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Why do tomatoes look so much like pomegranates?
The pomegranate fruit has been cultivated since ancient times, particularly in the Middle East and the Mediterranean.  It has a hard outer rind, and inside are several chambers, each of which contains a multitude of seed pods, consisting of a single hard seed wrapped in a protective cushion of liquid.
Take every detail of that description, make it a bit smaller, a bit softer, and a whole lot more edible, and what you've got is the exact description of the tomato fruit.  One could certainly be forgiven for assuming that they were genetically related, but if you look at the phylogeny of the two plants, you see that that hypothesis could hardly be more wrong--not to mention the minor little detail of tomatoes being native to the Americas, literally on the other side of the world from the pomegranate's home!
So what's going on here?

Would the downvoter care to comment?

Don't worry about it. it seems like some high-level botanist should be able to answer

Species evolve similar features in isolation - wings have evolved on multiple occasions for example. Besides that it seems your question is looking for some grand meaning behind their similarity, and is not a good fit for Bio SE.

So what's going on here?

Personally speaking, I don't think the tomato is anything like the pomegranate. However, generally speaking the appearance of similar traits despite widely divergent ancestry is called Convergent Evolution. Some traits -- let's say round fruit and red coloring -- may be so advantageous that they evolved multiple different times throughout history.
Take wings, for another example. Wings have evolved in insects, avians (obviously), and mammals. The last common ancestor (often shortened to "LCA") is billions of years back, but wings persist.
So, the real answer is not quite "by chance," but closer to "because they're very good traits to have."

We might also consider the effects of human selection: there are certainly similarities in the plants we choose to domesticate, and the traits in those plants that we select for.

Why do bats look a lot like birds?  Or hawk moths/hummingbirds, dolphins/ichthyosaurs, and many more.  Also, I wouldn't say that wings "persist", as the LCA didn't have them.  It's rather that they evolved independently, and the similarities are a result of aerodynamics determining that there are only so many ways to make a good wing.


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agglutination test using blood of the donor and the recipient
we were told that agglutination occurs when the matching antibody react with its antigen on the RBC surface (as antibody B with antigen B)....
Also when blood transfusion, Donors plasma with antibodies is diluted , so when o-donor gives blood to  B-recipient , B antibodies ( of the donor) is diluted
........
My question is in lab cross-matching test  when we put recipient's plasma(o with b antibodies for example) on the donor's RBCs (B with b antigens)..... is there agglutination, If so, how would we know the right group then?....if not ,Why not?
if the whole thing is misunderstood ,i wish to be told how it's done.

Disregarding Rh factor for a moment: when you add A-antibodies to a blood sample and agglutination occurs, this means the blood contained A-antigens (A-type). The same can be said for a sample of blood to which B-antibodies are added (B-type). If agglutination for both antibodies occurs in separate assays on the same sample of blood, it means the sample contains both A and B antigens (AB-type). If the sample is said to be O-type, this means neither A or B antigen would be present in these cells. It's safe to transfuse O-type blood into any recipient due to this fact. What you also want to watch out for, is attack on the recipients RBC's by antibodies in the donor's plasma. This can result in a hemolytic transfusion reaction (HTR), but it's noted in the following text:

Red blood cell incompatibility may also occur when the patient's RBC antigens are attacked by antibodies from the donor's plasma. This tends to be a minor problem because of the small amount of antibody present in the donated plasma, which is further diluted on transfusion into the recipient's circulation.

If you're in the lab doing a Coombs test, for example, you're checking to see if there are any extraneous antigens present that might results in a HTR. In a normal result, ergo there aren't any antibodies to RBC's in the sample mixture, you wont see any agglutination. This is for considerations outside of ABO antibodies, generally. If you're adding to B-type RBC's a plasma with known antibodies to B antigen, like O-type plasma, you can probably expect an event. To my knowledge, O-type plasma wouldn't be safe to give to anyone but an O-type recipient.
additional source

what i know is that o is the universal donor what i don't get is how do we know it's compatible when its plasma has the antibodies or is it not done this way at all(mixing donor's RBCs and recipient's plasma)?

O group RBC's lack antigens to either A or B antibodies, making them suitable for donation to any blood type. The recipients body wont attack the donor RBC's. The donor plasma contains antibodies to both A and B antigens, however. The assumption we're making is that out of total blood volume, donor + recipient, the amount of A/B antibody in the O group plasma will be dilute enough that there's a deleterious effect on hemolytic events involving donor anitbodies. What you wouldn't do, is give O group plasma to anyone other than an O group recipient during a plasma transfusion.

