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Physiological reason why leaves got twisted when treated with indole acetic acid
I want to know the physiological reasons of why the leaves of my study plant got twisted when treated for 10 days with spray of indole acetic acid. I want to treat seeds with IAA, and I'm thinking about testing what will happen when I treat the leaves.
Here is a picture of what the plant looks like:

thanks

Please add some images - ideally both treated and untreated leaves.

Add study species as well. Also give some background; why did you perform the experiment in the first place? Why indole acetic acid?

IAA induces growth. perhaps that is leading to twisting. But unless you upload a picture and provide more information about the methodology it will be difficult for people to answer this question

@legend I think you need 10 reputation before you can add images yourself. I've added the picture now.

Speculation on my part: since IAA can induce growth, spraying it mostly on one side of the leaf (by spraying from the top) might cause the upper part to growth faster, which would lead to the leaf twisting downwards. From the picture, this seems to be what is happening most of the time. +1

IAA seems to act partially through cell elongation (http://www.biosynth.com/index.asp?topic_id=139), so differential elongation due to uneven spraying seems a likely explanation

how can I measure cell elongation or compare with untreated plant? is there any method for measuring?

Disclaimer: Not my area of research

Since IAA (auxins) can induce growth, partially acting through cell elongation (http://www.biosynth.com/index.asp?topic_id=139), it seems likely that the explanation to your result is differential growth/elongation rates on the upper and lower side of the leaves. This could result from uneven spraying, e.g. by spraying the leaves from the top. Faster growth on the top part of the leaf would lead to downward twisting, which seems to be what is happening most of the time.
You could test if this is the case by doing a simple experiment where you carefully apply IAA with a brush on both sides of the leaves for some plants, while others are sprayed. If uneven application is the cause you should see twisting when spraying but not when applying with a brush.
However, auxin is toxic to plants at high concentrations, so you also need to consider the concentration you are using.

The concentration was 50 ppm.

@legend I have no idea if that is considered high or low.


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Why cannot there be multiple sources for same species origins?
We often associate Africa as the geographical location of the origin of humans. Why cannot there exist multiple geographic locations of origin (given same environmental conditions)?
The same argument exists for other species as well. So what is the basis of the common ancestor (from single geographical location) theory?
Please give me references so that I can read more on this subject.

Partly depends on the resolution at which you look (both spatially and temporally) but the further you zoom in the harder it becomes to define where one species becomes two because its a gradual process which takes place over time and space. It's relatively easy to show that humans originate from Africa, harder to show that humans originate from east Africa ~400,000 years ago, and harder to show that humans originated 378,058 years ago in northern Kenya. One part of the problem is pinpointing when homo erectus (?) became homo sapiens which depends on the definition of a species...

@rg255 Why cannot there be multiple sources of origin say for at Australia and Africa?

There is no reason why it cannot be. Just that the likelihood (of two exactly similar events happening at the same time) is less.

To me, it is unclear what you are asking. Are you asking if two different taxa can give rise to the same species at two different locations (i.e. A -> C and B -> C, if they all would all co-occur you would have A, B & C)? If so, how do you view the relationship between A & B - can they be sister taxa?

@fileunderwater : I think question will make it clear. Why cannot homosapiens independently originate at may be europe and africa?

Why is this question voted for closure because it is unclear? It sounds OK. Also because of the hypothesis that Neanderthal and hominids may have successfully interbred. Both were deemed unrelated. Although it's not my expertise and although i cannot answer this question, i feel it is a good question. Vote to leave open here.

@dexterdev So evolving from H. erectus to H. sapiens independently at two different locations?

@fileunderwater : Yes. That's what I mean.

@dexterdev: But why (and how!) would two separate populations of H. erectus both evolve to the same H. sapiens?  Closest you could get would be two subspecies, which later interbreed to form a single species again.  (Which might indeed have happened with Neandertals...)

This is a very fundamental, and in my opinion, interesting question. You might not find many sources that directly cover this question because it is hard to test. If speciation did happen in two separate locations and the resulting species were so similar that they could breed with one another and not the original species, how would we be able to tell if the species originated in separate locations and that the new species didn't just travel to the new location? Below I'll try and explain why it's safe to assume they probably didn't have different locations for speciation.
Thought Experiment
Here is what happened in hypothetical land. Species X exists in happy land. Individuals of X then move to water land. Some more individuals from X move from happy land to H2O land (very similar to water land). Species X undergoes speciation in water land to species Y and speciation of X also occur in the H2O land to species Z.
Can Z and Y be the same species with different origins where the niche conditions are the same?
As you can imagine, the longer after geographical isolation the more mutations occur and the less likely it is that the new species will be able to breed successfully with similar species.
Although the two environments may seem identical, ecology is notoriously complex and chaotic, and so in reality as far as ecology is concerned, they are very different environments. Even the slightest difference between niches will naturally select different traits that could make Z and Y sexually incompatible.
Furthermore, when dealing with the geographical origin, you must assume that there was geographical isolation between the two speciation event locations. Since there is typically no contact between Z and Y species, there is no selective pressure to remain genetically compatible and given enough time, they will become unable to breed.

Humans
There is a contentious claim that ancient humans bred with chimpanzees after both speciation events from our common ancestor to humans and chimpanzees. Broadly I think this has now been dismissed. However, it is reasonably well accepted that in a more recent "Tolkien-esque" world humans bred with Neanderthals.
But ultimately I don't think there is a single example (I am thoroughly open to being proven wrong!) in the natural world of two similar geographical isolation events driving exactly the same species to evolve and both versions of the new species are more genetically similar to one another than they are to the origin species. The odds are just too slim even if to us the conditions seem identical.

References - Wiki article about the theory of multiregional origin for humans. The wiki article clearly states up front that this is "an alternative explanation to the more widely accepted Out of Africa model". One issue brought up in this article, is although there doesn't seem to be any unique localized single feature, there has been unique combinations of localized features found in early fossils in locations like Australia. The wiki article includes further references.
http://en.wikipedia.org/wiki/Multiregional_origin_of_modern_humans
The more accepted theory is "Out of Africa". Wiki articles:
http://en.wikipedia.org/wiki/Out_of_Africa_I
http://en.wikipedia.org/wiki/Recent_African_origin_of_modern_humans
http://en.wikipedia.org/wiki/Early_human_migrations
Another article that explains why "Out of Africa" is the more accepted theory:
http://www.actionbioscience.org/evolution/johanson.html
Note that all of this is with respect to modern humans. I don't know if there are any animals or plants where multiple source for the same species is the more accepted theory.
Hybrids (the offspring of two compatible, but different species parents) could occur if the parents where multi-regional. You can do a web search for polyploid hybrids and tree frog for examples of this, but these are hybrids, not mutations.

Citing wikipedia alone is risky, as its contents are dynamic and often based on questionable sources

@AliceD - The OP asked for references. The wiki article clearly states up front that this is "an alternative explanation to the more widely accepted Out of Africa model", and the wiki article contains links to references (again, what the OP was asking for). I updated my answer to make this more clear.

Those references may be disputed or deleted altogether over time. Cite the primary references if they are good.

@AliceD - the wiki article was originally created July 2014, and has been continually updated since by multiple people. The references have been there during much of this time, and should have been deleted by now if that was an issue. I would assume that less accepted already means it's disputed, and the wiki article covers this. The talk page should include discussions about the article or disputed references.  I'm not a proponent of this theory, and only posted the link since the OP asked for references.

All good. I'm just explaining my downvote. I'm not saying wiki is per definition not OK, I'm saying I am not a fan of wiki-only answers. That's all. You might get a bunch of upvotes from others. Because of your research into the wiki page I'll remove the -1 :)

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Is life expectancy linked to intelligence in animals?
For example, animals that live only a few days or a few years are often not very intelligent. In contrast, the most intelligent animals seem to live longer.
Is this true? Are there any studies to prove or disprove this statement?

I imagine that the first problem a study like this would run into is how to objectively measure intelligence in a wide variety of animals with vastly different modes of life. I do not have a clue on how to answer this, but "problem-solving" ability in their natural living environment could possibly be one criteria.
Have you done any background research (e.g. on life expectancy in different groups of animals)? The question is very vague and broad.

it would be nice if you can provide references to your argument.. there are several "unintelligent" animals which live long (such as some fishes and echinoderms)

@WYSIWYG I agree that there are exceptions. But on average animals like insects, fishes, small mammals, birds don't live very long. Again, on average. I have one explanation and that is that the heart(or lower forms of heart) is pumping slowly for bigger organisms, (and because each organism has preprogrammed the same ammount of heart-beats per life (as well as mitochondrial "replications"), on average, of course , therefore hummingbird (fast metabolism) lives shorter than a whale or a human. But I am curious if it correlate with the intelligence too and if there is some study.

Could you at least list a couple of "intelligent" (longlived) and "non-intelligent" (short-lived) examples that you have as a starting point? Then others can contribute counterexamples or examples that support your claim. You cannot build an argument on anecdotal evidence based on a handful of species. You name fish, birds and insects, but there are quite a few species in these groups that are long lived (and unintelligent?). There could also be an assymetry, so that all "intelligent" species are relatively long lived, while "unintelligent" species can be both short and long-lived.

