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What makes humans omnivores, and not herbivores?
Some vegans claim that humans are herbivores, not omnivores, and that we are not physiologically designed to eat meat (see here: http://www.peta.org/living/food/natural-human-diet/).

"According to biologists and anthropologists who study our anatomy and our evolutionary history, humans are herbivores who are not well suited to eating meat. Humans lack both the physical characteristics of carnivores and the instinct that drives them to kill animals and devour their raw carcasses.
  Although many humans choose to eat a wide variety of plant and animal foods, earning us the dubious title of “omnivore,” we’re anatomically herbivorous."

They go onto claim that we don't have tiger claws and teeth for catching and eating meat, that our jaws and teeth are designed for grinding plants not meat, that our stomach acid is too week to break down meat, that our intestinal tract is long like a herbivore for digesting plants and that it takes so long for meat to pass through that it rots and poisons us causing cancer, that we lack a hunting drive, that meat with it's cholesterol and protein is the cause of all disease so obviously its poison that we are not supposed to eat, that we get food poisoning from meat (like that never happens with vegetables...) and that the only reason humans started eating meat was to survive in times when there was a lack of plant foods available but according to our anatomy it's clear we're actually herbivores not designed for eating meat.
Can this be debunked?

Not an anthropologist myself, but a quick web search turned up this  https://www.vrg.org/nutshell/omni.htm  which seems credible, although it does lack references.

Look at our teeth - our front teeth are the teeth of a carnivore. Compare that to the teeth (or lack thereof) of horses, sheep, cattle, etc.

Relevant: https://www.quora.com/Why-do-some-people-say-we-are-omnivores-evolutionarily-speaking-when-for-most-evolutionary-history-we-came-from-great-apes-and-before-them-monkeys-who-were-most-all-vegan

relevant: http://www.beyondveg.com/billings-t/comp-anat/comp-anat-2a.shtml

relevant: https://ourspiritwillliveon.wordpress.com/2008/09/25/the-carnivorous-primate-monkeys-who-think-like-wolves/

"Debunk this nonsense" sounds like a cognitive bias. But that's just my opinion

Although we are omnivores (as most of the answers below explain), the main problem is the amount of meat that we consume. There is a very good chance that in the beginning of our species history, we didn't have access to so much meat. So, I would say that we need a better balance and we are naturally more herbivores than carnivores. And if you check the diet of people 100 years ago, meat was more the exception, rather than the rule.

@BioGeo: The other half of this is a sedentary lifestyle, which doesn't consume the extra calories & fats of meat.

The fundamental (no pun intended) problem here seems to be the idea that human are "designed".  We evolve, and we do that by exploiting new environmental niches.  The "eat meat when you can catch it" niche seems to be one that our ancestors moved into before they split off from the chimpanzee lineage.  A more recent example of such evolution would be the preservation of lactose tolerance into adulthood among humans whose ancestors were herders.

Just a note: PETA is a highly ideologically-charged organization that is in no way an expert on scientific facts. I would take absolutely anything they, or similar agenda-focused organizations, say with a grain of salt. Remember, not everything you read on the internet is based on facts ... -_-

Also, both "canine teeth" and the entire state of West Virginia (or, for non Americans, every rural town or village in the world that sustains a large population of game hunters) are pretty good evidence against the "facts" that PETA provides in this link.

@theforestecologist: Anecdotal evidence at most ... There is nothing to really debunk in the PETA statement. It's just a slightly one sided view on the history of human diet. Just as one sided as the claims that humans wouldn't have evolved a really big brain without consuming animal products (which I hear over and over again, even in anthropological sciences). So far we just don't know, though it seems like human groups changed diet from vegan to omnivorous - never carnivorous for sure - and back quite frequently and opportunistically. I will give a more detailed answer in a few days.

@AlexDeLarge: I think the key there is "opportunistically".  If I would eat meat if I could get it, but  eat a vegetarian diet because "some other bugger pinches the pig", does that make me an herbivore, or just a deprived omnivore?

It is worth noting chimps also hunt and eat meat. https://www.nationalgeographic.com/science/2007/02/chimps-use-spears-to-hunt-mammals-study-says/

Recently became vegetarian, and I wanted to correct some things that I've read here. Humans by definition are omnivores, because we can eat meat. "Chimps eat meat" is a claim I've read. Great. Do you know how much meat chimps eat? 7 days out of the year chimps will eat meat, other than that they're eating fruits and veggies. So 99% of the time most omnivores are NOT eating meat.

"omnivores have canine teeth, just like us humans" - their canine teeth is drastically different than ours. And I wouldn't hold up America, especially rural America, as any bastion of good health.

As the answers given already point out, humans are generally considered omnivores that are able to use food sources available to them opportunistically. Apart from that, there actually is not much to debunk in the PETA statement - it is just a slightly one sided view on the history of human diet. Just as one sided as the claims that humans would not have evolved a really big brain without consuming animal products. Especially the canine teeth cannot be seen as evidence for prehistoric hunting, as in great apes the size of canine teeth is ridiculously well explained not only by defensive but mostly by mating behaviour; apart from that, humans do not even have those, and that most likely is caused by the trend towards monogamy which reduces inter-male aggression.
However, coming back to the actual question, in the relative short history (approx. 200-300ky) of our species there is evidence for 'several transitions towards or away from a vegetarian diet in humans' (Nielsen et al., 2017).
And in fact, there even is a human-specific evolutionary derived haplotype (younger than the Human-Neandertal split) that shows signatures of positive selection and is associated with increased efficiency in the synthesis of long chain fatty acid from plant precursor molecules - which would not really be necessary for meat eaters, as these fatty acids are readily available in animal products (Ameur et al., 2012). More specifically, the genes lying on that haplotype belong to the FADS cluster that seemed to have had adaptive value - also for synthesising long chain fatty acids from medium chain plant precursor fatty acids - in some African populations even more recently (approx. 85 kya, Mathias et al. 2012).
This finding has been supported by a more recent study by Kothapalli et al. (2016). They investigated a 22bp-indel allele in the FADS2 gene that is associated with both higher blood levels of long chain fatty acids and exhibits high frequency (signature of positive selection) in some populations in South Asia and Africa for which they claim a long tradition for plant-based diet.

Conclusion:
Modern humans (and this is relevant, as diet varies strongly between species and therefore the species comparison does not need to be very informative) appear to have changed diet frequently but there even is evidence for human-specific molecular adaptations towards plant-based diets.

Thank you. Well thought through.

There are several claims in this that could use sourcing, like that eating meat was instrumental in human evolution is one sided, your links only confirm this view.

But you also show some adaptations AWAY from a plant based diet, so your own evidence does not support your conclusion. Also I would like to see support for your claim that South Asia and Africa have a long tradition of plant based diets, any claim about native African populations a a whole is immediately suspect.

@John: 1) My conclusion is that there appear to have been many transitions away from or towards a more meat/plant-based diet in modern humans, and I think the evidence presented shows both directions, thus supporting the conclusion. I explicitly mention evidence for only one of these transitions because of the phrasing in the OP; it was asked to debunk the claim that humans are herbivores but humans show adaptions expected in herbivores. I would have phrased it the other way around if the OP had asked to debunk the claim that humans are carnivores.

@John 2) The statement about a long tradition of plant-based diets in South Asia and Africa is taken from the Kothapalli et al. (2016) paper, it's not mine. I agree that this is definitely not a true statement for all modern human populations in South Asia and Africa and therefore edited the post to make that more clear (i.e. tone down the statement). I agree that statements about an African (meta-)population as a whole is definitely suspect and that is not what I meant. I was talking about some modern human populations in Africa and South Asia, not all of them.

The simple answer is humans are omnivores – physiologically – because we have the capability to digest both plant and animal matter. Many humans are behavioural omnivores as well, consuming both as part of their diet, although many people can and do live while consuming only plant products.
Most if not all humans can or could digest animal products in some form - a brief search doesn't bring up any counterexamples of people who cannot physiologically do this (in the same way that many people cannot digest milk well in adulthood as they are lactose intolerant). Even if some people do not have this capability, they would be exceptional and broadly speaking you could describe humans as omnivorous, at least physiologically.
The Wikipedia page for omnivore is a good starting point if you want to know more about consumption classifications.

What about B12 deficiency and anemia risk in vegans, isn't that a clear indication humans are not designed as herbivores? Vegans have to take supplements, which is a modern invention, without supplements and fortified foods vegans risk serious deficiencies which can prove fatal if untreated from a lack of animal products in their diet. We can't get sufficient b12 from plants but herbivores can because their  digestive system works differently, right? Can you explain about that please if you can?

Furthermore, fossil record shows humans have been eating meat in the last milions of years.

@BigSkeptic Vegetarians also drink more milk and lots of milk-products (curdled milk, sweets, butters, curd, etc) (and also used in many worships, sometimes in wasting amount). But milk is actually source of animal-proteins.

B12 is only sourced from dirt. Whether you are getting it from a supplement or animal meat - the source of that vitamin was found in the dirt. Humans used to get it from the dirt off fruits, veggies, etc. Now? Every bit of b12 you get comes from supplements. Even the animal meat you consume, the b12 you get from them was supplemented to them

Deer, generally considered herbivores, also have the capability to digest animal matter. https://academic.oup.com/jmammal/article/68/1/195/1041038

There are several lines of evidence.

Behavior, we regularly eat meat.

This is the one that matters most, omnivore is a behavioral classification. All humans societies eat meat, a few eat little else or nothing else. The fact that a small subset of well off people in developed countries don't does not change this. Our two closest relatives also eat meat and many of our ancestral species show direct signs of eating meat.

Gall bladders.