The way we find out if it's compatible, is we add A and B antibodies to separate samples of blood to determine if agglutination occurs. For O group blood, you wont see any of this. To confirm, you can back type the blood. Take the O group serum, and add either A blood cells or B blood cells to separate samples. You should see clumping in both cases (you're type AB if no clumping occurs in back typing).

is cross matching done with the blood of the donor and recipient or not ?

It's done with the serum of the recipient, and the donor's packed red blood cells.

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Does anyone know what kind of caterpillar this is?
I was out hiking, and was walking along the side of a road, and saw this little guy on some gravel. Hes a light blue/grey color, hairy, spotted with red,and looks like he has horns and a tail. I've been trying to search for what species it is. If anyone knows, please share!

(Click to view full image)

Nice picture! Where and when did you take the photograph?

In colorado springs, Cheynne mountain, and just a few days ago!

Looks similar to a Rusty Tussock Moth (Orgyia antiqua) caterpillar, but you might want to check the bugguide page for the species, or submit your photo there for a second opinion.

Thank you so much! I looked the moth up and there was a youtube video of one. Thats definitely my little guy. once again, thanks!

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Are mitochondria transferable between cell types, individuals and species?
I'm curious about what happens when you insert organelles from a cell into another. In particular, mitochondria.
Take two cells from your own body. Somehow extract a mitochondria from one cell and somehow insert it in the other cell.
Will the cell with the foreign mitochondria make use of it (respiration), or will it dispose it?
What if the foreign mitochondria comes from someone else's body?
What if the foreign mitochondria comes from another species' cell?

There is evidence that cells can exchange mitochondria. There are some donor cells that transfer mitochondria to recipient cells via cytoplasmic nanotubes (within the same species). This happens endogenously and triggering factors may include stress.
References:

Pasquier et al. 2013
Ahmad et al. 2014
Wang and Gerdes. 2015
Hayakawa et al. 2016

On interspecies mitochondria transfer.
In a study by Yang and Koob, the feasibility of mitochondrial transplants was studied. Mitochondria isolated from donor cells were initially injected into mouse oocytes/embryos. Then mitochondria, along with a chunk of cytoplasm and membrane was taken out; these cell-like structures were called  mitocytoplasts. Then, these mitocytoplasts were fused with recipient cells (mouse rho0 cells - these lack mitochondria) with the help of a viral fusion protein.
They found that the recipient cells supported mitochondria from the same species (donor species include mouse, rat, Mongolian gerbils and Golden Syrian hamsters).
The success of the "mitochondrial xenograft" depends on how different the species are and as shown in the abovementioned experiment, a donor cell (mouse) would not support the mitochondria from even a closely related species (rat). This incompatibility would primarily be based on the dependency of mitochondria on the nuclear genome which may be different for different species. It is possible that "mitochondrial xenografts" may be accepted; the impossibility of it has not been exhaustively verified.

Interesting stuff. +1 great answer

I'm not entirely sure about cross species organelle transfer (lets focus on mitochondria), but some people have already made three parent babies, therefore mitochondria are at least transferable between individuals of the same species.
The reason for the operation was to cure a disease that was inherent to the mitochondria of the mother (mitochondria always come from the mother, never the father). They used the genetic material from the nuclei of the mother and father, and used the mitochondria of a "foster" mother.
http://www.bbc.com/news/health-31594856

Interesting! But this looks like transfer of the nucleus, rather than transfer of mitochondria. So it doesn't answer the question of whether a cell would accept "foreign" mitochondria I think.

Another keyword for interspecies mitochondrial transfers is "xenomitochondrial". Carlos Moraes' lab is probably one of the the main groups that study this over the years, finding that mitochondria from only some great apes could functionally substitute for human mitochondria in cell lines.
Kenyon & Moraes "Expanding the functional human mitochondrial DNA database by the establishment of primate xenomitochondrial cybrids" PNAS 1997
http://www.pnas.org/content/94/17/9131.short

this is a comment that adds nicely to the pre-existing answers, but is not a stand-alone answer by itself.