@Derfder: let me put this argument in this way.. it is wasteful for a shortlived organism to invest in a complex machinery like intelligence or cognitive ability.. it rather aims to fulfill the primary motive of reproduction

whales and elephants are more intelligent than we are?  not sure, but its hard to be smart when you live only a few days on the other hand.

not too big not too small ;)

Limiting the conversation to mammals, and taking relative brain size as a proxy for intelligence (which, of course is not necessarily "true", but at least is quantifiable), the answer is yes: body-size relative  brain size correlates with   body-size relative longevity in mammals.

using a global database of 493 species, we provide evidence showing that mammals with enlarged brains (relative to their body size) live longer and have a longer reproductive lifespan (González-Lagos et al.).

They present data by species in the paper, which is available free online, but so as to have something on SE, I've mocked up a chart based on the averages they give for each mammal order:

 González-Lagos C, Sol D, Reader SM. 2010. Large-brained mammals live longer. Journal of Evolutionary Biology 23: 1064–1074.

Nice graph. Did you make it (smells like ggplot2)? I cannot find it in the paper.

Thanks and yes! I used GraphClick to estimate the data, then made the graph in ggplot2 and added the custom symbols in Illustrator. This version is based on figure 1 in the paper. In fig 2 they display the variation within orders, but it's pretty crowded (there's a point for each of the 493 spp, and they use 18 different symbol/color combinations for the different families) so I thought I'd simplify it a bit (mostly because I didn't feel like GraphClicking 493 points!).

@Oreotrephes Absolutely gorgeous, and definitely above and beyond.  I'm an R n00b but am setting some time next week to try to pick it up; replicating this is my new target.

This is too long to be a comment. Life expectancy is apparently affected the size of an animal, and this is especially evident in mammals and supported by the heartbeat hypothesis. This hypothesis says that all mammals have a similar number of heartbeats, and that the larger an animal is, the less heart beats it has per minute. Therefore, the larger an animal, the longer it lives. A larger size is also associated with a larger brain (which is associated with higher intelligence, although this is not true in all cases since for example some dinosaurs were very large but had very tiny brains). All I'm saying is that any correlation between intelligence and life expectancy may not necessarily be brought about directly by intelligence, but by the size of the animal. Hope this helps.

I'd imagine it's more correlation than causation , just like you suggest, and can find no evidence of a causal relationship

Are you referring to a relatively larger brain with larger body size, or just a larger brain in absolute terms? To me, the first case should be most interesting for intelligence (see brain to body ratio), since, everything else equal, a bigger brain is required to control a larger body.

[cnd]: ... Therefore, the 'residual' brain size should be most interesting for higher cognitive functions. However, this seems to be an area of discussion (see e.g. Marino, 2006. Absolute brain size: Did we throw the baby out with the bathwater? PNAS 103(37).

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How do pet gecko lizards pose a health risk?
Does having gecko lizards living in your house pose any health risk?

If you're referring to keeping geckos as pets, like all reptiles, amphibians and birds, they come with a small but finite risk of contracting salmonellosis. Having said this, the infection is easy to avoid if you maintain basic hygiene.
On a personal note, I know dozens (perhaps hundreds) of people who keep or have kept reptiles as pets and have yet to meet anyone who contracted salmonellosis. Basically, if you wash your hands after touching the gecko, keep it away from food preparation areas and don't put the lizard in your mouth, you should be fine.
If you're talking about geckos living free in your home, as is common in many tropical places, I have never heard of any health risks associated with them. If anything, I would think that the geckos would reduce health risks by eating insects such as cockroaches and mosquitoes that are prominent disease carriers.

I have geckos in my home too! They get rid of cockroaches, mosquitoes and flies. Plus, I love watching them, they have great personalities!

I especially love watching young geckos try to use stealth.


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Where do butterflies sleep?
Do butterflies (insects) sleep, and if so, where??
I have googled for information but didn't get an exact answer.

It would be better to say that they go into an inactive, low metabolic state. This low metabolic state is often driven by the temperature in the air itself; ectothermic butterflies require outside heat-energy to become active. Basically they use this time to digest their food and produce sperm/eggs. (reference). At night, or during inclement weather, most butterflies perch on the underside of a leaf (this provides them with a bit of shelter from the rain and makes them less noticeable to prey), crawl deep between blades of grass or into a crevice in rocks, or find some other shelter to rest (reference).  In short, I would not call it sleeping but just a state of rest. Butterflies cant even close their eyes from the lack of eyelids (reference).


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Do chickens always lay eggs?
http://de.wikipedia.org/wiki/Hühnerei says it takes up to 24 h for a chicken to produce an egg.
Is that dependent on the chickens nutrition, i.e., if it does not get enough food or the wrong kind, meaning it can survive on the food but it does not have everything to produce an egg?
Do we have data on this?

In short; yes. It depends on the breed (not all lay up to 1 egg/day), the age of the bird and on nutrition. High yielding breeds of chicken are e.g. dependent on supplements of calcium to be able to produce new shells rapidly (e.g. in the form of ground-up shells). Some information on the nutrient requirements of chicken can be found at Feeding the Laying Hen. Egg production will also fluctuate over the year, and will generally decrease e.g. during molting, since energy and nutrients are then diverted to the production of feathers (see info at e.g. The Poultry site).

Ok. That means they always lay eggs, it can take just a little longer sometimes depending on resources available to the chicken. I guess it might stop at some point, when they are really starved.

They will stop laying entirely if severely malnourished, but may also stop completely during molting.

every 24 hours they can lay an egg new young chickens that are for the first time laying eggs could possibly  but there is no breed that lays two eggs a day. and note it might be about a year for some to start so don't think if there not producing eggs there is something wrong, my chickens didn't lay eggs (note i have Plymouth Rock chickens) and they didn't lay until they were about a year. they may stop for molting or stop every here and there randomly and this is important to them laying eggs they need lots of calcium.

rockinboy3303 please use standard grammar while writing As and Qs. In Eng language sentences start with capital letters.


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Measuring body size in flies/insects

"Mesothorax length (the distance from the tip of the scutellum to the
  most anterior part of the mesothorax)"

From Bergland et al 2008.
Would that be this distance (green line)?

If not, how would you describe that distance?

I think you are correct, but I'm not an expert in Diptera/Drosophila morphology. Since the prothorax (pronotum) and metathorax are greatly reduced in flies, you mostly see the mesonotum in dorsal view, and this includes the scutellum. Personally, I think it would have been more accurate of them to label this structure mesonotum, or at least dorsal mesothorax length, since mesothorax could just as well imply a ventral view (mesosternum).
More information can be found at this webpage: Flies - Morphology and anatomy: Thorax, which state that:

The mesonotum occupies most of dorsal view of the thorax. In order anteroposterior we can identify four parts, called as follow (McAlpine, 1981): prescutum, scutum, scutellum, and postnotum. The scutum is the most large, condition considered apomorphic for the entire order of Diptera.

Also see this picture of the mesonotum from diptera.net


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Difference between Medical and Airport scanner radiation
What is the difference between radiation doses of a medical scanner and airport security scanner (X-Ray full body scan)? Is it the same kind of radiation? Does it pose any danger for people who fly often?

What medical scanner are you talking about? An X-Ray machine? Ultrasound? MRI? Immunoscintigraphy? Optical tomography?

I think this question should rather be asked on physics.SE.

@Terdon: Ultrasound and MRI don't use X-rays.

@RamManoharM neither do any of the others. The OP just mentioned "medical scanners" not X-rays, which is one of the reasons why this is a very hard question to answer. As you point out, diffent scanners use different methods.

The type of radiation is quite different in a medical X-ray vs. an airport scanner.
Medical X-rays are high frequency (beyond ultraviolet) radiation, typically on a wavelength of a few angstroms.  While I would emphasize that @Ram is right to point out that there is not very much radiation in a medical X-ray since electronic detectors have been in place over film, the radiation itself is capable of penetrating the entire body and causes ionization.  The body can tolerate a certain amount of this, but that's why we use X-rays - they go through just about anything but bone/minerals and metals.
Airport security scanners emit terahertz radiation, which has a wavelength between microwave and infrared.  This is a very low level of energy per photon.  Terahertz radiation will not penetrate more than a centimeter of light material, which is more suitable to find hidden metal objects (which reflect terawaves).  Relative to X-rays it causes practically no radiation damage.  The intensity of the radiation is also pretty low since these scans are also detected by digital cameras, which are quite sensitive.
Compare the machinery.  X-ray technicians, who might have to take dozens of X-ray exposures a day, usually go behind a protective screen to take a medical x-ray.  The airport body scanners are open to the air and the terahertz radiation spills out into the crowd and the workers stand by it every day.  It has practically no expectation of being hazardous.  This device is pretty good as frequent fliers can have as many scans per year as are needed and health concerns are not significant.
Its always possible we might find some issues with Terahertz radiation in the future, but its hard to imagine it - its safer than standing 2 feet away from a working, closed oven.