One somewhat useful piece of evidence is humans have well developed large gall bladders. Gall bladders function to store bile, a large one functions to be able to break down large quantities of fatty foods eaten all at once, which really only occurs in carnivores, omnivores. (there is also a weird thing ruminants do, but we are not ruminants so it can be ignored)

Dentition

Our dentition is that of an omnivore, Its not specialized for a meat or plant diet. As an example gorilla show signs of specializing in a plant diet. Our detention however does show specialization for eating cooked food. Which we do to both meat and plant products.

Digestion

We havelarger powerful livers able to breakdown toxins better than many related animals, We are also more sensitive to the smell of rot. Some have argued this is a sign of being a scavenger but this is more likely another adaptation to eating cooked food, the toxins we are best a breaking down are those that come from cooking meats and plants.
Humans are also better to digesting iron from animal sources than plant sources, and show adaptations towards this.  We also show adaptations for digesting some plant materials better supporting an omnivorous line of adaptations.
Humans lack any of the specialized gut features seen is exclusive herbivores, we have no way to breakdown cellulose nor a structure to house bacteria that could do it for us, that means you could classify us as a frugivore at best if trying to argue for herbivory. Our gut length is what is expected form an omnivore, longer than a carnivore shorter than an herbivore.

B-12

We can't make vitamin B-12. Humans and all our other great ape relatives get b-12 from eating animals.
Now some people argue humans should be classified as cucinivores (a unique classification) as well as omnivores, becasue we are specialized for eating cooked food.

We are not herbivorous because our digestive system is too short. Humans do not have many of the features required to digest plant matter efficiently. We do not have a multi chamber stomach like ruminants have. We do not have an enlarged cecum like rabbits
In fact, the human gut as a percentage of body mass is half that of a chimpanzee, (10% vs 20%). Also the composition of that gut is different, 50-60% are small intestine in human vs 20% in chimp. The human colon is also reduced: 17-23% in human, vs 52-54% in chimp.
http://www.beyondveg.com/billings-t/comp-anat/comp-anat-6c.shtml
Also gorillas, which are more herbivorous than humans, have cecum (7% of the Gut volume compared to 0% in humans.) http://huntgatherlove.com/content/human-colon-evolution-part-1-comparative-anatomy
If anything, the argument that the human gastrointestinal system is long like a herbivore's is false. It is short and reduced, and does not have the right components to ferment plant matter. However, it is longer than an obligate carnivore.
As a species, human are an ape (a fruit eating animal) that has started to evolve to eat meat. It is an intermediate species so to speak, it still doesn't digest meat well. It has many features of its fruit eating ancestor, but has already taken step to eating meat, while having lost features (like large gut size and big colon) that digest plant matter more efficiently.
Put a child on a vegan diet and the kid might die from B12 deficiency, insufficient calories, and lack of fatty acids.

Some apes eat meat as well, chimps f.e.

That is true. Estimated that Chimps obtain 6% of its calories from meat. Gorilla are more herbivorous and have larger percentage of their gut  devoted to a cecum (7% in Gorilla, 5% in Chimp and N/A in humans). http://huntgatherlove.com/content/human-colon-evolution-part-1-comparative-anatomy

I think when you say humans "digest plant matter efficiently", you are perhaps over-simplifying.  Humans seem to digest many fruits, seeds, and vegetables quite well.  We just don't have the extra machinery to digest things high in cellulose, as grazers do.  So like many other species, including some (like wolves/dogs) that are popularly supposed to be carnivores, we eat both.  Though some human groups, e.g. the Inuit, have traditionally lived on an almost exclusively animal diet.

I don't think you realize that those added machinery is required. The vegetable and fruits that we eat today are no way similar to the non domesticated versions of the same plants. It is like saying bananas are very easy to eat... only problem being the wild version of bananas are small, gummy sappy, full of large hard seeds.. and really only edible by straining out the seed and cooking the resulting pulp. The plants we are familiar today are the product of thousands of years of domestication. wheat is the product of nearly 12000 yrs of selective breeding.

@JayCkat: But there are many fruits, nuts, and vegetables that have not been subjected to that 12K years of selective breeding (and which aren't sold commercially in any large quantity), yet which sustained native populations.  Hereabouts there are pine nuts, cattail roots & pollen, camassia bulbs, elderberries, wild blackberries, and much more, all of which I eat on occasion.

Elderberry, black berries has been domesticated. Camassia bulbs show signs of domestication. The cattail... I can't find info about domestication of this plant. But it has been harvested for human consumption for over 30,000 years. I cannot imagine a plant being so heavily used not be artificially selected. Just because a plant is not commercially sold at the super market does not mean it is not domesticated.

Gut anatomy is the most swift and convincing argument that humans are not evolved to be strict herbivores. Since the OP mentioned it, there's an interesting discussion here on the evolution of stomach acidity.

Humans benefit from a plant based diet. The B12 argument is only valid at face value as domesticated animals that are raised to be slaughtered are given B12 supplements as they would to obtain enough of it through a "natural" diet. B12 is found in bacteria in the soil so washing vegetables and removing the dirt is also removing the B12. Animal products are high in saturated fats which is the main contributor to atherosclerosis and therefore heart disease which kills millions of people around the world each year. True ominovores do not have the ability to develop atherosclerosis.
 The argument that humans had always eaten animal products renders us complete omnivores is downright wrong as eating something for survival is completely different than eating for optimal health. Our ancestors had no concept of biochemistry or the effects food has on the cellular level of our body. Our ancestors also usually died at rather young ages of nutritional deficiencies.
It is not difficult to obtain protein, fatty acids, or calories for that matter as many nuts, beans, seeds, and legumes are high in unsaturated fats and flax seeds them selves are a better source of Omega 3s than fish. Lentils, dark beans especially are high in iron and, and virtually every food has some sort of minor iron content and vegans have an infinitesimal chance of becoming anemic compared to an omnivorous diet or a vegetarian who consumes dairy. Dairy products are known to hinder iron absorption.
Animal products also raise levels of a hormone called Insulin like Growth Factor 1 or IGF1. IGF1 is known to cause insulin resistance, promote cancer cell growth and release free radicals throughout the body.
The argument of what we are is really a nonsensical argument as it does not matter what the label is as opposed to what kind of diet we can optimally benefit from in the long term.

Welcome to Biology.SE. Please take a look at what is considered a good answer on this site. Some of your statements might be challenged, so please provide reference to any claims you make. Thanks!

This posting contains lots of wild claims - please add serious references for them.

B12 deficiency in livestock is due to cobalt deficiency, these animals can manufacture their own B12 ( well the bacteria in their complex gut can), they lack cobalt mostly due to human agricultural methods which prevents animals from wandering and eating a more diverse diet. Humans can't get B12 by this method. Also the nutrient content of modern crops is meaningless for our evolutionary history, since they are highly modified compared to their ancestors, more importantly most of them don't occur where humans evolved so mentioning them is pointless.

You didn't explain how Cobalt deficiency leads animals to be b12 deficient. You also didn't explain how they'd get more Cobalt if they had a more diverse diet. Humans get b12 the same way animals get b12. Bacteria in dirt.

@JustinBeagley if you want a full breakdown ask it as a question but a good summation can be found here.  https://www.agric.wa.gov.au/livestock-biosecurity/cobalt-deficiency-sheep-and-cattle. And you are wrong ruminants GUT bacteria manufacture their B12.

It is physiologically possible for a human to be an omnivore, carnivore or herbivore. It's not what we are, but what we can be or what we want to be.
Strictly speaking, it seems that humans can not be strict herbivores, because natural plant foods do not contain enough of the essential nutrient vitamin B12 and they are vegan/vegetarian websites that tell you that (Vegan Health, Vegetarian Nutrition Dietetic Practice Group).


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DAPI staining showing unknown artefacts?
Dear fellow researchers,
I have been facing some problem with staining nucleus with DAPI. I use the standard protocol for fixation 4%PFA+0.1% TX-100+2%BSA.
I use 0.2ug/ml conc. of DAPI for 5 minutes. Before mounting my cover slides, the nuclear staining is very specific and no artefacts were visible. However, after mounting (with Sigma-Aldrich mounting medium), I have started observing artefacts. Images are attached for your reference.
I usually keep my samples at room temperature for an hour to let the mounting medium settle down and then move samples to 4 degrees overnight and observe them the next day. I do not think that temperature here is an issue because the other marker did not show any problems.
Another issue is that the artefacts of nuclear staining are not ubiquitous. Even after mounting, some cells stained nucleus fine but others showed cytoplasmic or membrane staining.
Is there any reason that you guys can think of? Or if you have encountered similar situation before? Thanks in advance.
Why is DAPI giving artefacts with nuclear staining? - ResearchGate. Available from: https://www.researchgate.net/post/Why_is_DAPI_giving_artefacts_with_nuclear_staining [accessed Sep 18, 2016].

Hi Udesh. Welcome to Biology.SE. Can you post the images here? It would be easier for people to check them here instead of visiting other websites. Also, can you please mention what cells were these? Did you try gentle washing to remove excess DAPI?

Hello! Unfortunately I could not attach the images here. But, in my post there is a link to the same post on research gate. Could you take a look at it? It has images attached there.
Yes, I washed three times but it did not help. These were MDA-MB-231 breast cancer cells.

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What causes pinkish hue to some skins?
I know it is caused either by blood vessels beneath skin , or some pigment called "pheomelanin" . But what is it in fact?

Please clarify your specific problem or add additional details to highlight exactly what you need. As it's currently written, it’s hard to tell exactly what you're asking. See the How to Ask page for help clarifying this question.

The answer lies in hemoglobin, which is responsible for the transportation of oxygen throughout our bodies. It is the protein found in red blood cells, and thus it has a reddish hue to it. When an organism has lightly pigmented skin, the oxygenated hemoglobin causes the pinkish hue that you are describing.

then , this happens if the skin is not much pigmented, and if there are much melanin pigments , the hemoglobins in blood cant be visible, isn't it ?