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What form of reproduction did the first land animals use?
What form of reproduction did the first animals on land use*? Were they hermaphrodites, or did they have male and female sexes? [Is there a proper term for sexual separation in a species?]
Were any land species believed to have evolved from hermaphrodite ocean species (that crossed to land on roughly the same geological time periods that land creatures first evolved)?
*I know that 'first on land' is a complicated concept itself, since it could mean first creatures be able to survive on land at all, first to freely travel between land and water, or first to only live on land, or anywhere in between.  I assume all three categories were sexual though?

Are you thinking of vertebrates or non-vertebrates?

Your questions are quite wordy. Please be to the point. Condense the question by cutting the fluff, reducing details and exclude irrelevant random thoughts.

I think the term you are looking for is sexual dimorphism. Or just sexual reproduction.


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Why are there no complex hermaphrodite land animals?
The title says it all.  I know that 'complex' is a pretty ambiguous term to use, but I can't think of a more scientific term/definition for my meaning.  I can't think of any large (larger then a small rodent) hermaphrodite species, or any that we tend to think of as having complex structures; hermaphrodite species all seem pretty boring really.
I get why sex is a huge advantage, but by that regard hermaphrodites seem quite powerful.  The ability to both produce your own young and impregnate others allow for more young.  Plus, it provides the opportunity for a species to choose to self fertilize if no mate is available.  I realize sexual reproduction is preferable, by it's nice to have Autogamy as a backup option just in case.
I understand why there are advantages to two sexes, particularly in terms of sexual dimorphism which allows male to be better at potentially reproducing with many females by specializing in it.  I completely understand how two genders would evolve and be successful.
What I find odd is that nearly all larger or complex species seem to have genders.  I would have thought that, like many other mating strategies, there would be variance across species; with some choosing to be hermaphrodites to increase the maximum children they can produce as a species, by having twice the child bearers, and others choosing to go the sexual dimorphism route by having roles that they are best at.   I mean even Obligate parthenogenesis has evolved separately many larger specie like lizards, despite it arguably being an evolutionary dead end in the long term due to the lose of the advantages of sexual reproduction.  If adaptations that completely toss away the power of sex evolve all over the place why do new hermaphrodite species never seem to evolve, and existing hermaphrodite species never seem to grow bigger or more diverse?
In particular sequential hermaphrodite, like many aquatic fish use, seems a pretty effective strategy.  When your young, and small, play a female role to have guaranteed offspring, only once your big and at your most fit bother competing as a male for access to multiple mates.
A related question, associated with my own attempt to explain why existing hermaphrodite species don't seem to take as many varied forms; but which I'm not really sure I buy.  Is it possible that the lack of sexual conflict (primarily, but not limited to, competition between males for mates, driven from the fact that males would have more drive to compete then hermaphrodites since it's their only reproductive strategy), would mean there was less of a drive towards adaptation in hermphrodite species?  A sort of red-queen scenario, where your own species is the red queen?

I'm no biologist, but what is your definition of "complex"? Land snails and earthworms are hermaphrodites, which makes sense because they move rather slowly and therefore have fewer opportunities to find a mate. Do you mean "vertebrates"? If this is what you mean, the probable answer is that simultaneous hermaphroditism is something that hasn't existed in the verterbrate ancestral lineage for a very long time, if ever, and therefore it needs to "re-evolve." Given that vertebrates are highly mobile and therefore have frequent opportunities to mate, it seems unlikely to happen.

"I can't think of any large (larger then a small rodent) hermaphrodite species, or any that we tend to think of as having complex structures; hermaphrodite species all seem pretty boring really." !!! There are snails much larger than mice. And "boring" is very opinion based.

Please reduce the text by at least two-thirds. Add only info relevant to the Q

@steveverrill Evolution of hermaphroditism is likely not difficult, see http://icb.oxfordjournals.org/content/53/4/736/F1.expansion.html

I was really happy to see this question, cuz it's been bugging me for years too. (Like, I remember trying to get a satisfactory answer from my grade 12 bio teacher.) But it seems like the community in general isn't quite getting the intent, the way you phrased it (it makes perfect sense to me, but then, we're obviously in the same mindspace on this point already). Maybe try making it more concrete?

Like... sketch out an idea for how a species of birds could evolve hemaphroditism, maybe? The selective pressures you think could create and maintain it?

Abstractly, the possible answers to our question that I can think of are: {1 Our ideas of how pressure for hemaphroditism would be generated in species like this are wrong because...?} {2 Our ideas aren't necessarily wrong, but there would be stronger pressure against it because...?} {3 There would be a stable net pressure maintaining hermaphroditism, but there's a barrier against it initially re-evolving from a [antonym of hermaphroditic] population because...?} So write the question to try to focus on concrete examples of those possible explanations, I guess?