As per the American Association of Physicists in Medicine the radiation exposure from full body airport scanners is equivalent to what an individual receives every 1.8 minutes on the ground from natural background radiation or equivalent to every 12 seconds during an airplane flight.
http://www.aapm.org/pubs/reports/RPT_217.pdf
The Back scatter full body scanners at airports use X-rays.


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Why do chickens not try to get up if laid on their backs?
I've seen a few videos about chickens being laid on their backs for a few seconds after which the chickens stay in that position until they are turned over. Comments around the video suggested that lying on their backs is a very unnatural position for most birds and so they don't have any reflexes or instincts that would help them get back up. But this is only speculation. Why is that really happening?
Here's one video demonstrating the effect:
https://youtu.be/R9mzz9jxNsM
I've been told Chicken hypnotism is related to this.

This phenomenon is called tonic immobility. And those speculations you've mentioned are wrong: they do get back on their feet, only remain in that state for a prolonged time, which depends on the distance and eye contact with whoever laid the chicken on its back, as stated here.
From this experiment, it can be concluded, that this behavior in which the animal is immobile is a defense against predation, because most attackers sense motion primary.

+1 would you have a reference for the primary motion-detection of predators?

Sharks do the same thing! I'd link to the Wikipedia article on tonic immobility (https://en.wikipedia.org/wiki/Tonic_immobility).


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Did Darwin ever reach the conclusion that selection will remove variation?
According to simple models of selection the genetic variance in a population should be reduced by selection. (Fisher's fundamental theorem states that the rate at which a population can evolve is limited by its variance). If we select the next generation from one population we will only ever capture as much, and probably only a subset of, the variation that exists in a the first generation.
Did Darwin ever discuss this loss of variation? What did he conclude?
(For now lets ignore the potential roles of sexual antagonism, pleiotropy and such)

A little clarification on my question:
Darwin saw variation in phenotypes, and variation in fitness dependent on phenotype - an effect he called selection. He also saw that this variation was heritable (but did not know how). This is the basic concept of evolution, and is mathematically speaking, the breeders equation:
$r = h^2 s$
He also would have realized that life must therefore have started out as a simple unit, and new variance in traits (and whole new traits) must have arisen over time, i.e. that some kind of changes (mutations) were going on in the heritable information (genes). However, what I'm asking is, did he realize that selection would act to reduce the variation in a population? This would reduce the rate at which evolution can occur over time (Fisher's fundamental theorem - assuming no influx of variance or potential for pleiotropy to maintain variation). Or was it Fisher that first formally discussed the concept of lost phenotypic/genetic variance?

I don't think you can simply ignore mutation like that. Each generation may have its variation reduced by selection but novel variants will also pop up through mutation and copy errors. We'd have to take both rates (that of loss and that of gain of variation) into account to answer this.

Do you mean genetic variance specifically? Since Darwin didn't really know about "genetics" in the same sense as Fisher, I doubt Darwin could have come to this conclusion. Phenotypic variation is another question, though.

@terdon I mean I'm not worried if he considered mutation and other effects which may maintain variation. I mean he realized there is selection, and some kind of heritable information, and therefore did he realize and discuss that selection would take away from the pool of information over time

@kmm yes loss of variation in the information/trait from one generation to the next is what I'm thinking of - mentioning genetic variation was not so deliberate.

This might help

@terdon is right - in practice over time the rate of variation will reach a steady state if there are no environmental changes

After reading your question, I had a vague memory that this subject was indirectly touched upon in "On the Origin of Species", so I did some text searches (in this pdf version I found online). From what I can see, Darwin never used the technical term 'variance' (I don't know how old this use of the word is), but 'variability' is often used, both with regard to accumulated variation but also meaning variation between individuals within a population.
All-in-all, I could not find clear support for the idea that selection will decrease the amount of variation. However, there are number of passages where the subject of variation vs selection comes up (often indirectly), but, to me, these just as often (most often?) indicate that Darwin saw no risk that selection would reduce variation as the opposite. Here are the most interesting passages I could find (searching for combinations of 'variab*', 'selection', 'decrease' etc), with page references referring to the pdf version and a short comment below each quote:

A large number of individuals,
  by giving a better chance for the appearance within
  any given period of profitable variations, will compensate
  for a lesser amount of variability in each individual,
  and is, I believe, an extremely important
  element of success.
  (p. 44)

This is clearly discussing amounts of variation within species, where large numbers can compensate for a smaller amounts of standing variability, by increasing the chance of advantageous mutations.

Nothing can be effected, unless favourable variations
  occur, and variation itself is apparently always a very
  slow process. The process will often be greatly retarded
  by free intercrossing. Many will exclaim that
  these several causes are amply sufficient wholly to
  stop the action of natural selection. I do not believe
  so. On the other hand, I do believe that natural selection
  will always act very slowly, often only at long
  intervals of time, and generally on only a very few
  of the inhabitants of the same region at the same time.
  (p. 103)

Not directly related to selection vs variation, but deals with the rate of evolution vs amount of variation.

But what here more
  especially concerns us is, that in our domestic animals
  those points, which at the present time are undergoing
  rapid change by continued selection, are
  also eminently liable to variation. Look at the breeds
  of the pigeon; see what a prodigious amount of difference
  there is in the beak of the different tumblers,
  in the beak and wattle of the different carriers, in the
  carriage and tail of our fantails, &c., these being the
  points now mainly attended to by English fanciers.
  Even in the sub-breeds, as in the short-faced tumbler,
  it is notoriously difficult to breed them nearly
  to perfection, and frequently individuals are born
  which depart widely from the standard. There may
  be truly said to be a constant struggle going on between,
  on the one hand, the tendency to reversion to
  a less modified state, as well as an innate tendency
  to further variability of all kinds, and, on the other
  hand, the power of steady selection to keep the breed
  true. In the long run selection gains the day, and we
  do not expect to fail so far as to breed a bird as coarse
  as a common tumbler from a good short-faced strain.
  But as long as selection is rapidly going on, there
  may always be expected to be much variability in
  the structure undergoing modification.
  (p. 141)

This is maybe the most interesting passage, which to me indicates that he saw little risk that selection could/would limit variability (see especially beginning and end).

For forms existing in larger
  numbers will always have a better chance, within
  any given period, of presenting further favourable
  variations for natural selection to seize on, than will
  the rarer forms which exist in lesser numbers. Hence,
  the more common forms, in the race for life, will tend
  to beat and supplant the less common forms, for
  these will be more slowly modified and improved.
  (P. 162)

Also on limitations for variation that selection can act on, and the value of large populations.

... firstly, because new varieties are
  very slowly formed, for variation is a very slow process,
  and natural selection can do nothing until
  favourable variations chance to occur, and until a
  place in the natural polity of the country can be better
  filled by some modification of some one or more
  of its inhabitants. And such new places will depend
  on slow changes of climate, or on the occasional immigration
  of new inhabitants, and, probably, in a still
  more important degree, on some of the old inhabitants
  becoming slowly modified, with the new forms
  thus produced and the old ones acting and reacting
  on each other.
  (p. 163)

On the limiting nature of variation, but does not connect selection to decreased variation.

It cannot be asserted that organic beings
  in a state of nature are subject to no variation; it cannot
  be proved that the amount of variation in the
  course of long ages is a limited quantity; no clear
  distinction has been, or can be, drawn between spe-
  cies and well-marked varieties.
  (p. 425)

On variation over the long run.
These are the most interesting sections I found on the subject from my (quick and limited) searches. I hope you find them useful. However, this is only based on the first edition of "On the Origin of Species", and it is possible that it is is modified in later editions or that he touches upon this in his other writings. However, when looking at these particular passages in the sixth edition, I cannot see a major change in his thinking.

I now see that the pdf version I used is unavaliable at the moment. At the Project gutenberg page for On the Origin you can find the first edition as html and the sixth edition as epub, as a complement.

Fantastic research on your answer, from this I would conclude that Darwin wasn't aware/hadn't considered that selection reduces population variation (and therefore reduces the rate at which evolution occurs) I'd credit that observation/idea to Fisher. Would you agree?

My guess would be that it came from the Modern Synthesis, but I cannot say who should be credited for the idea (could be Fisher, Haldane, Wright, Dobzhansky ++). Even if Fisher developed it theoretically, somebody else might have voiced the concept earlier. I do not know the literature well enought to say.

However, I would tentatively conclude that Darwin did not have any well developed ideas on the relationship between selection and within-population variability.

I think Darwin just stuck to the empirical observation that variation exists.  Without knowing about genetics and mutations, he didn't know the mechanism that generates variation, and he knew that he was lacking that, but he knew variation was being generated.


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Tree census data for Sweden/Scandinavia?
Is anyone aware of any attempts to count or approximate the number of trees there are in Sweden or Scandinavia? I have a small popular science side project for which this would be useful

This site says 51 billion but there is no source http://www.sverigeturism.se/smorgasbord/smorgasbord/natrecspo/nature/forest.html

I would definatley look at data from Swedish National Forest Inventory (Riksskogstaxeringen). They have time series data of multiple variables (DBH, size classes, species, dead wood etc) from plots all over the country. Extrapolations based on these data should produce reasonable estimates of total tree count, and probably the most accurate one that can be obtained at the moment. As an example, this report (in swedish) includes graphs on trees/km$^2$ for different species and areas (page 17 ff), but this is only based on areas that can support productive forestry.


text:
Why estimate linear and full (linear, quadratic, and correlational) selection coefficients separately?