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Can estimating the likelihood of protein sequences adopting functional enzyme folds show life is too complex for evolutionary timescales?
An acquaintance provided me with this article1. I can't understand for sure what it is about.
My acquaintance said that it proves that time for generation of even the simplest proteins is on a larger timescale than evolution history (billions of years).
I'm asking you, is that a valid conclusion to be made from this paper? What is in this article that might drive someone to that conclusion?

Axe,D.D. (2004) Estimating the prevalence of protein sequences adopting functional enzyme folds. J. Mol. Biol., 341, 1295–315. http://www.ncbi.nlm.nih.gov/pubmed/15321723

In addition. As i understand, this man considered linear exhaustive search of nucleotides. As i understand it is wrong, because genetics and evolution algorithms are optimized exhaustive search.

I appreciate the way you phrased your question in terms of appropriateness, and the good will of the person that gave you an answer, but this is really not an appropriate question. The main reason is that it is not comprehensible as it stands. First one is required to go elsewhere to read a paper (which happens to be behind a paywall), and second the paper (at least the summary) makes no reference to evolutionary time. Thus, we do not know what argument your acquaintance is making. So, with reluctance, I am voting to close the question unless you can edit it to make it fully self-contained.

@James — I have no objection to Elsevier charging for what is there's. Your language is another matter. Even if the article were not behind a paywall the question is unsuitable for SE Biology as it requires one to read a paper and then imagine a third party's attitude to it. If you ask similar types of questions they too should be closed. The guidelines on writing questions are quite clear.

@David I've asked similar questions about skeptically analyzing conclusions drawn from articles. It certainly shouldn't be closed because of Elseviers shameless paywalls. Often abstracts don't include some observations, particularly long technical papers with advanced and nuanced methods like this. +1 good question.

@David The guidelines on questions aren't entirely clear in this case. This could be seen as a give me teh codes question, however I think the complex methods are indeed exceptional and asking whether they can have conclusion X drawn from them is a valid question. We disagree on Elsevier's right to ownership (they legally own it, but I'm an open access idealist), but you're right; you've lost when you start swearing!

You might find some useful analysis of the paper here: http://pandasthumb.org/archives/2007/01/92-second-st-fa.html

I think your acquaintance is trying to fit real science to some of his personal beliefs (that are obviously wrong).
If you read the article you'll see that it's not about evolution at all, but about protein folding and what proportion of possible sequences gives a working protein. It turns out random sequences are not that likely to fold, which leads to some conclusions about the probable mutational pathways to folded proteins.
The argument of your friend is sort of analogous to the infinite random monkey theorem. If you put a monkey behind a typewriter and wait long enough, eventually he'll write the complete works of Shakespeare. This doesn't mean we waited billions of years for this monkey to type it up, because the world doesn't work like that. There was just a guy with a brain.
In case of the proteins, evolution doesn't work by generating newly (random) 300 residue proteins that work 1 time in a billion. Probably in one generation a copy of the protein is made with the same function, and during many generations the function of this protein drifts towards a new function, while all the intermediate proteins stay folded because they're not that different.

For some background on the author of the paper (Douglas Axe) see for example http://rationalwiki.org/wiki/Douglas_Axe. My personal opinion is that the paper looks interesting from a quick scan, but there may be some agenda behind it.

Also from the wiki: Axe himself says his work does not support intelligent design. So there might be a conflict of interest, but the data in the paper doesn't prove anything regarding evolution anyway.

Conclusions from the paper.
The finally line in the article should actually be read first as it clearly spells out where the paper fits in the scientific literature.

So, if re-creating a fold by ordered assembly of sections of sequences
  that already adopt that fold is not a simple matter, generating new
  folds from parts of old ones may be much less feasible than has been
  supposed.

A popular hypothesis at the time was that some folds emerged at some point or another from substantially different folds.
This paper used advanced statistical analysis (well, they're convoluted, not particularly advanced...) using a very simplified and uncertain model to show that the chimera theory of fold genesis is unlikely. It is a critique of that model at the time, and does not seek to show how long it took for evolution to come up with the fold.
This is an incredibly important question to answer. This paper was probably accepted because it shows a genuine attempt to quantify the probability of a general hypothesis. However, almost every step of their method introduces over-simplification, arbitrary thresholds, and convolution of the biology. As I see it, the only thing the paper can say for certain is "that in a small subset of simple folds, with a tonne of caveats and conditions, it might be less likely than other people think that the fold formed that way".
What your friend is drawing from this.
It would be incredibly difficult, many philosophers would argue impossible, to prove how folds were formed. But to build up lots of different scientific hypothesis and disprove them as much as possible is more achievable. That, broadly speaking, is the scientific method and this paper generally adheres to that line of thought.
This paper is saying "The current hypothesis surely can't be the right method! Look how improbable it is." and your friend has drawn from it "A scientist said more time would be needed, which proves evolution needed longer than it had". A simple misunderstanding; a scientist said a model had problems, a layman thought this meant the problems were the truth. The paper is not aiming to prove anything (The author may be especially careful about doing this given his close ties to intelligent design movements), but I think your friend might be incorrectly using the paper to prove something!

The study by Axe (a creationist) is fatally flawed. See these comments on it by Arthur Kent, a biologist at the University of Kentucky. To summarize: Axe did not study the native form of the protein he was looking at (TEM-1 penicillinase), but specifically, a variant that both had lower activity and was especially temperature-sensitive. His results, then, can't be generalized to even the native form of the enzyme under investigation, let alone any other enzyme. As Kent points out, more recent techniques suggest a substantially larger proportion of functional variants than Axe's method suggested. In any case, experimental and observational evolution has settled this debate: we see proteins with novel functions constantly evolving from pre-existing proteins all around us (how do you think new bacteria are constantly emerging which can digest all sort of novel artificial synthetic plastics never before seen in nature? how do you think viruses switch hosts?), and so it is 'out of question' as to whether there is sufficient time for new proteins to emerge. We can see it happening ... all the time!

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How to find the radius of gyration for a protein?
While going through the paper titled "GEOMETRIC ANALYSIS OF THE CONFORMATIONAL FEATURES OF PROTEIN STRUCTURES" by Manish Dutt, it talked about finding the radius of gyration of each protein structure. I am unable to understand how the radius of gyration has been obtained for the entire protein. I first find the root mean square distance between the centroid and the C alpha atom. Is the average of these distances the radius of gyration?

Pretty sure that there are library methods to calculate this - otherwise the formula for the radius of gyration of a set of points is on wikipedia? in any case, more of a bioinformatics question than a biology one...

Radius of gyration (https://en.wikipedia.org/wiki/Radius_of_gyration) is a basic-physics concept. If we rotate freely a point-mass, we can quite easily derive various inter-related variables from other-such variables (like mass, speed, radius, etc); but if it is a complex object (say a wheel or stone), it is complicated, but we can imagin an EQUIVALENT point-mass in rotating; whose mass is same as whole object, and radius, speed, frequency-of rotation etc. all characteristics are exactly same to our object.

there are square-roots in derivations for radius of gyration, and they are looking like (root (a. b. c. d... (r^2))) pattern. But I can't tell whether it is r.m.s. of that distance, or not. (from my H.S school physics textbook)

@Rishika you could go-through the paper slowly, and mark statements and sketches which could be useful. Then add some more details to question. You could provide a link to the paper. Is it freely accessible paper?


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Can viruses replicate in a cell that's already dead?
Suppose a virus randomly lands on a cell that's just lying around. This cell may have just recently died, or died a while ago. This cell may also be part of tissue of a dead organism.* Does the virus know that cell is dead? Would it attempt to inject its DNA into the cell?
*If it's a single cell, not part of a tissue, I imagine a "dead" cell would be lysed, so a virus landing on a "single dead cell" wouldn't happen - pleae correct me if I am wrong. So I'm asking how it would be for a dead organism because we can still see those dead tissues ..

Which virus, which cell?

Sorry, I don't know much about different types of viruses and their specific hosts so I can't give a specific example.. If anyone could recommend some examples that could help. @James

A lysed cell may be defined as a leaky one, which doesn't have to be dead yet. I think the question hinges on 'What is a dead cell?' and what is 'a lysed cell?'

You wrote, "would it attempt to inject the DNA into the cell" ... viruses do not have any nervous mechanism, so they can not "attempt" to attack any cell. They just get spread through air/water/etc (which is its proper propagation-medium). When they come in touch with the right host (with the right receptor-proteins), they bind, enter and cause disease. Now if the 'dead' (but not too distorted) cell can yet maintain the right binding-sequences in their membrane proteins, virus would bind, but probably it would not be phagosized. Or if it uses penetration/fusion methods, but wouldn't multiply.

I agree with @Christiaan; without an operational definition of 'death' at the cellular stage for multicellular organisms, this is too vague to answer.


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Can 5 alpha reductase inhibitor drugs work for life or do they lose effectiveness?
Do 5 alpha reductase inhibitor drugs like finasteride and dutasteride lose their effectiveness over time? Why do some drugs, like in an HIV regimen, work for a prolonged time without tolerance whereas other drugs, for example antidepressants, have tolerance issues after a short time?

This is a very broad question. From the [help/dont-ask]: Your questions should be reasonably scoped. If you can imagine an entire book that answers your question, you’re asking too much.