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Why isn't the upper limit of pain lower in humans?
From what I understand, pain is an useful mechanism that signals us that something is not quite right with our body (in particular, we're under attack). It's good - it alert us and tells us that we got to do something (stop the threat, or run away, etc). From Wikipedia:

Pain motivates the individual to withdraw from damaging situations, to
  protect a damaged body part while it heals, and to avoid similar
  experiences in the future.

However, there are damages that cause too much pain. If you are stabbed in a particular place, you will most likely have so much pain that you simply can't fight back or run away. The shock makes it incredibly hard to do something or even think properly.
So my question is: is there a reason why pain can elevate to such high levels? I'm just assuming that if we had some sort of hard limit on the amount of pain we receive, we could perform better in several dangerous situations. In other words: instead of hurting so much that we can't even think properly, it hurts enough to let us know we are in grave danger but still capable of assess the situation and perhaps even act accordingly.
Obviously some physical damages will render you unable to act anyway. Like, damages on the spine that may cause your limbs to malfunction. But I mean damages such as a large open wound on the abdomen: if that didn't hurt so much, I'd imagine you could probably stand up and run away (you'd probably bleed out but at least you'll have a chance to escape the threat).
My guess is that it "cannot be helped". Pain are signals from different parts of the body to the brain, and once a signal is sent, the brain has no choice but to process it accordingly.

There is no hard upper limit, but there is a soft (dynamic) upper limit. An injury that will result in you being paralyzed with pain would be almost unnoticeable if you are in shock.

You are assuming that fighting back with a bad wound would be more useful than dropping to the ground. That is not always the case.
Dropping to the ground and ceasing activity is very adaptive in almost any situation involving potentially significant blood loss. Becoming prone or supine prevents loss of consciousness, the most critical aspect of survival. Decreased movement is also likely to decrease the rate of blood loss (though not in as significant a manner as consciousness).
Certainly with a significant abdominal wound, running would increase cardiac output, which would increase bleeding. Is running from a traumatic event advantageous if you pass out before escaping? On the other hand, lying prone and holding the wound (instinctive) may reduce bleeding and prolong consciousness and life.
What "cannot be helped" (like withdrawing a hand from a flame) is usually advantageous.
An infant's cry changes during circumcision (an involuntary reaction to pain). The cry in turn naturally produces a visceral reaction in nearby adults that compels action (causes a state of strong sympathetic nervous system activation.) The adult either avoids the cry by trying to distance themself, or responds by coming to the infant's cry.
The infant cannot help changing the intensity of the cry with intense pain. If a "certain level of pain" was as far as one could feel, the baby might not elicit the sense of urgency in adults which it does.
Newborn pain cries and vagal tone: parallel changes in response to circumcision.
ASSESSMENT OF INFANT CRY: ACOUSTIC CRY ANALYSIS AND PARENTAL PERCEPTION

The upper pain limit is far above the the worst cry though. I suspect from reports on runaway pain disasters that cutting it in half would make no difference.

@Joshua - I'm not sure what "runaway pain disasters" are, and as someone who worked in an emergency department wherein pain management is a necessary skill, it seems I should know about runaway pain disasters. I agree, though, that there is pain in excess of our ability to express it, but, again, as an ED doc for many years, I have only seen it a few times. What can't be expressed as words (or cussing) is expressed in body language, and there is only one time that the pain seemed so great it was truly inexpressible. It was hellish for me, too, watching and trying to treat that.

I wondered how I might answer, and then much later I remembered how a dog has a much lower pain awareness or a much higher pain tolerance. I've never seen the human having too much fun to let us see if the mouth bleed is a problem, but the dog sure wanted to play despite the mouth bleed from what we could only think was a thorn. But if that's all the pain experience a dog needs (which doesn't have a good enough head to know what needs treating otherwise) than why do humans need so much more pain experience?


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Genetic Diversity in Mitochondria
As I was studying for my GRE exam, I was reading on Mitochondria. I then remembered that they undergo replication similar to bacteria. So I googled for info and found on Wikipedia that there is a " near-absence of genetic recombination in mitochondrial DNA"
https://en.wikipedia.org/wiki/Mitochondrion#Replication_and_inheritance
So then, if there is a lack of genetic diversity, how can these mitochondria still be functional? If we assume they are affected by random mutations as DNA can be. Is it the case that they replicate infrequently enough to not suffer ill-effects of low diversity?