"We then fitted a linear regression including all three life-history
  traits to estimate the vector of linear selection gradients, β, for
  each sex (Lande and Arnold 1983). A quadratic regression model
  incorporating all linear, quadratic, and cross-product terms was then
  used to estimate the matrix of nonlinear selection gradients, γ, for
  each sex. "

This is from the paper Evidence for strong intralocus sexual conflict in the Indian meal moth, Ploida interpunctella. I am not sure why they estimate these gradients separetly rather than taking them just from the one full model - any suggestions? Is this normal or have they done it for a reason?
For some similar work see these two papers:

Gosden et al which seems to use only the linear gradients from one model with sex as an effect.
Stearns et al which uses linear, quadratic and correlational estimated from one multiple regressions model per sex (similar to the main paper I cite first but not using a linear terms only model for the linear coefficient).

I have mailed the corresponding author on the quoted paper to ask why, I will let you know what he says if he replies

This is directly following the advice of Lande & Arnold (1983), saying:

Linear multiple
  regression can be used first to estimate the forces of directional selection, $\beta$, and their standard errors. Then a quadratic multiple regression (16) or (Al), can be used to estimate the forces of stabilizing selection, $\gamma$, with their standard errors. The regression (16) provides the best quadratic approximation to the selective surface (although valid estimates of $\beta$ can be obtained
  only from a purely linear regression, or by using the orthogonal regression (Al)).

The reason is that the estimates of direction selection is influenced by the higher order terms in the full model that includes quadratic and correlational selection, and the linear model therefore has the best estimates of the change in mean value over a generation of selection ($s = \bar{z}_{after} - \bar{z}_{before}$). However, the full model is the better representation of the fitness surface. There are also other methods to approximate the fitness surface.
For the record, I used the same approach in my master's thesis many years ago.

Thanks - what did you do your masters thesis on and who with? (I did mine on multivariate nonlinear selection in a secondary sexual trait hence I should have known the answer to the above, it's just been too long!) Talk in chat?

Actually, after rereading the Lande Arnold paper, this will be problematic only "If the character distribution before selection displays multivariate skewness (non- zero third moments), the linear and quadratic terms are correlated and estimates of β, depend on whether or not the quadratic terms are included in the regression." Thus, if I understand correctly, you can use orthogonal polynomials using poly(x,2) in R or run a model with only the linear and a second model with both the linear and the quadratic term. Is that correct?

The third moment in the sentence means the skewness. Does that mean the same thing as covariance = 0?

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Need for proper air filter for bioreactor?
I am going to build a simple bioreactor for microalgae growth.
I already have fluid filters pore size: 0.2um, diameter: 25mm
https://nl.vwr.com/app/catalog/Product?article_number=514-4039
I wonder if I can use them for air filtration to avoid the bacteria when pumping in the air.
Or do I necessarily need air filters?

What are your end goals?  These determine your sterility requirements.  Generally if you are aiming for mass protein production you want to filter air both in and out of the reactor.  Normal hippa filters should be sufficient.  I've not known of any liquid filters that could do double duty as air filters, but that doesn't mean it won't work.

The goal is to maintain and growth the microalgae without getting infected with the bacteria (They would stop the culture from growing) and I will get some samples from bioreactor, occasionally, for imaging. I also think there should be filters both for air in and out. But don't know what would be a sufficient filter (lower price is better of course) for this purpose. It seems that pore size and filtration area are important parameters.

Well then you need to get a filter specific for air filtering.  I recommend Polytetrafluorethylene PTFE membrane filter.  Now the only issues are size and "how sterile."
There are a lot of vendors out there that supply these.  If your institution has an agreement with VWR, they certainly have them.  If not, I have used Sartorius in the past, but I don't have any particular brand loyalty to them.
Let me know if you need any more help.


text:
What's the name of this flower?
I photographed this flower in Central Europe. I looked in online databases but can't really identify the actual flower, since there are so many that look quite similar. Can you help me? What's the name of this flower?

It looks like the common Geranium sylvaticum (also called wood cranesbill or Mayflower), and it is at least a close relative (member of the Geranium genus). This plant is commonly found across Europe and in parts of Asia (see map below), and it is sometimes planted in gardens. It is a perennial herb that grows in many types of habitats (woods, meadows, road sides, mountain areas), and the flowers are most commonly violet to blue, but can also be white. Geranium pratense is very similar, but usually has more narrow leaf lobes and bent flower stalks. However, it might not be possible to separate these two species based on your picture.
There are also similar relatives found in North America (e.g. Geranium maculatum) and Asia (e.g. Geranium himalayense) and many hybrids of plants from within this genus are cultivated.

(picture from Swedish Wikipedia)

(distribution map from the Swedish Museum of Natural History: Den virtuella floran)

Superb example of a good answer to an ID question!

@Oreotrephes Thanks. The same species is just about to start flowering in my garden.

My guess would be the meadow cranesbill (Geranium pratense), see this image (from here, more images are available there):

The flower is quite common on meadows in europe, see here.

This is certainly a possibility, and I have updated my answer to explain why I feel that G. sylvaticum is a better fit.

@fileunderwater I think we can be pretty sure that it is from the genus Geranium :-)


text:
How to best conserve a beetle inside a jar?
Few days ago a giant beetle appeared on my house. Well, it's dead now. Since it attracted some attention from my little girl, I'd like to preserve it inside some jar. What's the best way to do it? What products should I use?
I've researched a bit in the internet, and it's said not to use formaldehyde because the specimen would become too hard (that's not a problem to me, but I don't like using such strong products considering that a child will probably handle the jar).

The answer to this question depends on how you want to preserve it - as a pinned specimen (also dry preservation, most common) or in a liquid. If you want to pin it, placing it in a jar with a cottonball soaked with ethyl acetate (also used in killing jars) is good because it softens the muscles and makes the insect easier to pin and mount. Beetles are then usually pinned with a needle through the right elytra (wing cover), but there are also other ways to pin them. You can also glue the beetle to a piece of cardboard, which is then pinned. Gluing insects generally helps to protect them (so that legs and antennas dont fall of when handling them), but makes it more difficult to see the ventral side and it can also be cumbersome to have large glued beetles in a collection.
If you want to keep it in a liquid, 70-80% alcohol (ethanol) is a good choice, but not stronger (95% alcohol makes the insect stiff and brittle and might distort smaller insects). As you say, formaldehyde is generally not used since it's very toxic and it can also make the insect stiff.
Here are some more good tips on collecting and conserving insects from the University of Minnesota.


text:
What is the minimum population size that Hardy-Weinberg calculations can be applied to?
I'm trying to find out if a particular allele is in Hardy-Weinberg disequilibrium, but the data is poor. What's the minimum population number that you can use to get any sort of respectable conclusion?
I've heard it's 5 individuals minimum for each genotype but can't find a source on that.

You can use power analysis to work out answers depending on the specifics of your data. The things you need to consider are:

The power of the test. This is the probability that the test will
fail to reject the null hypothesis even if in truth it is false
(Type II error). If the population is not in equilibrium, what is
the probability that the test will fail to detect this? This will largely depend on the costs of a Type II error. If the experiment is expensive in terms of time/money/animals used etc. you would want to make sure it will give a sold answer at the end.
The significance level. 0.05 is commonly used. The probability that
the null hypothesis is rejected even though it is true (Type I
error). If the population is in equilibrium, what is the probability
that the test will erroneously say it is in disequilibrium.
The degrees of freedom. The number of alleles.
The effect size. This is how far away from equilibrium you expect
your samples to be. The largest effect size would be extinction of
one allele. However, if two alleles are in a ratio of 100:101 across
the full population, this is a small effect size.

For the Pearson's Chi-squared test we can use (in R)
library(pwr)
pwr.chisq.test(w = 0.3, N = 40, df = 4, sig.level = 0.05 )

A rough guide for effect size (w) is 0.1, 0.3, and 0.5 for small, medium, and large effect sizes. There is more detail here. N is the total number of data points, df is the number of alleles. This function will give us a value for 1 minus the power of our test. A value of 0.9 means there is a 10% chance of failing to detect an effect that truly exists.
If we want to work out a suitable number of data points to collect we must decide what power we want. Say we decide that a 0.01 chance of doing the test, but failing to detect disequilibrium if it exists is acceptable.
pwr.chisq.test(w = 0.3, df = 4, sig.level = 0.05, power=0.99 )

tells us that 280 data points are needed.
Without estimates of effect size or a number of genotypes it is hard to give a straight answer to your question, but 5 per genotype seems very small.
If you have only two genotypes, you might choose to use the Fisher Exact Test in which case you can use power.fisher.test() in the statmod package. The definitions of effect size and degrees of freedom are slightly different but the idea is the same.

+1: nice to see power analysis mentioned every once in a while... too often biologists tend to skip on these things.