As noted in a comment, a truly thorough answer to this question would require one or more books (1,2) or scientific journals (3), but a simpler, necessarily incomplete answer can be provided.
The short answer is: transmembrane drug transporters of the ABC family (4)
But what are those? Well, you should read the wikipedia article for a detailed description, but essentially they're proteins that burn energy in order to remove a broad range of drugs from the cytoplasm, making them less "bioavailable". The answer to why some drugs (or broad spectrum treatments with multiple drugs) are more or less susceptible to export by ABC family proteins is much more complicated (buy books from (1) and (2) or similar texts(5)), but the broad spectrum HIV regimen prevents resistance by a completely different mechanism (6).
Briefly, ABC transporter-mediated resistance involves no evolution, simply a "transcriptional response" to the presence of harmful drugs, while HIV actually evolves to become resistant or immune to antiretroviral drugs. However, it's difficult or impossible to be virulent (fast replication) and hardy (drug resistant and/or immune system resistant) at the same time, so mutations which increase resistance to one drug also decrease virulence - if you treat HIV with enough drugs then the mutations required to be resistant to all of them will result in a virus that has very poor virulence.
(1) http://www.wiley.com/WileyCDA/WileyTitle/productCd-0470927941.html
(2) https://www.amazon.com/gp/search?index=books&linkCode=qs&keywords=9781782620693
(3) https://scholar.google.com/scholar?q=human+drug+transporters&hl=en&as_sdt=0&as_vis=1&oi=scholart&sa=X&ved=0ahUKEwjVh6-a8aPPAhVK1B4KHfxABSsQgQMIGjAA
(4) https://en.wikipedia.org/wiki/ATP-binding_cassette_transporter
(5) https://www.google.com/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=human+drug+transporters&tbm=bks
(6) https://en.wikipedia.org/wiki/HIV_drug_resistance


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What is cytoplasmic localization?
I was studying development of chick but didn't understand what is cytoplasmic localization. My book says:

After third cleavage , the rest of the cleavages are irregular and completely delimited cells are formed all over the germinal disc which is termed as blastoderm. This outcome of cleavage called cytoplasmic localization helps seal the developmental fate of each cell's descendants.

"Cytoplasmic localization" is a very general term and it means that something is present in the cytoplasm. For instance (hypothetical but there are known examples), you can say protein-X is localized to cytoplasm or the cytoplasmic localization of protein-Y is reduced upon phosphorylation. Similarly, there are terms like "nuclear localization", "ER localization", "mitochondrial localization" etc.
The usage mentioned in your excerpt is actually unclear and misleading. There is no process called cytoplasmic localization. What it actually means is that there are proteins/RNA inside the cytoplasm of the embryo that are asymmetrically distributed. When the cell divides, these molecules are therefore asymmetrically sorted to the daughter cells. Depending on what (and how much of) molecules the daughter cells receive, different cells adopt different phenotypes. Also note that the axis of division also plays a role; if lets say the distribution of a given molecule is asymmetric only about the anteroposterior axis and the division happens along that axis then both daughter cells receive the same amount of molecule and both the cells would be similar (w.r.t that molecule). This won't be the case if the division is along left-right axis. See the figure below.

From: Berika et al., 2014

I am not sure which book you are following but Developmental Biology by Scott F Gilbert is a good book and explains these processes nicely.

That's absolutely terrible phrasing in that quote.
I think it's referring to one mechanism of cell fate determination: a transcription factor can be transported out of the nucleus (which will result in it being localised to the cytoplasm rather than the nucleus - "cytoplasmic localisation"), and thereby that transcription factor won't perform its function anymore. The resulting changes in gene expression can be involved in the developmental fate of that cell and its descendants - depending on which transcription factor it is.
In the early embryo, various factors (for example chemical gradients of a signal) cause different cells to apply this mechanism to different transcription factors, thus resulting in different cell fates. However, unlike the statement in your quote, that is not an outcome of cell cleavage.


text:
Calculate signifficance of SNP in specific trinucleotides
So, I have calculated the frequency of all SNPs (single nucleotide mutations) in some samples and have also found the nucleotides on the 3' and 5' sides of the mutated nucleotide. So I have a list of 192 possible permutations like this one:
AAA -> ACA 43
AAA -> AGA 35
AAA -> AAA 134
.
.
TGA -> TAA 345
TGA -> TCA 25
TGA -> TTA 97
.
.

What is the statistical approach to show that a particular set of 4 of these mutations is significant?
I have little knowledge in statistics so I welcome a for-dummies explanation!

Please do not suggest it is a good assumption to assume you are an idiot. It is wrong and you should work on knowing it better. I edited your post.

If you are wondering about statistical significance, it means that you want to do a statistical test. In order to make a test, you need a question to test. What is your question? Is it "Is a given SNP under selection?" or "Does the SNP really exist or is it just a sequencing error?"

Hi, the stupidity I was referring to was statistics-specific :)  But, you are right. Anyway, I am trying to prove that the SNP is under selection. Specifically, that there is a higher frequency of TCA>TTA and TCT>TTT.

Cool. You should clarify in your question that you are trying to detect selection. Also, what samples do you have exactly. Do you have different species or a single species? Do you have a structured population or a panmictic population? Do you have candidate genes (or SNPs)?


text:
Is there a meaningful difference between direct and indirect light
I don't see a basis for a distinction, but I've heard several people distinguish between direct and indirect light for people, claiming that indirect light would be better in many cases. "Direct" means that the light goes from the source to your eye without intermediary, and "indirect" means that the light bounces one or more times off other objects before entering your eye.
An example of indirect light, for the purposes of this discussion, is sunlight or indoor artificial light, reading an old-fashioned print book or a non-backlit Kindle. An example of direct light would be any modern computer screen, or a backlit Kindle. The one context I've heard of direct light being preferred is a light alarm clock, where it was stated to be an advantage that light from the alarm clock goes directly to your eyes and is not exclusively bounced off objects in a room.
Now I can see one or two obvious differences; direct light tends to come from a small source (we don't tend to cover walls with LED's), while indirect light is more likely to bounce off everything or at least much more of what you can see. Furthermore, all other things being equal, direct light should be brighter as I am not aware of anything that reflects fully 100% of the photons that strike it (maybe some odd variant on superconductors)? However, I see only superficial distinctions between the two, and not a reason why, if all other things are forced to be equal (e.g. an indirect source being made brighter to compensate for the photons that physical surroundings absorb instead of being reflected), there should be the fundamental difference between direct and indirect light that I have repeatedly heard from people I trust.
Is there such a basic difference, or not, and if there is a difference, what does that difference consist of?
TIA,

Welcome to Biology S.E.! If you need additional assistance, please visit The  http://biology.stackexchange.com/help Help CenterHelp Center

If the lights from 2 source, is creating same intensity of light for all points of  retina, I don't think there could be any difference of effect.

@AlwaysConfused That thought is part of why I asked the question (instead of simply agreeing with my friends). I see possible differences in a (theoretical) blackbody room where everything was covered with low-light LED's so that theoretically there is only ambient light but it is 100% direct and 0% indirect; or light not visible to the viewer could bounce off a single object the light was shining on and that object would seem isomorphic to a direct light source. Part of the assumption that led me to post here rather than physics.SE is I'd expect any valid answer to be biology, not physics.

I don't know if really such biological experiment/evaluation took place or not. So I didn't go to write any answer, and wrote as comment. Thanks.

I'm voting to close this question as off-topic because it is more suitable for Physics-SE

The best difference I can find is not a different in physics. There is a difference (I don't know what significance it does or does not have for biology) between light that comes through a large area of a person's visual surface, and light that comes through a concentrated area. There are occasional differences with that reformulation (a fire in one's surroundings may provide direct light to a large portion of your visual surface), but that may be a more biological question.


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What does fail-safe mean in transmission at electrical synapses?
I'm reading a book named Neuroscience:Exploring the Brain recently. And in the chapter about synaptic transmission, it says "Transmission at electrical synapses is very fast and, if the synapse is large, fail-safe." So what does fail-safe mean? And why is that transmission fail-safe when the synapse is large?
And when is comes to EPSP, it also mentions that "The neuromuscular junction has evolved to be fail-safe; it needs to work every time, and the best way to ensure this is to generate an EPSP of a huge size." I don't understand the meaning of the word and the whole sentence.

To understand what failure means in this context, we need to know a bit about how signals are communicated from one neuron to another.
Types of signals
First of all, it's important to know that synaptic signaling (communication between neurons) comes in two flavors: chemical and electrical.  The signaling is done at the interface between two neurons, known as the synapse.  There are generally dozens to hundreds of synapses between two connected neurons.  At chemical synapses, a chemical (the neurotransmitter) is released into the space between the pre-synaptic site on the axon and the post-synaptic site on the dendrite (or soma).  At electrical synapses, no chemicals are released.  Instead, porous proteins called “gap junction channels” bridge the space between the cell membranes of two neurons and create pores that allow electrical current to pass directly from one neuron to the other.
Signaling is probabilistic
Second, it's important to appreciate that neurotransmission is probabilistic, rather than deterministic.  That just means there’s a chance that signaling from an upstream neuron might fail to evoke a response in a downstream neuron.  There are several reasons why transmission is not 100% efficient, at both the pre-synaptic and post-synaptic ends.
Some of these reasons have to do with spontaneous opening and closing of channels in the membrane.  When researchers examine electrical currents flowing through single ion channel proteins they find that each channel randomly flips between open and closed states.  This is caused by molecular-scale fluctuations in the protein's shape that cause it to either block or allow the passage of electrical current (or ions).
In addition, random fluctuations in how well electrical current is able to be integrated by the downstream neuron add to the variability in signaling that makes responses probabilistic. You probably already know that "response" of a neuron refers to the firing of action potentials. And you probably also know that action potentials are generated when the membrane of a neuron becomes sufficiently depolarized - the result of a process known as synaptic integration.  A simple view of synaptic integration is the summing together of all electrical currents flowing across the membrane from different synapses in a short window of time.  If this current integrates to a total greater than some value (the firing threshold) the neuron fires, otherwise it does not.  What some may not realize, though, is that this process isn't perfect - current can leak out of the cell, other neurons can "siphon off" current, and receptor proteins in the downstream neuron can become inactive and stop contributing to the overall current flux.
All of these factors conspire together to make the signaling process probabilistic. Because there's always less than a 100% probability that signaling from an upstream neuron will sufficiently excite a downstream neuron, there will be occasions where a downstream neuron fails to fire.
So taking these things into account, we can define the following:

SUCCESS = Neuron A fires -> causes Neuron B to fire
FAILURE = Neuron A fires -> Neuron B does not fire