Your claim that "there is a lack of genetic diversity" in mitochondria is not correct. There is no connection between recombination and mutation rates per se. In fact, mitochondria have much higher mutation rates than nucleus and different types of mitochondrial DNA can even co-exist in one organism, a phenomenon called heteroplasmy (which is found at a frequency of ~90% in human).
But: there is a connection between mutation fixation rate and effective population size. Because mitochondria are normally inherited through maternal line, effective population size for their genome is smaller than that of the nuclear genome, and thus any mutations in the mitochondrial DNA reach fixation faster, but again this is counteracted by high mutation rates.
There is no problem with functionality: as always if something gets broken (and it is easy to break something in the mitochondrial genome, since genes are normally tightly packed in it) respective genotype is eliminated or reduced in frequency by natural selection. In the case of mitochondria this selection acts both upon the level of individual organisms (intra-individual somatic pool of mitochondria: positive and negative selection) and the level of populations (mostly purifying selection in humans). It is nevertheless true, that given the virtual lack of recombination, selection becomes the only force of purging deleterious mutations.

Since mitochondria have a very small genome, with very little intergenic DNA, the mutations are likely to affect the essential respiratory genes (amongst others). Since many of these genes perform vital functions, many mutations may not be tolerated. I am not sure about it but would this also lead to loss of diversity? On the other hand, I had read somewhere that mutation rate in mitochondria is higher: perhaps due to high ROS concentration (my guess). Basically, how strong is the selection pressure against variation i.e. is there a sort of permanent bottleneck?

@WYSIWYG Yes, the fact that the mt genome is mostly coding reduces the potential allelic and nucleotide diversities in comparison to a randomly mutating sequence. And yes, mt mutation rates are much higher than in nucleus. Concerning the bottleneck: I've added a ref to a review. Nevertheless, there are always enough neutral mutations (3rd position and others) to contribute to the genetic diversity.

@WYSIWYG        Yea I guess I wasnt thinking about how important mitochondria are, and that a mutation would have to be purged out.


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Database of Geographic Range of Species
Is there a database of organisms which would contain their queriable geographic location?
I would need to perform a rather simple query, such as Animals of <Location>, where Location is some well defined geographic area such as Czech Republic or Europe.
So far I have found multiple lists on Wikipedia and other webpages, however they seem to be quite incomplete as their intersect is quite small. Moreover, I have found EOL (Encyclopedia of Life) collections but they appear to struggle the same way.

What taxa are you most interested in and for what purpose are going to use the data?

The data are supposed to be used for online tool for learning biology (in non-taxonomy matter). So for now I am mostly interested in vertebrates, but later some subselection of plants, fungus and other kingdoms will come to play.

This is to a large extent a question of how reliable the data in the database needs to be. Reliability (and spatial scale) will differ between datasets and between species groups within datasets, and it is difficult to give a general recommendation. I doubt that you will find a single database with good coverage over all taxonomic groups, even if it is in the form of country checklists. For the most reliable information, curated country checklists for specific taxonomic groups will probably be best, but these have to be searched for individually for each taxonomic group of interest.
As a starting point, you might want to look at the occurence data that can be found in gbif.org (The Global Biodiversity Facility). The data found there is certainly not complete, and it will be misleading for many species. However, for the current distribution of relatively well-known groups of species it will give you a good idea of their distribution. This has to be evaluated on a case-by-case basis though. You can access the data in gbif using external tools, for instance using R through rgbif (there is also tools for python or other languages). At the blog recology.info you can find a tutorial on how to get a species list for a particular country using rgbif (more specifically the function density_spplist).

The data completeness will always be problem, however with your suggestion of GBIF and triangulation from various sources mitigate this problem to much lower level. Thanks! :)

The GBIF database that was suggested can give you locations of occurrences given a specific animal. But you asked for lists of animals given some location. An excellent tool to give a list of animals given a location in the world is the Map of Life. Click on "Species by Location" which gives a map of the world, and click anywhere to get lists of species that could occur there.

Also seems very interesting and relevant, thanks for sharing!