Thanks, whilst I asked this a long time ago and it's not very relevant to me now I'm sure this will help people in the future!

Yes I was aware it was old. But as you say hopefully useful for others. Having got information from stackexchange a million times but never asked a question, I know that it's potentially true.


text:
How can homosexuality evolve despite natural selection?
I would imagine that the answer to this question would be population control, especially since even if one sibling is homosexual this does not necessarily mean that the other siblings will be too.

I suggest you change the question to "How can homosexuality evolve?"

I suggest a title change too. Evolution does not assume a purpose. I suggest "How can homosexuality be maintained genetically in a population?"

Why does it need an evolutionary explication? Not everything needs to be selected for. This is like asking why myopia (which in certain parts of the world can have a prevalence of >70%) evolved despite natural selection...

@nico because it seems like homosexuality would be heavily selected against but it appears to be highly prevalent anyway, seems to me the OP is interested in possible explanations as to why it seems natural selection has failed to get rid of it - i.e. how can a seemingly negative trait persist? does it have some kind of benefit which may slow/reverse the effects of selection?

@rg255 you're right.

@rg255: I reapeat my point on myopia. Furthermore you should consider that homosexuality does not in any way imply sterility.

@nico Correct, it does not imply sterility but, reproductive success does require the combination of both male and female gametes. If someone is homosexual that is far less likely to occur. The evolution of homosexuality, and the subject of myopia, is not a question of "why does X, a seemingly pointless trait, evolve?" but instead is more "why does X, a seemingly detrimental trait, evolve?" - I think it is a valid question because when we consider the effects of selection then homosexuality is paradoxical, hence several theories have been developed to try and explain it.

@rg255: I think the main problem is that whe should not ask "why X evolved", but rather "why X was not selected against" which is a very different thing.

@nico I think that is what this is- by asking why it hasn't been eradicated? They are effectively asking what possible benefits could save the trait

nothing evolves despite natural selection - its a contradiction to the definition and forces behind evolution.  Any trait that shows up which is not selected for does not last long.

@nico Ah, but it is extremely useful to seek an evolutionary explanation of myopia. The key is not to ask why it evolved, but instead to ask, as shigeta points out, why it has not been eradicated by natural selection despite being highly heritable. Searching for the answer leads one to the role of early environment (interacting with genetics), suggests possible interventions, and provides one of the classic examples of disease caused by mismatch between modern and evolutionary environments. One example

@corvus point is asking "why x evolved" implies the fact that evolution is somehow finalistic, which it is not.

@nico Huh? Asking why something evolved is not finalistic at all. E.g. "Why did penicillin resistance evolve in E. coli around 1945?" "Because people started using penicillin as an antibiotic in 1943, thereby selecting for penicillin resistance in human commensals."

@Corvus OK, my previous comment didn't come out quite all right. What I mean is that thinking that every single thing in existence evolved for a reason implies evolution is finalistic. Certain things are just not selected against, despite not giving a clear evolutionary advantage. Penicillin resistance is a good example of a trait that was positively selected, but that does not mean (as many put it) that "the bacteria evolved the resistance because there were antibiotics around" (finalistic view), but rather that "some bacteria which happened to have the AmpR gene were more fit and expanded"

@nico I totally agree that many traits are not adaptations. And I agree that final cause explanations are generally inappropriate forms of evolutionary explanation (though teleological language be an acceptable shorthand among researchers who are all clear on the subtleties). I think we're pretty much on the same page here.

@Corvus BTW: Your assumption about antibiotic resistance is wrong. It didn't evolve in 1945, it is a quite old mechanism. Almost as old as the "development" of antibiotics in funghi is.

@Chris I specified "in E. coli". Of course a wide range of resistance alleles have circulated in bacterial populations for tens of millions of years. But penicillin resistance was rare or nonexistent in E. coli when penicillin was introduced in the early 40s and became common within a few years. This change in allele frequencies in a specified population is the very definition of evolution.

@Corvus I wouldn't exclude that there are some E.coli in the wild which where resistant. It is a new phenomenon to a human environment, but the mechanisms are old. They simply acquired it from the environment.

@Chris of course. The resistance alleles were doubtless acquired by horizontal gene transfer, probably from soil microbes.

Several years back, results of a twin study (Zietsch, et al., 2008; popular press in The Economist) suggested that genes associated with homosexuality make heterosexuals who carry the same genes more reproductively successful. This would explain the observation that, for example, sisters of homosexual males have more offspring.

We show that psychologically masculine females and feminine men are
  (a) more likely to be nonheterosexual but (b), when heterosexual, have
  more opposite-sex sexual partners.

So if more sexual partners in heterosexuals is correlated with more offspring, then the genes associated with homosexuality may lead to more offspring in heterosexuals that carry them. So these "homosexuality" genes could easily be maintained in the population by conferring a reproductive advantage to siblings.
The authors conclude:

Taken together, these results suggest that genes predisposing to
  homosexuality may confer a mating advantage in heterosexuals, which
  could help explain the evolution and maintenance of homosexuality in
  the population.

do the authors discuss the possible effects of having a homosexual twin sibling? being raised with a homosexual twin might influence their sexual behaviours in a social and psychological context (i.e. the number of partners, rates of courtship, courtship style...). & how to separate these effects of nature vs nurture? I guess one could compare identical twins separated at birth but this is not perfect and would be highly limiting on sample size. Also non-related adopted siblings in which one is homosexual could test the nurture effect.

This study only suggests that genes effect promiscuity. That would explain the observation that sisters of homosexual males have more offspring, as well as why, when heterosexual, they have more sexual partners. Gay men are also known to be statistically more promiscuous. The study suggests that the tendency is genetic, but that the tendency is promiscuity, not homosexuality.

Obviously selection would appear to not favour being homosexual, in an evolutionary sense it represents somewhat of a decrease in fitness: Homosexuals fail to reproduce successfully due to the requirement of both male and female gametes and reproductive organs, therefore significantly fewer than the average heterosexual couple. Certainly I don't think it would have evolved as some kind of population control method - group selection theory is generally discarded in favour of a gene-centred theory (see Dawkins for popular science literature)
There is debate about whether someone can be biologically "preprogrammed" to be homosexual, this can occur genetically or epigenetically. Genetic models have used kin selection, overdominance, sexual antagonism in the past and are briefly discussed in the following article on epigenetics. Recent work has looked at possible models by which heritable homosexuality could arise by epigenetic markers and this was covered in a lot of mainstream media (1,2.. just google epigenetics homosexuality). This quote is from their abstract and explains one reason it is difficult to pin down heritable causes of homosexuality:

Pedigree and twin studies indicate that homosexuality has substantial
  heritability in both sexes, yet concordance between identical twins is
  low and molecular studies have failed to find associated DNA makers.
  This paradoxical pattern calls for an explanation.

By their readily testable model they have shown possible (& plausible) conditions under which the "epi-marks" which cause homosexuality could spread through populations.
Genetic studies of twins where one is homosexual have also revealed links between genes and a mating advantage. For example if in a pair of male identical twins one is homosexual, the other has a mating success greater than that of the average male. However, it could be that this link is found because of social reasons (perhaps someone who has grown up with a homosexual sibling may have a different mentality or lifestyle socially which could help them increase reproductive success).

Note: I have no problem with a person's sexual orientation & the rights/ethics of homosexuality is not the topic of this question & answer. This is purely an answer to the obvious evolutionary conundrum.

Comments are not for extended discussion; this conversation has been moved to chat.

This is not a subject I know well, but I can point to several recent textbooks on homosexuality in animals, all with an evolutionary perspective. I remember that Bagemihl's book got good reviews when it was published. In general, I think it is important to acknowledge that homosexuality is common in many animal species and not just humans:

Bagemihl. 2000. Biological Exuberance: Animal Homosexuality and Natural Diversity
Sommer & Vasey (eds). 2006. Homosexual Behaviour in Animals: An Evolutionary Perspective
Roughgarden. 2009. Evolution's Rainbow: Diversity, Gender, and Sexuality in Nature and People
Poiani. 2010. Animal Homosexuality: A Biosocial Perspective

For a good review, see Bailey & Zuk (2009) Same-sex sexual behavior and evolution. Trends in Ecology & Evolution, 24(8):439-446. (link to a pdf: http://www.thestranger.com/images/blogimages/2009/09/14/1252958575-evolution_of_homosexuality.pdf)

Do any of these books demonstrate that animals are born gay? Animals do all sorts of things sexually, but what evidence does anyone have that animals are born to behave that way (that they are not simply more promiscuous)?

@CarlSmith I don't know exactly what you mean with born gay, especially in relation to non-human animals. What we can observe is behaviour, and homosexual behaviour (which might be roughtly translated to sexual preference), not thoughts and intent. I don't know this literature well, but there might be studies of sexual preference across time for individuals of certain species, which might get closer to the issue of being born gay. Individuals that only engage in homosexual behavior would (sort of) imply that. However, in some species, sexual behavior varies a lot within the same individual

Thanks for the clarification. I don't understand how anyone could possibly determine which animals were born gay. Still, I'm a computer programmer that never studied biology, so it's probably just total ignorance on my part.