An example
If a synapse has 100 channels, and each channel has a 50% chance of being open at any moment, then we expect that, on average, 50 channels will be open at any given time.  If each channel can allow 1pA of current to pass through, this synapse will transmit on average 50pA of current from Neuron A to Neuron B.  Let's say 25pA is needed to bring Neuron B to threshold and cause it to fire.  Then this synapse will typically transmit more than enough current to evoke a response in Neuron B.
But here's the catch.  Because the inactivation of each channel is spontaneous, sometimes there will be more than 50 channels open, and sometimes less than 50 - just by chance.  On some rare occasions, fewer than 25 channels will be open, and if Neuron A fires at one of these crucial moments, our 100 channel synapse will transmit less than 25pA, and fail to bring Neuron B to threshold.  This is how an electrical synapse "failure" occurs. You can imagine how, evolutionarily, this might be a bad thing if that failure to fire Neuron B occurs at a crucial moment when the muscle under control of Neuron B is needed to jump out of a predator's reach.
This leads us to the question:
Given these definitions, how would we increase the chance of success, and correspondingly decrease the chance of failure?
Scaling up
Well, probability makes things a numbers game, and here's where size comes into play.  One way we could make sure that Neuron A has a really good chance of firing Neuron B is to mitigate the risk from spontaneous channel inactivation.  We could do this by simply scaling up the synapse - making it larger and adding more channels.  If we had 200 synapses, rather than 100, and they all still had a 50% chance of being closed at a given moment, then the chance becomes incredibly remote that, at a given moment, fewer than 25 channels (the number needed to fire Neuron B) are open and able to transmit signal.  This is what's meant by being made fail-safe.
It's easy to see that another means to the same end is to scale up the corresponding response in Neuron B - the EPSP - as observed at the neuromuscular junction.  By scaling up the strength of the response, it becomes less likely that random, uncontrollable influences on the cell (or muscle) would cause a failure to fire.
Hopefully, now you can see how neurons may fail to signal, and why scaling things up can, in general, make a synapse more fail-safe.

It would be great if you can add some references that people can go to if they need to know the details. References are, in general, always appreciated.


text:
Hundreds of Red Spiders in Individual Webs
I live in the USA in south Louisiana. I woke up this morning to find my yard covered in hundreds of spider webs.

Each of those little white puffs is a spider web. Inside of each web is one little red spider.

The spiders are pretty small. Less than half an inch long.
Anyone know what they are?

http://xkcd.com/8/

@CDspace Seriously, there's an XKCD for absolutely everything...

It is a black-tailed red sheetweaver, Florinda coccinea.
Identified by its red body colour , location (USA) and black caudal
tubercle.

More images to be found on bugguide.net

It is a species of web-building spider belonging to the family Linyphiidae. It is the only species in the genus Florinda. It is sometimes known as the red grass spider. This species is common in the southeastern United States, inhabiting grasslands, lawns, and agricultural fields.

Reference: Wikipedia

You say "It's a rare species.", but the quoted text says "This species is common in the southeastern United States" could you please clarify?

Rare worldwide and common in a location.

I have seen these suckers before. Usually their web is most visible in the early morning when the grass is dew covered.  They seem to need a lot of space. I have seen them in large yards and fields but never small yards. There a little neat, but mostly harmless. Birds should come soon and eat most of them. You should try to avoid mowing them. I'd be surprised if they were there for more then a couple of days, assuming your don't have a mosquito problem.

@anothersackofchemicals Thanks for pointing out. It was my mistake to put it in that way. I actually meant they are rare worldwide as coteyr said. I've removed it.

Hey, I saw a couple of these in my yard just this morning. This one missed a meal

@WayneWerner I loved the plot twist at the end of your video. It was like deus ex machina, or dog ex machina :-)

Cat ex-machina, actually. She decided that I should be petting her instead of taking videos of boring grey patches on the ground.

@coteyr Yeah, they were gone when I got back from work that evening.


text:
Can the NADPH/NADP+ ratio affect the FMN to FMNH2 ratio in the complex I of the mitochondria?
This is the reaction:
FMNH2 + NAD(P)+ <-> FMN + NAD(P)H + H+
The reaction works either with NADH/NAD+ or NADPH/NADP+
I know that the NADH/NAD+ ratio affects the FMN to FMNH2 ratio
But does the NADPH/NADP+ ratio affect the FMN to FMNH2 ratio in the complex I of the mitochondria?

No, because FMN is bound to the complex covalently.

@SciEnt — if you are going to answer questions please do so as an answer not as a comment. When you click on the comment link this is made quite explicit. Ignoring this injunction undermines the way Stack Exchange operates.


text:
Is it possible to estimate the age of a wasp nest by its size?
Long story, but briefly I am debating knocking down a paper wasp nest. I don't want to kill the wasps, because (1) they're beneficial wasps, and (2) I would not have even known they were there, except I came face-to-face with the nest (~1 foot) and they didn't act remotely aggressive at all (karma).
My concern is that I've been out of town for a couple weeks, and I don't know if the nest has been under my deck all year and they were actually relatively sedate, or if the nest has developed recently. I mow regularly, and my big concern is that the noise of the mower and weed eater is going to agitate the wasps into stinging.
The wasp nest is under my deck, and my dog crosses the deck to get to the back yard frequently. I also have a toddler, but we generally play with him in the front yard, which is separated from the back yard by a fence.
So, tl;dr - A wasp nest is a little smaller than a baseball and covered in about 15 wasps. Has this nest been under my deck all year (and I can mow without worry as I have in the past), or has this nest sprung up since I stopped mowing (about 2 weeks) and I should remove it before I mow again?

It sounds like a small nest that can very well have developed recently. However, the size of the nest is also species dependant.

What season and climate is it where you are living? Most (or all?) colonies of social wasps in temperate climate only last one season. So it will go away in the autumn. (Also, nice to see someone caring about wasps!)

@picapica - I'm in Southwest Virginia. Being mid-September now I figured they were probably on their way out, but I mow every Saturday morning, except I've been out of country for two weeks. The nest is in an obscure location that I found on sheer coincidence after I got back (scouting for a DIY project). I thought I had read that they generally form the nests in Spring or early Summer, and if that's the case then I'd leave it, but I'm worried my mowing kept them away and when I stopped they built that nest, and if I mow again I'll get swarmed. I don't want to kill them if I don't have to.


text:
To what extent do fossils change over time?
Fossils are formed over millions of years. How do scientists quantify the extent to which a particular fossil has changed in shape/relative tissue density/etc. over geological timescales (if at all)? I ask this (as a non-biologist) because we are often presented with fossils as being exact copies of the original species, as it was when it was alive. I wondered if this is indeed the case and imagine that the answer will vary for fossils of soft versus harder tissue composition.
If organisms do indeed retain their shape almost entirely, what experiments are carried out to mimic geologic timescales and processes to demonstrate this?

There won't be a single answer to this question -- a skeleton will be different from an insect from a leaf. But taphonomy is study of the process of all the things that go into making a fossil a fossil. Start there and maybe refine your question.

Fossils typically are millions of years old, but they can form rather a lot quicker than that.


text:
Why does vision gradually becomes dimmer in bright setting?
I don't know if this is only happens to me, but if I am in a well lit room and I stare at one point or just look at one area without moving my eyes around my vision in that specific light setting becomes dimmer. I can look around and everything feels like it is dim and lacks the bright light that originally radiated through the room. So I was wondering how and why this happens? I suspect(I am quite dusty in my ophthalmology) my eyes maybe relaxing and taking less notice of the intensity of the light, if so what makes it do so? As a side note this occurrence hasn't affected my life, I am just curious as to why it happens. Another note response to some of the comments, this isn't like walking into a well lit room and get bombarded by the light and eventually adjusting to it. This is like sitting in a well lit room for 15 minutes and then things just become dimmer and less intense. I've also observed this only happens with artificial light and may have some link to the type of light bulb.
I would like to add that this happens if I concentrate on one area or object. So if I were to read a book or be on my laptop, the light around me would feel dimmer. I suspect it has something to do with my eyes focusing on one source, if I were reading a book and this happens, the words become more prominent.

You mean when you just enter a bright room then things appear bright and they seem to dim down after a while?

Answer is linked to expression of proteins and sequestration of those proteins as amechanism to adjust light intensity percived by eye

WYSIWYG not really, I understand what you are saying, this is more like sitting in a well lit classroom for 15 minutes and suddenly everything becomes much less intense and much more dim and gloomy.

This is a very normal vision-mechanism, that happens to everyone.    https://en.wikipedia.org/wiki/Adaptation_(eye)#Light_adaptation and https://en.wikipedia.org/wiki/Adaptation_(eye)#Dark_adaptation. But can't tell how-severe is yours one and is it okay or not.

There are 2 places of rejecting the background-illumination (noise). 1 . Pupil become narrower (like camera's small aperture), and 2. Changes in signaling pathway in retina. On more light, a protein, arrestin (https://en.wikipedia.org/wiki/Arrestin). It inhibits the receptor's activities in various ways.

Always Confused I feel like your description of pupil becoming narrow might have something to do with this I'll look it up and see, but if any of you could beat me too it I would be grateful.

There is nothing to beat you since it as a natural phenomena... to adjust the vision. And perhaps the light-adaptation is much faster than dark-adaptation, (perhaps because excess light can do damage). But I can't tell how-severe it is in yours case, so you could visit an ophthalmologist (not optometrist) who have facility to predict glaucoma (https://en.wikipedia.org/wiki/Glaucoma) .

Always Confused, this is not the case, as the issue only occurs after some time. Light-adaptation is not nearly that slow, so that explanation is invalid.

I get this too, but I understand exactly what you mean unlike previous comments. Only happens when staring, can be almost blurry sometimes.


text:
Single celled organism and immortality
My biology book says:

No individual is immortal,except single celled organisms..