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A tool to get annotation features by position in the reference genome
Previously, when I needed to find a genomic feature (promoter, CDS, repeat etc) that underwent mutation (SNP) I used my own scripts to load an annotation file, parse it, map the SNP's position and output the sequence of the feature. Now that I'm moving from microbes to mammals with huge annotations, introns/exons and huge genomes, my scripts don't work that well and I'm sort of lazy to optimize the code or rewrite it in a faster language, since I'm sure there should be some prominent tools for the task. That's it, could you recommend me some tools that do the following:

Given a reference genome, annotation and a VCF (or similar variant file) match the SNPs to genomic features in the annotation
Output the entire feature that underwent mutation, e.g. if the SNP happened in a protein-coding gene, I need to have the entire protein-coding sequence not just an exon/intron.

Thanks in advance.

The GTF/GFF format is universal. Why would your scripts not work? Try stream reading. It can be done in python and is default in awk.

@WYSIWYG My scripts is in fact written in Python. It pulls out the annotation region it hits. In bacteria there are no introns in protein-coding sequences, hence if I get an annotation hit I can simply pull the region. In mammals the script sometimes pulls a piece of a gene (an intron or an exon), though I know how to fix that issue. More importantly,  my script stores the entire annotation file in memory as a hash-table of ranges. That's not too much efficient.

The second column in the GTF is the feature name. You can parse only for exons. There are programmatic ways of limiting the memory usage; one easy way is to run the script chromosome-wise and just store the features that you are interested in.

I'm voting to close this question as off-topic because it is about programming, not biology.

Well, after 2 weeks and several thousand lines of code I got a demo-version of my revamped annotator up and running, but then I was told to take a look at SnpEff. The tool makes everything I was to implement in my own one, so if anyone ever wants to annotate SNPs with regard to genomic features they hit and possible effects, give SnpEff a try. It's really fast.

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There aren't any animals like hornets that hunt large prey (like a rabbit, or even up to a deer), right? Why not?
There aren't any eusocial animals (hives of wasps, ants, termites, etc) that hunt large prey, are there?
I'm thinking prey in the size range of, say, a rabbit, or even a deer.
I can't see a rabbit or a deer having any real effective way to defend against a swarm of hornets, especially if you supposed that the hornets' venom could easily be adapted to be particularly effective against such prey.
Intuitively, this seems like it would be a lucrative little niche.
Like:

A swarm could bring down a kill without risking losing too many members.
The return seems like it could be very high.
There shouldn't be too much of a risk of losing much of the kill to scavengers or whatever.
And after starting down the evolutionary pathway into such a niche, they could easily develop methods of preserving meat (I'm imagining a horrifying hive full of natural ham, here).
Protecting this ham-hive wouldn't be any more difficult than protecting a honey-hive from bears etc.

And such a niche doesn't seem that evolutionarily distant from where hornets already are.
Like:

They already do seriously hurt or even kill large animals that they perceive as threatening their hive.
They already do scavenge large animals they find dead, and even steal the occasional chunk of flesh from living animals.

But as far as I know, nothing like this exists, right?
Why not?
(And, like... maybe the most important question: How can we make sure it never comes into existence?)

Army ants regularly kill and eat birds (although they primarily hunt insects). Dorylus, or siafu ants consume rats and are considered a menace to humans with restricted mobility. And [invasive] bees do kill humans although we are not prey.

@Luigi Yeah, that kind of stuff is essentially what I meant about them already being pretty close to that niche. That is, those are examples of eusocial insects with behaviors on the edge of the "ham-hornet"-like niche. My question is, why haven't any species fallen right smack-dab into the middle of it? Ya know what I mean?

I wonder whether hornets &c can effectively sting through fur?  Then there's the sheer number of stings that it would take to kill a non-allergic animal.

@jamesqf In case you think sting victims who die only die of allergy reaction (anaphylactic shock), some species of hornets actually have a sting that contains neurotoxins, and some can cause kidney failure. E.g.: the Asian giant hornet

They're not fast enough
A hornet has a top speed of around 40 kph, while a rabbit is only a touch faster, a deer can hit 75 kph (all figures from Wikipedia). In order to act as hunting insects they need to match the speed of these large animals in large enough numbers to surround and overpower them but these animals could easily match their speed or outpace them. Let's suppose they can overcome that limitation somehow and bring the prey down. They've now bagged a big lump of protein but it's a long way from the hive because they've had to chase it down first. That means that a long round trip is required every time they visit the kill and thus reduces the energy yield as well as increasing the chance of losing it to scavengers.
Against this you have the simpler option of eating smaller, easier to catch, prey as they do now.