There is an interesting theory coming from a slightly different, yet related, field. It was developed by Paul Vasey and Doug VanderLaan of the University of Lethbridge, they are both evolutionary psychologists:

An Adaptive Cognitive Dissociation Between Willingness to Help Kin and Nonkin in Samoan Fa’afafine (or direct link)

They called their theory the "helper in the nest" hypothesis. It basically states that gay people compensate for their lack of children (this has been been covered thoroughly in the other answers) by offering an indirect benefit through enhancing the survival prospects of close relatives. And they do so by being “helpers in the nest”, by acting altruistically toward nieces and nephews.
Their study was conducted in Samoa, and they chose the country because males who prefer men as sexual partners are widely recognized and accepted there as a distinct gender category (called fa’afafine - neither man nor woman), which makes for a clearly defined sample for study. It's worth mentioning though that the authors see Samoan culture as very different from most Western cultures. Yet, they affirm Samoa’s communitarian culture may be more—not less—representative of the environment in which male same-sex sexuality evolved eons ago.

Looks like only the Abrahamic religions are against homosexuality. In no other mythology I've found anything against homosexuals.

Apparently, Buddhism is homophobic and transphobic (and discriminates against people with disabilities too): https://en.wikipedia.org/wiki/Buddhism_and_sexual_orientation

There are a lot of theories about how homosexual behavior might be maintained in a population or provide some evolutionary advantage. One thing to remember though is that there is a big difference between homosexual behavior and obligate homosexuality. One could quite easily confer benefits, like any other intra-sex social interaction. The other carries a huge fitness cost. However it's not clear that obligate homosexuality has been common in humans. It is in our current culture, but historically, it's possible that most people (particularly women) would have had children because of cultural pressure to do so, regardless of sexual orientation. Without knowing more about cultural influences on reproductive rates, we can't say if there even is a mystery to be solved here.

Humans have a wide variety of triggers for sexual arousal. I think that having a variety of triggers can beat having too few - ie it can result in more consistent reproductive success, especially within humans who do not have strong and obvious fertile periods and will have relatively few offspring. Where a strong sex urge exists and fertile mates are not available having other outlets - masturbation and homosexuality - may reduce the occurrences of harassment and rape and prevent strong sex drives being injurious or socially destructive.
Being homosexual does not prevent the ability to have hetero sex and many people who are homosexual by preference still persist in hetero relationships and have children. It isn't the preference but the inability to have hetero sex with fertile partners that would select against homosexual behaviours.

Are you saying that gay people have as many children as normal people, on average? If you're correct, then there is no evolutionary disadvantage to being gay.

I don't know how much so, but would expect less offspring, but my point is being "gay" does not, by itself, prevent most gay people having children, or even the desire to have them. I don't see any evolutionary advantage/disadvantage as independent of the social group and it's cultural imperatives. If it results in reduced conflicts over mates and supports positive contributions by those who don't have children then it raises the group's reproductive success. Any such individuals will share most of their DNA with the offspring of others - to no overall evolutionary disadvantage.

I think I understand your argument. You're saying that having some people adopt gay and lesbian lifestyles (that are often not lifelong), actually causes their tribe to be more successful overall?? So, even though gay people probably have less children themselves, they care so much more for other people's children that it more than makes up for their lower mean fertility (just like Dawkins' selfish gene)??

@CarlSmith - yes that is what I am saying - although I think caring for other's children directly, more than average, isn't necessary; just contributing to the group as normal, with less conflict over mates raises everyone's chances for survival. Yes, like Dawkin's Selfish Gene.

Ah. I see. That makes sense. I was looking for something more specific and tangible that could counter the obvious disadvantage, but reality doesn't owe me that. On reflection, what you're suggesting does seem perfectly plausible. Thanks for taking the time to clarify your argument for me, and also for not judging me for wanting an explanation. I honestly couldn't conceive of homosexuality evolving. I kept an open mind, just because I don't know much about the subject, but it seemed scientifically impossible to me. Thanks for changing my mind, mate.

A recent study using a massive pool of genetic data suggests that indeed genetic factors associated with homosexuality also confer a mating advantage to heterosexual individuals in the sense of being "more attractive".  Some quotes from the article:

According to an abstract the team submitted to the American Society for Human Genetics, whose annual meeting is under way this week in San Diego, the DNA signals linked to gay sexual experiences also appeared more often in straight men who had a larger number of sex partners. The team also notes that straight men with the gay-linked variants were, on average, judged more “physically attractive” than others (the researchers decline to say who did the judging). This, the scientists conclude, could mean that these variants also “confer a mating advantage to heterosexual carriers.”
Such trade-offs are a fact of evolution. For instance, gene variants that can cause sickle-cell anemia also lend protection against malaria. The resulting balance means the sickle-cell gene doesn’t die out. The researchers say their new findings about non-heterosexual behavior, though not conclusive, are consistent with such a Darwinian balancing act.

PS: I know this is in line with the most upvoted answer, but the nature of this study, I think, singles out the need for a new and more recent answer.


text:
Why Can't A Male Mule Have Offspring?
I've read that female mules can sometimes have offspring, but that male mules are incapable of doing so. Why is that the case? Is their sperm not capable of entering the egg or is their a genetic reason?


text:
Are there echolocating insects?
Echolocation is the ability to obtain spatial information of the surroundings from echos generated by the animal. There are bats and other vertebrates that naturally use it.
I was wondering if this is limited to vertebrates, or if there are examples among the invertebrate, especially insects.

Some moth actually do use clicks for their own echolocation: "Noctuid moths (Noctuidae) are the only group of invertebrates for whom echolocation was
demonstrated":

Lapshin & Vorontsov 1998
Lapshin et al 1994.

Cool. Thanks for the references. It's good to know some people believe in it, but those articles have no citation and are published in somewhat minor journals. So I must say I don't fully trust them. Do you know of any other group replicating their results?

Well, I would of course keep some degree of skepsis. And I'm not aware of something published by other research groups: it's true, that they provide principally only self citations. But this, coupled with the fact, that nearly all of the papers of this lab were originally published in Russian, is just another example of the continuation of the Soviet school. I can confirm, that the author still considers his findings valid and has a very elaborated description of the story and his experiments (in Russian): http://www.lapshin.iitp.ru/project1/index.htm

As others have indicated, I also haven't seen direct evidence of echolocation in insects. However, there is much evidence that the auditory system of e.g. moths can hear ultrasound generated by bats (Waters, 2003). According to Waters (2003) moths mainly use this to avoid predation. The review also contain many useful references and examples of moth ultrasound detection, and specifics on the physiological adaptations. Since moths apparantly can detect ultrasounds (and generate them), this also opens the possibility that some species could use it for echolocation. But from what I have seen, no direct evidence.
In general, many insects use high-frequency sounds, but we often do not know exactly for what purpose. If you are interested, this webpage on sounds in butterflies (in Swedish) have a couple of examples that you can listen to (recorded by a professor emeritus as my old department). Look at the subpages for each species for embedded .wav where the ultasounds are played in slowmotion. Again, the exact use of these sounds are mostly unknown, but they are believed to be used to attrach mates or scare predators, but might potentially (if we are speculating) be used for echolocation in some species.

My understanding (as a PhD holder in toothed whale echolocation) is that insects do not use echolocation themselves as a means of hunting or sensing their environment more generally, but some do produce clicks which serve to jam/confuse a bat's echolocation. This is an anti-predation strategy. Their production of clicks being a means of defence is supported by this recent publication (O'Reilly et al., 2019, Scientific Reports), which shows that even deaf moths exhibit this behaviour. Additionally, this recent PhD thesis (T. Hugel, 2020) thoroughly explores this predator-prey interaction between bats and moths.

Welcome to Biology.SE. This looks like the start of good answer. Two suggestions for improvement: 1) Can you add more support for saying that insects don't use echolocation — as written it sounds like some moths are clicking to "jam" bats, but that doesn't seem to disprove echolocation in moths let alone all insects; 2) Please include the complete reference information since links can (and do) break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information.

As far as I can tell, the answer is no.  It's hard to prove a negative so the best I can do is that none of the articles in the literature I've been able to comb through have any mention of invertebrates at all.  What I can give you is that some moths use clicks to jam bat echolocation and some fish are sensitive to echolocation, "raising the possibility that fish may exhibit negative phonotactic behaviour in the way that moths do."


text:
Why do I smell flowers after sneezing?
Often when I sneeze, I smell flowers for a few seconds afterwards.
I've done some searching on the internet, and apparently it's something that is at least not entirely uncommon, although the exact smell description seems to differ. It's sometimes also referred to as a 'honey sneeze'.
Just to be clear, there are no flowers anywhere in sight when I sneeze.
Biology has never been a field of study of mine, but the scientist in me finds it fascinating. I've yet to come across any real explanation for this phenomenon, only guesses.
Does anyone know what causes this, or can you at least give a somewhat likely explanation?
Edit:
When I sneeze through my mouth, I do not get the same smell sensation.

it might just be the sneeze might be pushing air around the nasal cavity, putting the flower pollen and other molecules into contact with more olfactory sensors.

Every time I sneeze really hard, it smells like beeswax rather than flowers.  Not sure what the cause is, either.