I think that such conclusion aries from the necessity of binary division in many single celled organism to reproduce.
Is the book's conclusion biologically correct and why?

Possible duplicate of http://biology.stackexchange.com/q/21111/3340

I don't believe this question is an exact duplicate of the question at Do bacteria die of old age?, however all of the comments and answers provided there are relevant, and you should read them before continuing to read this answer because I won't repeat what's stated there.
In addition to bacteria and yeast which produce certain "rejuvinated" cells that can divide indefinitely while other cells become senescent or "aged", all multicellular organisms actually employ a remarkably similar strategy. Under certain culture conditions, embryonic stem cells can propagate indefinitely (1).
During early embryogenesis they divide "symmetrically" to the extent that all of the daughter cells are fully undifferentiated until after gastrulation (2), but there is a certain degree of asymmetry that defines the axis along which gastrulation occurs prior to gastrulation (3). This asymmetry is mediated by a large number of signaling pathways (3), some of which become asymmetric during the very fist cell division of the embryo. Adult stem cells also divide asymmetrically primarily as a precursor to differentiation, but this is thought to also be involved in the asymmetric distribution of damaged components to their more differentiated daughter cells (4), as occurs in yeast and bacteria. Currently there is less research on this in adult or embryonic human stem cells than in bacteria or yeast, but it stands to reason that our embryonic cell line does the same thing beginning at its first division, and our germ line is immortal (we're no "older" at birth than our great-great-great-great-great-great-grandfathers) for the same reasons that unicellular cells are immortal.
References:
(1) https://en.wikipedia.org/wiki/Embryonic_stem_cell#Propagation
(2) https://en.wikipedia.org/wiki/Embryonic_stem_cell#Pluripotent
(3) https://en.wikipedia.org/wiki/Gastrulation#Loss_of_symmetry
(4) http://www.ncbi.nlm.nih.gov/pubmed/25966295

Book is technically wrong relative to now, but maybe not when it was written.
For examlple, the hydra are immortal.
https://www.sciencedaily.com/releases/2012/11/121113091953.htm
I also believe there are starfish that are also technically immortal.
That said nothing is trully immortal like Dr Manhattan, and energy.
You are right about the trade off between reproduction and longevity. Reproduction, esspecially sexual.
Big topic


text:
What determines the sex of hybrid offspring?
I'm aware of the usual definition of Haldane's rule, which says that, if the offspring of inter-specific hybrid offspring are sterile, then the sterile offspring will be of the heterogametic sex. That is, for example, females in birds, and males in mammals. But I'm a bit confused. This implies that non-sterile hybrids are also produced, which rarely happens.
So, I have two questions, please:
 1. Does Haldane's Rule really mean that only offspring of the heterogametic sex are produced?
And 2. If so, please account for the exceptions. Crosses between Golden Pheasants and Lady Amherst's Pheasants regularly produce female as well as male offspring, as do crosses between Ring-necked Doves and Barbary Doves. Thanks!

XY and ZW are the heterogametes - males in mammals, females in birds

Yep sorry - wrote it the wrong way around

I am detecting a bit of confusion in you wording of Haldane's rule.
Haldane's rule makes predictions on the fertility of offspring from an inter-specific cross, not the sex-ratio of the offspring from the cross.
"if inter-specific hybrid offspring are sterile, then the sterile offspring will be of the heterogametic sex."
In inter-specific crosses there is not an effect on sex-ratio of the resulting offspring, but a effect on the ability of the F1 offspring to reproduce.
For the offspring, those of the heterogametic sex, males in mammals (XY) and females in birds (ZW) will be sterile while the homogametic offspring will not be affected by hybrid sterility.

Thanks. But that's what I don't quite understand:  virtually all mules, for example, are females. Virtually all canary mules are male. And virtually all hybrids are sterile, including the mules of both. It seems to be the opposite of Haldane's rule in both cases. Sorry for my late reply, by the way - I didn't realise I had answers.

With these mule examples, it is important to consider how distantly related horse and donkey are. Haldan's rule could be acting, but there are likely other effects on top of it causing a different result. Many 'miscommunications' could mess up development when the diverged horse and donkey genomes are mixed. Haldane's rule is illustrated more clearly with closely related sub-species or species because there are fewer incompatibilities which would affect development. The effects much stronger in the XY or ZW hybrid offspring.

Many thanks. It seems there are still a lot of unanswered questions relating to hybrids. Interesting stuff.

As already stated Haldane's rule doesn't always apply to odds of sex being born, it usually applies to the odds of that hybrid being fertile based off of whatever sex it actually was.  Haldane's rule can also apply to the odds of a sex being born at all, though this situation is run into less often.  So in short, no the vast vast majority of the answer to your first question is no, it doesn't mean that only one sex is produced.  The majority of the time when Halden's law applies it only affects fertility of the offspring not the production of them.
Let me get into more specifics though, to help clear things up better.  I think I detect two main conceptual mistakes which may be leading to your other confusion, so let me address them and see if it answers all your
confusion. At least one, maybe both, seem related to the way you quoted Haldane's law, so let me first quote a slightly more accurate version of the law, straight form wikipedia:

When in the F1 offspring of two different animal races one sex is absent, rare, or sterile, that sex is the heterozygous sex (heterogametic sex)

Halden's rule doesn't apply to all hybrids
The law starts by saying "when in f1 offspring one of 3 situations occur it will be the heterozygous sex.  I think the first confusion is simply an attempt to apply this rule a little too broadly instead of limiting it to these categories.  In your example of the Pheasant's it appears that both sexes of hybrids are fertile.  Since neither sex is rare or sterile Haldane's rule simply doesn't apply, the precondition isn't met so you can't say anything about they heterozygnous sex.
In the case of the doves, well I'm not an expert at this but as far as I can tell Barbary and ringneck are two names for the same dove so I'm not sure that is a hybrid at all.  I may just be misunderstanding dove nomenclature/classifications here, but in any case it looks like most doves hybrids are fertile so if I had to guess Haldane's rule doesn't apply in this case either.
However, just because your specific examples may not apply that doesn't necessarily invalidate the entire question.  It is certainly possible species where Halden's rule applies where children of both sexes are born, in fact this is usually the case.  Thus let's get to the other confusion.
Haldane's rule applies when one sex meets listed conditions
One confusion you seem to have is that the rule seems to imply that fertile hybrids exist despite the version of the rule you quoted specifically saying that halden's rule applies when hybrids are sterile.  That's because the actual rule applies only to one sex, meaning that one sex will be infertile and the other sex fertile.  If both sexes are infertile, as with the mule, Haldne's rule doesn't actually apply since it's not a trait unique to one sex(except when it does...I'll come back to that).
When precondition X applies the heterozygnous species demonstrates that condition
The law states that if offspring are "absent, rare, or sterile" that sex is the heterozygnous one. Those are three conditions any of which can apply, this doesn't mean all the conditions apply.  The most common examples of Halden's law your likely to run into is where one sex is sterile, in which case that sex is sterile, that doesn't mean it has to be sterile and rare and absent.  For that matter in cases where one sex is rare it's possible that the sex will be fertile on the odd example it's born despite being rare.
So back to what I said at first, most often Halden's law means two sexes that are equally common, but where one sex is sterile when it's born.  The best example that I can think of right now is with bovine hybrids, where cattle were often crossed with other bovines to get the 'best' bovine to raise for meat was common.  Crossing bison with Cattle produced more resiliant and better animals that were easier to raise, the only problem was that males were born infertile while females were fertile.  This resulted in an inability to keep hybrid breeding populations without males to mate and thus keeping a 'feral' breeding pool of bison cows to mate with cattle bulls; which was a problem since bison weren't domesticated and keeping breeding stock was an issue.  Thus a very common hybrid ran into issues due to Haldane's rule, keep this issue in mind, I'm coming back to this example later for my last point.
It is true that some hybrids have only one sex common due to Haldne's rule, I can't think of an example right now but there are many, just none exist in the common big/domesticated mammals I'm most aware of.  Usually if a sex is rare that sex is likely to also be infertile, the issues that cause the sex to be rare will usually also make it infertile.  However, as I understand the genetics it's entirely possible for a species to have one sex be rare, but that sex be fertile when it is produced; in fact id love an example if anyone can suggest one!
Laws are really just rule's of thumb
You don't want to apply this, or really any genetics law, too exactly or biology is going to decide to throw you a curve ball.  Because of the oddities of the ways genes are combined, and even the possibility of random mutation, many 'impossible' situations still come up.  Look at mules, thought to be infertile and yet a half dozen fertile mules have been documented at least, in fact most common 'sterile' hybrids I know of have examples of fertile hybrids being produced.
Which brings us back to the beefalo example above.  Remember keeping bison cows for breeding stock was a major problem for them?  Well that problem solved itself when a fertile male beefalo was born.  Even though they are almost always infertile this male was fertile, as were both sexes of his offspring.  This was due to random chance (I don't know if it was mutation or just the combination of the genes specifically), but a rule was broken by genetics.  Thanks to this we were able to start up hybrid breeding populations of beefalo, all decedents of this male, beefalo are the most common bovines raised for meet now of days!
The point being go in expecting any rules to be bent in genetics at time.  There are exceptions to most of these rules, life finds a way yadda yadda.
Hope all that rambling gave you a better idea of how the rule applies.

Many thanks for taking so much time to answer this. Apologies for not replying sooner - I have only just found the answers via Twitter, which I rarely use

Apologies also for confusion over Ring-necked Dove - I'd intended to write [Eurasian] Collared Dove but was distracted. Husband has bred some of these and they do appear to be sterile and occur in both sexes. Certainly canary hybrids with finches are virtually all sterile, and virtually all males. I had recalled reading an explanation of this in Tim Birkhead's book The Red Canary which, (as far as I remember) attributed this sex bias to Haldane's Law - hence my confusion. Many thanks, once again.

