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4037311/


text:
Can HBV pseudotyped oncolytic viruses be used to treat hepatocellular carcinoma?
Chronic hepatitis B is the leading cause of hepatocellular carcinoma (HCC). Oncolytic virotherapy (OV) is an emerging tool to treat cancer. However, one challenge of OV is that our immune system may produce neutralizing antibodies, which impaired its efficacy.
While on the other hand, antibody production against surface glycoprotein of HBV is inhibited in chronic hepatitis B. So can we use the HBV glycoprotein to pseudotype OV (e.g. VSV, measles, MLV), thereby circumvent the host humoral immunity? Can such viruses be used to treat HCC caused by chronic hepatitis B?