I have experienced this weird floral smell too.  I can also confirm that other people generate this smell after sneezing.  Someone sneezed next to me and then I smelled it.  When my husbands allergies kick up and he sneezes all day the whole house smells like that weird floral smell when you walk in the door.

I knew an italian at school who liked to stick straws from grass up his nose to intentionally sneeze. He would say "it's great man, when you sneeze your body releases opiates for a moment so I get high for free"

This will be a hypothetical answer for the moment, so take it with a grain of salt until I can find sources or someone else does:
My best (educated) guess would be that the smell is there all the time, and when you sneeze you reset what's currently being "ignored" (in that you are not aware of it, though it is being sensed) by your brain momentarily. The source of the smell may be up in the air - it could be cologne/perfume, fabric softener residue on your clothes, what you ate for breakfast and are currently digesting, the bar of soap in the kitchen, etc. - but I haven't heard of "scent illusions" before.
One very quirky way of possibly testing that out is to remove yourself from your regular environment, sniff some ground coffee beans for half a minute, and then re-enter your home or smell your clothes to see if any of the scents match up with what you do smell when you sneeze.
My apologies that this isn't a thoroughly-sourced answer, but hopefully it acts as a good starting point.

My observations agree with this. We're unconsciously filtering out a lot of, even olfactory information.

I have my doubts.. the smell is quite pronounced, and always the same. Even when I haven't been near a flower for a week.

It doesn't have to be a flower, it could be anything that has a floral scent. Fabric softener, deodorant, cologne, soap, lotion, hair products (shampoo, conditioner, gel), aftershave... We filter out a lot of scents. If you don't believe it's something you're encountering in your daily life, then it might be a product of your own system - maybe a compound in your nasal mucous that encounters the receptors when you sneeze. Haven't heard of that happening, but it's not my best area.

You may have some liquid in your nose after sneeze. This liquid can contain microbial flora, which can have a smell, which is interpreted by you as of flowers. Check your health with a doctor to be on the safe side.

Another starting point (apologies if this has more considerations than a 'thoroughly-sourced answer') ...
A sneeze is a violent, temporarily mechanically stressful event. See How much force is generated by a sneeze?
(Temporary) mechanical stress on the brain can have many effects.
One point you should consider for your Testing Hypothesis: If you sneeze through your mouth, do you still have this effect?
I would also suggest looking into the interplay of short mechanical stress, serotonin, and the olfactory system...

I rarely sneeze through my mouth, but I'll try to pay attention next time :)

I forgot to update earlier, but when I sneeze through my mouth, I do not seem to get the smell.


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Which poison makes seastars inedible to possible predators?
In the new citizen science project (see: Sea Floor Explorer), numbers of seastars, scallops, crustaceans and other animals are counted. Already one can see a heavy bias in favor of seastars, both the fat and brittle kind.
I would be interested in why this creature is so succesful, especially if it is poisonous to e.g., crustaceans, and what poisons exactly are responsible.

it may not be that they are poisonous. seastars have extraordinary reproductive capabilities

That is the other factor of success. But they are really poisonous, see the answer.

Asterosaponins are the class of compounds - they have a cholesterol like organic core.
Apparently, these saponins make pore-forming complexes with Δ5-sterols of cell membranes, and so are deadly to all usual kind of life, including bacteria and fungi. Quote:

Starfish and sea cucumber cell membranes are resistant to their own
  saponines due to the presence of Δ7- and
  Δ9,11-sterols, sulfated Δ5-sterols, and
  β-xylosides of sterols instead of the free Δ5-sterols.


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3D models of adult male brain in the Blender software? Any open-sourced version for research?
I am trying to find 3D model of brains. I am particularly interested in adult-male -brains in Blender-model. I could find such 3D models of brains for sale here but because I am researching I would like to use some open-sourced candidate so anyone could preview things. So does there exist 3D models of brains in Blender?

I am interested in this as well

...this movie under cc3 and some brain model: http://mango.blender.org/gallery/

A side note, for those interested in mouse brain anatomy: you may want to have a look at the Allen Brain Atlas website, particularly to Brain Explorer

Am I the only one who initially (mis)read "adult male brain in a blender"? :)

There is a model of an adult, male, real human brain here:
http://brainder.org/download/brain-for-blender/
It can be imported into Blender or any other 3D application that can read Wavefront OBJ or Stanford PLY formats.

http://www.turbosquid.com/3d-models/max-human-brain/580672
That one is only 30 which really isn't bad for a model. You will have trouble finding an  anatomically correct model for free.
I am curious, is the male brain that much different from the female brain? And do you want just the brain or a whole head with the skeleton and other anatomical features? And if you would like to elaborate, I am curious about what end product you are looking for.
Side note: Autodesk has 'student' license version of software --in case you want to try learning Maya or 3Ds max, the latter has Retopology tools.
You can download from here:
https://students.autodesk.com/?nd=download_center
ITKsnap is a program you could use to get 3d data from ct or mri scans
http://www.itksnap.org/pmwiki/pmwiki.php?n=Main.Downloads
MRI and CT data can be found here:
http://www.osirix-viewer.com/Downloads.html
I know you just wanted a free model, but the above are the steps to get to one at least.

Academia is mostly against the photo electricity of brains with mammals https://twitter.com/heoalov/status/274090762524848128 -- just curious: placebo or some other effect with led-tosslink-in-ear?

Err photosensitivity -- still requiring placebo test, easy trials: get cheap toslinks and different intensity light. Can you detect it? Does skin-senses become different after some use or just placebo? I cannot understand if not placebo, how does it work? If LEDs were UV, then D vitamin? Otherwise what is the physiological reaction? I do not know but pretty curious so investigating brains and ears etc

I think all models are too generic out there.
Radiological models you can find in imaios.com's e-Anatomy where the Premium access gives you some RTG, CT and MRI videos which you can combine to form some 3D models.
I am working with the visualization of CNS lymphatic vessels here where I would like to create thin membranes to visualize how deep the lymphatic circulation goes.


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Why only able to close one eyelid? Genetic reason?
Eye-dominance is a critical thing with bows: right-eye-dominant is recommended to do the aiming on the right eye here otherwise inaccuracy. This made me think whether all people are even able to do this. I have seen people who can only close one eye or two eyes at the same time but not two eyes separately. What is the factor determining this? Is this determined by genes, learning or by something else? Is it possible that the other side of the eye muscles are missing because they have not been needed for the survival? I discussed missing muscles with my medical friends and they mentioned that there are muscles that some people do miss such as in hands because they are not essential for survival. I don't know whether certain muscles in face could be missing with some people or is this just learning thing?

Without having any scientific knowledge on the matter, I imagine it might simply be a matter of having learned it or not. I remember I had to practice for quite some time as a child before managing to reliably close each eyelid separately.


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Extraretinal photoreception in mammals?
A Finnish firm Valkee sells light-ear-plugs against thing such as jetlag. I asked a researcher in Aalto university how do they really work and he responded "why would evolution have lead to photoreceptive cells in ears?" -No direct answer. I asked a well-respected professor who said she did not know this area well enough. Now Valkee guided me to the publications such as Penetration of light into the brain of mammals (1963) and Spectral characteristics of visible radiation penetrating into the brain and stimulating extraretinal photoreceptors (1979). Related to the first one, I found this (1980) from the references:

"It  is  now  fully  accepted that  the  perception  of  light  by  extraocular  photoreceptors  plays  a  significant  role  in  synchronizing  endogenous  rhythms  with  the  environmental  light-dark cycle  in  non-mammalian  vertebrates"

Things such as certain birds and lizards apparently have extraretinal photoreception aka photosensitive cells not in eyes (this is how I understand it). Now the publication continues

"The  limited  number  of mammalian  species  tested  to
  date  and  the  near  exclusive  reliance  on  nocturnal  animals  leaves  open  the  possibility  of  extraocular  photoreception  in  some  adult  mammals  (Rusak  &  Zucker, 1975;  1979)."

Now according to a skeptical researcher in my university, there is only one paper supporting photosensitivity in mammals' brains: Wade et al (PNAS 85 (1988) 9322-9326 with rats. My professor in system sciences was extremely scornful when I even asked this question on a seminar course about brain -- he did not specify his reasons and pretty much labelled my thinking as inexperience. Now I am not sure whether researchers are even speaking about the same issues: too large disparities between opposing and proposing teams for the assumed effect apparently through the mechanism called "extraretinal photoreception in mammals". I am very curious.
Helper questions

What are the mechanisms by which a led in ear would affect a mammal such as a homo sapiens? You don't get D vitamin because of no UV light. You get very-very light heat because of tosslink connection. So it cannot sense the heat as antidote against things such as SAD and jetlag. Other mechanism?
Is the "extraretinal photoreception in mammals" just placebo or does there exist scientific proofs for it particularly with large mammals about the size of homo sapiens?
Why would evolution have lead to extraretinal photoreception in mammals?
Do the terms "extraretinal photoreception" and "non-eye photosensitive cells" mean the same thing? Other terms for the same thing?
Now eyes are developed very late in cell-division with mammals. Do born-blind mammals and later-blinded mammals experience extraretinal photoreception differently? If led-light (non-UV light) has an effect on large mammals, then I expect this may be possible to see by analyzing results of mammals with different-developed visual-cortexes.
Does this statement "Light penetrates deep brain areas, eye's receptors have developed from receptors of old CNS." by Humancharger justify the extraretinal photorecetpion?