Thanks very much also for the information about beefalo - that was all very new to me and useful information.


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Does galactose occur before or after galactose transferase?
The follow shows a protein pathway pathway.

The question is "where does galactose (GAL) first occur" i.e. which block above is galactose first contained in?
A transferase is defined as (wikipedia):

any one of a class of enzymes that enact the transfer of specific functional groups (e.g. a methyl or glycosyl group) from one molecule (called the donor) to another (called the acceptor)

This definition of transferase is confusing as:

The question doesn't show any functional groups does it?
From it, I can't figure out whether the galactose transferase is the molecule that is the donor or acceptor

I can't decide if galactose first occurs in S (as a donor) and is transfered into an acceptor upon reaching T, or if another donor forms galactose (as an acceptor) after S, causing T to contain galactose.

Can you please explain this diagram and cite its source? I think it depicts the processing of a glycoprotein and shows how different sugars are added stepwise.

Yes, this is a biochemical pathway showing a scheme whereby proteins in the endoplasmic reticulum and Golgi apparatus become glycosylated on their way to the cell surface. The square boxes labelled with letters represent a generic protein substrate as it moves along the pathway. The arrows between the boxes are labeled with the names of the enzymes that are performing the post-translational modifications. Galactose is a carbohydrate, specifically, a hexose with a 6-carbon backbone. It would be one of the substrates for the Gal transferase enzymes.

You need to google for galactosyl transferases and find out what kind of reaction they catalyse. Then, if S and T represent proteins with growing polysaccharide chains (as @RosieF states, although I personally would have no idea) you should be able to work this out for yourself. But I think the question is unclear because of the schema and am voting for it to be closed.


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Do all microRNA isoforms need to be known and sequenced to obtain microRNA expression?
From what I understand, microRNA are short "hairpin" shaped nc structures. When sequencing and counting miRNA, isoform miRNA are "found" which are subsections of varying length and possibly with some mutations or other differences to the "canonical" microRNA. The total counts for a miRNA are the sums of the counts for the isoforms which relate to that miRNA. [Please correct me if this is all wrong]
With regards to Next Gen Sequencing, a 'library' needs to be added which tells it what to sequence. Does this mean only "known" isoforms be read and counted or can "new" sequences (i.e. mutations) also be read and counted which were not known before sequencing started?
With regards to qPCR - does this technique only look for individual isoforms? In which case, if I want to know something about a particular microRNA expression would I need to do qPCR for each known isoform relating to that microRNA. OR, is it in fact easier to sequence microRNA expression with qPCR since sequences can be matched to the main hairpin structure with higher probability. (By easier I mean compared to say wanting to get the expression for a particular isoform since it needs to be matched exactly).

With regards to Next Gen Sequencing, a 'library' needs to be added
which tells it what to sequence. In the context of NGS, the "library" is a pool of molecules which you sequence. You don't have to know their content to get their sequence.

I had worked on a similar problem and I am telling my experience.
First, you have to consider the fact that a mature miRNA can arise from multiple genomic locations i.e. many pre-miRNAs can give rise to same mature miRNA.
As you said there are products of pre-miRNA cleavage with heterogeneity at their ends i.e. there are sequences that do not exactly match the annotated mature region. While products with 3' heterogeneity can be called isoforms, products with 5' heterogeneity are likely to have different targets as the seed sequence is disrupted and hence they are technically different miRNAs (by definition).
Now, the best technique to analyse isoforms is small RNA sequencing (NGS). qPCR would not be a good technique as primers cannot always differentiate highly similar sequences (worsened by the fact that miRNAs are too small). A NGS library is a set of DNA sequences that you obtain from shearing the RNA/DNA followed by adapter ligation (reverse transcription for RNA). Since the adapter sequence is known, the sequencing reaction does not require you to know the sequence of the products. However, you would need to know the reference genome for finding novel miRNAs. This is primarily due to the fact that it is very difficult to sequence pre-miRNAs (low abundance and hairpin structure). You can identify new small RNAs very easily but cannot say that they are miRNAs unless you can map them to a stem-loop precursor (pre-miRNA).
You can very well discover new reads and people have discovered a lot of new miRNAs using NGS. I can tell you the methodology I followed to find atypical products of the same pre-miRNA. I for simplicity I call the 5' heterogeneous products as badseeds (because they have disrupted seed sequence) and 3' heterogeneous products as isomiRs. I used a methodology that is similar to that of a well known program – miRdeep.

Get the pre-miRNA sequences from miRbase
Get mature miRNA sequences from miRbase
Use bowtie-1 to build an index from the pre-miRNA sequences
Remove adapter from your fastq reads and remove low quality reads. There are many tools to do that. You can try Trimmomatic.
Map mature miRNA sequences to pre-miRNA index using bowtie to find the exact location of mature miRNA in pre-miRNA
Map reads to pre-miRNA region. Filter reads that do not map in a pre-defined window around mature region.
Classify the reads as badseed or isomiR

Now, isomiRs and reads that perfectly map to mature miRNA region can be considered as contributors to total miRNA expression. However, badseeds should not be considered as an isoform. You can likewise allow a certain level of mismatch and count these reads. Sequences with mismatch in seed region would again be badseeds. You can additionally have scoring schemes for your reads.
There are not many studies on such analysis. I did not get any publishable result with our data but the methodology is reasonably correct. You can go ahead an apply it for your study.

Ok, at least one answer to the question. The basic point in the answer that's really a comment is worth retaining: the library is the pool of sequences you obtain from NGS, and you sequence all the RNA of a particular size. You identify what you have sequenced in relation to a reference — it could be a reference genome in which the miRNAs are already annotated, or you can try to discover new ones, as you did. And you (or at least I) don't find any pri-miRNAs.


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Reproduction or Cell division
Most of the cells in multicellular organism undergoes cell division through Mitosis.
While most of the single celled organism reproduces through binary fission by mitosis.
In both cases,the offspring are very genetically similar to the mother cell.
But one is defined as Cell division and other is defined as Reproduction.
Why?

Both cells from unicellular organisms (for example, E. coli) and multicellular ones (humans, for example) divide by mitosis - you are correct. The daughter cells are not just very genetically similar, they are identical (if everything goes right, which it usually does). Both of these instances are called "cell division". It's also called "reproduction" in unicellular organisms because the entire organism just reproduced, in an asexual manner - it went from one to two copies of itself. On the other hand, many multicellular organisms (and some unicellular) can or must reproduce sexually. This involves (generally) at least one partner and a cellular process known as meiosis, which produces haploid gametes, which then meet somehow, one gets fertilized by the other, and the resulting diploid cell begins mitosis again.


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Self-thinning: slope of log (biomass) vs log (density) is -1/2 whereas slope of log (weight) vs log (density) is -3/2, why?
In self-thinning or intraspecific competition (more relevant for trees I guess) why does logarithm of Biomass vs logarithm Density give you a slope of -1/2 whereas logarithm of Weight vs logarithm of Density gives you a slope of -3/2? Biomass is mass (or quantity) of an organism per volume(or area), weight is mass scaled by gravitational acceleration which is a constant, unless the organism you are dealing with is very very tall. So the plots can be shifted accordingly but shouldn't slopes be more or less the same ?
source: Ecology: Concepts and Applications
by Manuel Molles
www.mheducation.com/highered/product/ecology-concepts-applications-molles/M0077837282.html
.

Welcome to Biology.SE. This is a question of statistics, not biology. You should give it a try on Stats.SE.

I would not expect the slope of y~x to be equal to the slope of log(y)~log(x) (to the exception maybe of when the slope is 1?). Consider this R code for example. x=rnorm(100,40,7);y=x/6+rnorm(100,0,1);plot(x=x,y=y);lm(y~x);lm(log(y)~log(x))

@Remi.b I understand log plots. For example, if you know Stephan's law of radiation; radiated energy E is proportional to fourth power of temp T, in this case, if we plot log(E) and log(T) we will get slope to be 4. But that (value) is not my concern, why are they different is my concern.

@Remi.b I don't understand how is this a Stats question, I think definition of biomass and physics are more relevant here !

I though your question was "why does y~x has a different slope from log(y)~log(x)?" but it rather seems to be "why does log(y)~log(x) has a different slope from log(k*y)~log(x)?" (which is still a stat question). Actually, they should not differ. So either your definitions of Biomass and or weight are wrong (in other words weight != k*Biomass) or you misinterpret / misplot your graphs. You should include your data (or link to the source) and explain how you treated them.

Oh ok, you are comparing graphs from the book you added I suppose. Most of us won't have access to the book so you should show the graphs and also the text that define the variables used in the graph.

@Remi.b I know that this is not exactly a Biology question, it is more about the understanding of those quantities, physics behind them and the mathematical analysis of it. I am not exactly sure where to post it. I googled definitions of Biomass and weight and crosschecked if there was any misinterpretation, but there wasn't any. And as far as I understand it should only offset ( y = mx + c, I mean c by offset ) the plot and not change the slope. BTW I still don't get it how is it a Stats question XD.

Let us continue this discussion in chat.

Biomass here refers to the total mass of all the organisms in the population (in a unit of area), added together.
Weight here refers to the average weight or mass of an individual.
If biomass decreases, that could be because the individuals got lighter, or it could be because there are fewer of them, or both.

Added
I think I see what's happening.
Let $W$ be the average mass of an individual, $N$ be the number of individuals, and $B$ be their total biomass. Then of course,
$B=WN$
Let's start with:

$W$ is proportional to $N^{-\frac{3}{2}}$
$N$ is proportional to $N$ (duh). Let's rewrite that though, as:
$N$ is proportional to $N^1$

But that means:
$B=WN$ is proportional to $N^{-\frac{3}{2}} \cdot N^{1} =N^{-\frac{3}{2}+1} = N^{-\frac{1}{2}}$
Density increases with density (N). Weight per individual  decreases with the -3/2rd power (W). So their product, biomass decreases with the -3/2 + 1 = -1/2nd power  (B=WN).