P.s. I presupposed in this question that extraretinal photoreception is the effective mechanism by which light-in-ear would affect a mammal. It is also possible that there are other mechanisms -- I am not an expert with the terminology here, anatomically and physiologically challenging.

Possible duplicate: http://biology.stackexchange.com/q/700/72

Its pretty well established that there are photoreceptors in cells besides the cones and rods in the retina of the eye.  Humans and most animals have four light receptor genes known (so far).  In addition to Rhodopsin - there are the short, med and long wavelength opsin genes.
While they are mostly expressed in the retina of the eye, they can be found in many other tissues as well. The first image from GeneAtlas below shows the relative amount of RNA found for short wavelength opsin in a variety of tissues - its expressed in immune and nerve cells ( cyan and forest green respectively) relatively well too.   This might imply that neurons are light reactive.  Compare that to that of medium wavelength opsin, which is primarily much more common in the retina.

This is not a psychosomatic effect.  Light receptors in the skin are known to help with seasonal affective disorder - shine a bright or blue light behind your knees.  These receptors are not connected to optical nerves, and so you don't get any image from them, but the information can affect your biochemistry anyway.
The idea of unconscious receptor inputs from other parts of the body probably applies to many sorts of receptors.  This last year there has been a great deal of interest in taste receptors which are expressed in the gut.  They can taste sweetness and other flavors a second time and register the gustatory response in the brain.  Its not a conscious input, but it registers in the brain in MRI.
Why would evolution do this?  It seems to me that this is a new way of looking at the individual life of a cell and makes a good deal of sense.  If every cell has all the genes' DNA why wouldn't a little bit of receptor expression be found in any cell which could use the information?  The conscious processes of the brain probably only take in a small fraction of the information that is sent in and there maybe hundreds of other such senses from various parts of the body to integrate, only a fraction of which we are aware of.
In addition, there are probably lots of cases where receptor signals are only used locally by cells that are sensing their local environment.  It really doesn't make sense that the individual cells must blind themselves.  Individual bacteria and fungi have scores of receptors.  It makes sense that cells that are part of an organism would have as many or more senses as well.

-1. It is well-established that opsins are expressed widely, but their functions are not known. It hasn't been convincingly shown anywhere that human opsins confer light sensitivity to any cells other than those in the retina. The knee study you mentioned has been refuted (see my comment here: http://biology.stackexchange.com/a/704/72). Also, a point of nomenclature, photoreceptors are cells that are sensitive to light, and opsins are called photopigments when they are bound to a chromophore and are sensitive to light.

Do born-blind mammals and later-blinded mammals experience extraretinal
photoreception differently?

This article in Scientific American here where they refer to "Circadian and vision neuroscientist Russell G. Foster of the University of Oxford" outlines:

"In 1999 we found that mice lacking rods and cones were nonetheless
able to synchronize their circadian rhythm to the light/dark cycle.
These observations led to the discovery of an additional
photoreceptor system in the retina of humans and other mammals
consisting  of a small number of photosensitive retinal ganglion
cells (called pRGCs). These cells are most sensitive to blue light,
and, significantly, blue light is most effective in alleviating the
symptoms of SAD." (I added italics to interesting points)

WSJ repeats the blue-light thing and recites:

"In 2002, German researchers isolated one from green algae—a class of proteins called channelrhodopsins—that responded only to blue light. -- Depending on just how researchers tailor the virus that carries the light-sensitive protein, they now can target almost any type of neuron they want to study."

So differently in a way that they lack the cones/rods in retina and some links to visual-cortex but no in a way of SAD: evolution have apparently developed methods for blind-born mammals to survive and to sync their inner clock. This resonates with the earlier facts by shigeta but I don't know whether there is any other thing to light -- perhaps UV radiation -- that could tune the internal clock.
It looks that they are trying to find ways to engineer bionic-visions things similar to dobelle without physical modification of skull. The viruses tries to propagate certain photo-receptive protein into some spot where they try to activate them though external radiation. This is called optogenetics where they are trying to control certain behavioral things with optics.
New puzzles

why do they use protein? Why not other things?

do we have many kind of photoreceptivity? Certain muscles (requires protein) activated by EM radiation? What about other cells such as fat-cells?

P.s. this is pretty fruitless to advance unless someone provides precise power spectrum of Valkee (requires apparently spectrum-analyzer) and polarization experiments. WSJ referred to trials where they use monochromatic light and coherent light in testing while Valkee-light can be pretty much anything.


text:
variation in antigen binding site of antibodies
Antibodies or immunoglobulins are proteins made by the immune system in response to alien(!) molecules. Each antibody binds to its specific antigen. This great diversity and specificity is cause of diversity in Antigen Binding Site of heavy chain and light chain of antibody. Although other sections of Antibody are highly stable, Binding sites are very mutant. What is the reason for this difference in mutation rates in different parts of antibodies?

The processes are called gene rearrangement and somatic hypermutation, and are used by maturing B-cells to generate very (very) large amounts of diversity in the antibody repertoire. If your institution has access, this great article in Annual Reviews in Immunology has all the details, or you can read about it in Janeway (slightly outdated edition). Essentially, the genes encoding the B-cell Receptor, or BCR, have many fragments of several different types in them, and through the process of gene rearrangement the final Complementarity Determining Regions, or CDRs (the antigen-binding sites), are generated into one mature sequence for each individual B-cell.
A mature IgG molecule (the soluble, secreted version of the BCR) contains four chains - 2 heavy (each of which are identical to each other) and 2 light (also identical). There are Constant or C regions in each chain that essentially don't vary much, and are not really involved in the process of antigen binding. On the "business end" are three regions (or types, from above) called V, D, and J in the heavy chain, while the light chain just has V and J. Those letters are from Variable, Diversity, and Joining, if you're interested.

Figure 4.3 from Janeway shows the number of "fragments" or gene segments of each type in humans. So, when the heavy chain is being made, 1 fragment out of 65 Vs is picked, 1 of 27 Ds, and one of 6 Js, then each is joined together in a process that can also introduce an additional amount of randomness at the joins. Combine this with an only slightly less complex process in the light chain (as there is no D region), and the fact that a single insertion/deletion of a base pair can drastically effect the resulting protein sequence, and you get a protein with a huge number of possible sequences, potentially in the range of 1011.
This process of gene rearrangement typically generates immunoglobulins with relatively low affinity for their antigens. During affinity maturation, a process called somatic hypermutation randomly changes individual base pairs (translated to amino acids) in the CDR in cells that are descendents of, and bear the same base sequence as, the original. Cells expressing antigen receptors that are of higher affinity are then positively selected and clonally expanded by the immune system, allowing your body to tailor its response to an infection or other exposure to what it sees as foreign material.

I don't understand what this is referring to: "the vagaries of possible frame-shifting during transcription".

@AlanBoyd - I'll edit that. I was referring to the fact that an insertion or deletion of a single base pair can change the frame in which the downstream codons are interpreted, leading to (potentially) very different protein sequences.

Antibody molecules or immunoglobulins (Ig) consist of heavy and light chains (e.g. two of each in IgG). Both heavy and light chains have variable domains at their N termini.
During development of the immune system the pro-B cells in the bone marrow undergo gene segment rearrangements, bringing V and J segments together for Ig light chain production, and V,D and J segments together for Ig heavy chain production. The V gene segments encode the variable domains at the N-terminus of light and heavy chains. There are a few tens of V gene segments in our genome - this is the first source of variability.
The second source of variability is the "sloppy joining" of the V (D) and J segments. This results in frame shifts together with short deletions and insertions. This V(D)J junction corresponds to the third hypervariable region of the variable domain.
Each immature B cell displays its antibody at the cell surface as a membrane-bound form of IgM. If an antigen binds to this antibody the cell is stimulated to divide (clonal selection). During the proliferation of the immature B cell it undergoes somatic mutation due to error-prone replication of the Ig loci. This allows for the production of Ig variants with improved binding affinities which are in turn stimulated to proliferate more rapidly, eventually maturing into antibody-producing plasma cells. This somatic mutation is the the third source of variability in the variable domains of Ig molecules.
See any immunology textbook for details and diagrams.


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Is (are) there any crucial gene(s) for the formation of flower in flowering plants?
I am interested in qualitative (flowers of some plants have petal or sepal, but some plants have not) and quantitative (number of flowers of plants) differences between flowers of different plants.
Formation of flower in flowering plants is under control of which genes?
Which genes are the most important ones in flower development, for example which gene tell the flower that you should have for example 2 stigmas. or which genes tell the plant that you should have 4 flowers or your flowers will not have sepal...
Thank you

I think this is far too broad (all flowering plants, different features, both initiation and development). You are asking for a textbook. Can you narrow this down?

I am looking for a brief description

I think you are looking for the ABC model of flower development