Plants do not get lighter, the loss of leaves is not considered in this theory and it would apply to all individual in the stand, only the stem density is discussed.


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Can birds suddenly suspend in the air in one position?
I don't know if it was my eyes fooling me or if it was real. I've seen birds suddenly get suspended in the air, flapping their wings but not moving. Like making non-locomotor movement on the air. Is there an explanation for this?

Do you mean hovering?

Doing a stationary flight is called hovering (as @kmm said in the comments).
With head wind
When there is a (relatively important) head wind, many birds are able to perform stationary flights. However, in the bird's referential the flight is not stationary. It is typically common to see that for see birds.
True hovering
In absence of head wind, most birds aren't able to hover. There are a few exceptions. Hummingbirds hover while feeding on nectar. Some birds of prey are able to hover (they do so for hunting purposes) such as the common kestrel for example. While fishing, the pied kingfisher is famous for its hovering behaviour.
Anatomy and metabolic cost
Generally speaking, hovering requires flapping its wings very fast and is therefore energetically very costly. From wikipedia

Most birds that hover have high aspect ratio wings that are suited to low speed flying. One major exception to this are the hummingbirds, which are the most accomplished hoverers of all the birds. Hummingbird flight is different from other bird flight in that the wing is extended throughout the whole stroke, the stroke being a symmetrical figure of eight, with the wing producing lift on both the up- and down-stroke. Some hummingbirds can beat their wings 52 times a second, though others do so less frequently.

Videos
Here are some videos of birds hovering:

Hummingbird hovering
Common kestrel hovering
pied kingfisher hovering


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What will happen if a poisonous snake bites itself?
I wonder if in general snakes are immune to their own venom. I would like to know studies or references about times snakes bit themselves and got sick or the contrary.

Have you tried to google your question?

Homework questions and questions that show little or no prior research effort are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

This is not a homework question at all, as well after some googling I found 2 sort of answers for this interesting question. Some wrote, The snake will become affected and die. Some other source tells, nothing would happen to it. only a few uses an example, and I found no original experiments reference. https://www.quora.com/Will-a-venomous-snake-die-if-it-bites-itself , http://www.thenakedscientists.com/HTML/questions/question/2276/ , http://www.venomousreptiles.org/forums/Toxinology/23.

“The conventional wisdom is that they have circulating antibodies in
  their blood,” says Stephen Mackessy, Ph.D., a Professor of Biological
  Sciences at the University of Northern Colorado and an expert in
  venomous snakes. “This would protect them from their own venom, as
  well of venom from another snake in their own species.”
Hypothetically, if a speckled rattlesnake bit another speckled
  rattlesnake, the immunity they’ve built from being exposed to low
  levels of their own venom—kept in glands behind their eyes and
  secreted when they bite—would protect them from a fatal wound. (Even
  though the glands are closed, they still contain blood vessels that
  allow the venom to circulate in their system, causing mild exposure,
  Mackessy says.) But a speckled rattlesnake that meets up with a cobra
  might have a different day entirely.

So in the case snake were to bite itself it wouldn't suffer as much from the poison compared to the actual bite it self-inflicted.

If you're quoting from a source, you should include the source in your answer so others can read the quote in context. Additionally, answers that are completely or almost completely made up of quotes from other sources are generally not good answers. Do research, find several sources, and synthesize a good answer in your own words. Make sure you include links and attribution for your sources, however.


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Is ATP produced in a different manner during glycolysis from that generated by the Krebs Tricarboxylic Acid Cycle?
The ATP in glycolysis is produced in the cell cytoplasm but that from the Krebs Cycle is produced in the mitochondria. The mitochondrial membrane contains an ATP-synthase protein complex that harnesses a proton flow into the production of ATP from ADP and Pi.
Is the ATP made in the cytoplasm during glycolysis made in a similar or different way?
https://www.youtube.com/watch?v=mfgCcFXUZRk

The ATP in glycolysis is produced directly in certain reactions of the type:

X-PO32– + ADP → Y + ATP

in a process is called substrate-level phosphorylation.
A key preceding reaction in the pathway is the one catalysed by glyceraldehyde 3-phosphate dehydrogenase, in which free orthophosphate is incorporated into a sugar phosphate in a reaction of the type:

Z + PO43– → X-PO32–

(I have used X, Y and Z because other changes occur in the structures.)
This is totally different from the oxidative phosphorylation that occurs in the mitochondrion. In both cases the (free) energy driving the generation of ATP comes from oxidation of sugars involving cofactors such as NAD+ to NADH. In oxidative phosphorylation the reoxidation of NADH in the membrane (ultimately by molecular oxygen) is used to set up a proton gradient, which can then be used to drive the ATP-synthase. In substrate-level phosphorylation the chemistry of the intermediates is manipulated so that particular reactions involve sufficient free energy change to drive the conversion of ADP to ATP directly. (The anaerobic reoxidation of the NADH does not produce ATP in this latter case.)
You should read a text-book of biochemistry for the details, which are too extensive to present here. Berg et al. Section 16.1 covers this well, and is available on-line.

I have edited my original answer that had the unintended implication that ATP was generated in the G3PDH reaction. I have also tried to illustrate the principle of substrate-level phosphorylation, but have used general reactions to avoid the distraction of the actual chemistry, which can be found elsewhere.


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Bird identification- Crane
What species of crane is this?

Today afternoon, I found this crane among a group of white cranes that were moving around a herd of buffaloes. I live in West Bengal, India if it matters.
Is it an eastern cattle egret,Bubulcus ibis coromandus in breeding plumage?

Some of the photos appearing in the avibase page for Cattle egret look really similar, for instance https://www.flickr.com/photos/33816646@N06/5834155140.

It does. I found a page of Avibase about Bubulcus ibis coromandus with similar photographs.

Yes, It is for sure a cattle egret.

Yes, this is a cattle egret displaying its breeding plumage.
The cattle egret (Bubulcus ibis) is a cosmopolitan species of heron (family Ardeidae) found in the tropics, subtropics and warm temperate zones.
Specifically, this is the eastern subspecies, B. ibis coromandus.

 B. ibis coromandus [source: Wikimedia Commons]

 B. ibis ibis © Larry Thompson, 2007-2015
The cattle egret is the only member of the monotypic genus Bubulcus, although some authorities regard two of its subspecies as full species, the western cattle egret and the eastern cattle egret.

The eastern subspecies B. ibis coromandus, described by Pieter Boddaert in 1783, breeds in Asia and Australasia, and the western subspecies (B. ibis ibis) occupies the rest of the species range, including the Americas.
The eastern subspecies (B. ibis coromandus) differs from the nominate subspecies in breeding plumage in that the buff color on its head extends to the cheeks and throat, and the plumes are more golden in color.

B. ibis usually feeds in seasonally inundated grasslands, pastures, farmlands, wetlands and rice paddies. Their name comes from their tendency to often accompany cattle or other large mammals in these areas, where they catch insects attracted to and small vertebrates disturbed by these animals.
Originally native to parts of Asia, Africa and Europe, B. ibis has undergone a rapid expansion in its distribution and successfully colonized much of the rest of the world in the last century.

 [Source: Discover Life]
Major Source: Wikipedia


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Phylogenetic algorithms: How to interpret multiple ML trees from the same dataset?
There's still something that confuses me about how many of these algorithms work, and how results are presented in the literature.
Let's consider a Maximum Likelihood based algorithm like MrBayes or RAxML: Users set a random number seed which generates the starting tree. For many of our datasets, different seeds which result in different ML results, as the algorithms are initialized with different trees.
I'm not entirely sure how one is supposed to interpret this, especially as my experience with ML methods is that the initial step is irrelevant to the global/local min/max in parameter space----the chains just take longer to converge.
How should one interpret these results? Are users to run 1000s of trees at different parameter values, and then chose the most optimal likelihood value? That seems rather ad hoc, as does bootstrapping, etc.
Is the dataset fundamentally flawed?

MrBayes is definitely not doing maximum likelihood, as its name suggests.

@kmm Was trying to make this question relevant to several algorithms, and failed. Thanks for the help! I'll try to edit

In short, you have chosen two examples that do not use maximum likelihood as you know it in other contexts. In most statistical contexts, the ML is a single number which can be calculated analytically, so it it always the same for a given data set. This is not the case for either MrBayes or RAxML but for different reasons.
MrBayes
The likelihood criterion in MrBayes is the marginal likelihood of the posterior, given effectively the data conditioned on the priors. This likelihood comes from a stochastic MCMC sampling of the parameter space. If all is well behaved, then the chains and/or runs will converge in the same general location. But then the different possible topologies need to be summarized in some way.
RAxML
RAxML generates essentially random starting trees by random sequence additions to build up trees. The subtrees are then rearranged to find a "best" tree. Again, different starting points may lead to different best trees. But if all goes well, analyses will end up with the same tree. This process is described in this chapter.
In both cases, if you start in a different place, you may end up in a different place. There may be many trees that are, within some criterion, equally likely. If you are familiar with parsimony methods, the analogy is that of multiple equally parsimonious trees.

I'm not sure I follow this: "If all is well behaved, then the chains and/or runs will converge in the same general location. But then the different possible topologies need to be summarized in some way." (1) If the chains converge in the same general location, wouldn't the topologies be equivalent? (2) How would one summarize the different topologies---consensus trees?

Also, " There may be many trees that are, within some criterion, equally likely. If you are familiar with parsimony methods, the analogy is that of multiple equally parsimonious trees." How does one proceed in the literature then? Do you report all equally likely trees? Use (again) consensus tree methods?

Rather than there being a single tree with the highest (maximum) likelihood, there are a family of trees that are all possible, just some more likely than others. The topologies don't have to be equivalent. A consensus tree is the summary of those trees considered most likely or credible (in the Bayesian sense). Yes, you would report the consensus tree (or as many as you want).