Alright, that's the first idea that feels like a potentially satisfying answer, thanks! :D So in order to wander into this niche, they'd need to at least start by hunting animals that can't accelerate away as quickly, but those seem like they'd be less common (so it'd be less lucrative) and/or much more massive (so they'd need to also happen to have stronger venom). Of course, it might also work if the hornets were able to sneak up and surprise animals, but those kind of stalking behaviors are complex and not very close to their current behaviors...

Alright, yeah, I'm starting to feel like I'm getting a sense of the kind of barriers that prevent a species from simply wandering into this "ham-hornet" niche. Thanks again! :D Think I should mark this as accepted? Do you have any other ideas to add?

Like, to be clear, I'm not convinced this is definitely the reason, and I still overall feel like I should be surprised that ham-hornets don't exist. It's not intuitively obvious to me that the net number of calories transported back to the hive per hornet per meter flown would be lower than that for honey bees. But your answer at least starts to suggest models you could actually test!

Moreover they have to masticate the prey to feed the larvae. It would not be feasible with big animals.

@Owen_R: The comparison between honey bees and hornets is moot; the comparison which is evolutionarily relevant is to investing their energy in hunting small prey as they do now. In order to start hunting large prey they need to get a benefit from ineffectually hunting these prey since they have not yet adapted to do it well.

While it is true that rabbits and deers run faster than hornets can fly, I'm not entirely convinced that speed is really a problem. All the hypothetical hornets/wasps need to do is to gather around the rabbit without disturbing the rabbit, and then go all in at the same time, before the rabbit has time to react.

@Kal: Do you really think that a swarm of hornets would be undetectable to a rabbit? Remember, as well, that even if this strategy would work first it has to evolve and for that you need to have functional, beneficial, intermediate steps - what do you think they could be?

I'd argue that it's not so much they aren't fast enough movers, more that they are not fast enough killers. The note below about the army ants killing a worm... that's a worm, not known for its ability to sprint, and it got 3m or about 10ft. They then butchered it in situ, rather than carrying it back in one piece.
For a flying hunter, you have better range, but still... I suspect that most large animals, being attacked by killer bees, will run away far further than is feasible to recover their flesh, and will also do what they can to harm the bees, rolling etc. Sounds maladaptive.

Why not the turquoise?

@JackAidley It's actually quite possible for the wasps to swarm and remain undetectable to a rabbit. The rabbit's hearing range is about 360 Hz to 42 kHz. Meanwhile, wasps beat their wings at around 200 Hz, so the sound of their flight would probably be undetectable to the rabbit. As far as sight goes, wasps are small and they can easily hide in foliage. Behaviour-wise, wasps and bees are known to have already evolved coordinated attacks against intruders, so it shouldn't be hard to evolve into a hunting strategy as long as there is an actual advantage.

They do exist. Many such examples can be found. Such as the most terrifying one, being social groups formed by Spiders, Anelosimus eximius documented here.
Colonies of upto 9000 individuals have been documented by the scientists in their report.
Also let's not forget Piranhas, another group of social animals, which take down much larger prey due to their larger colony size.
This particular phenomenon is concisely explained in this article in wikipedia under Cooperative Hunting
As the models explain and I also think the same, that the only reason a social aggregation would seem necessary to any animal is because it provides increased fitness or survival. This particular phenomenon can be viewed from the perspective of Human society as well. I given an income source X, would always choose to rent a private space for myself. If my income does not allow me such an option my best option is to cooperate with another in a shared system.
So the same can be said for Insects if availability of prey which can be candidates of solo hunting goes down, the only option left for the species to survive is to either compete if that is the only available source of food, or if larger prey is available for group hunting where individuals don't come into direct conflict, then to go for the option which provides the greatest fitness to the species as a whole. Obviously, in such a case you go for aggregation and not competition such as those seen in ant colonies.
Many more such systems exist I am sure, but I am no evolutionary biologist only a humble genomics guy. They will be able to provide much more comprehensive answers.

Well, that's interesting, but it seems like kinda a non-sequitur to my question. Eusocial insects seem like they'd be really effective in a niche focused around cooperative hunting, especially if they bring down prey hundreds or thousands of times more massive than an individual member of the swarm, and then store the meat in their hive. But apparently they don't do that. My question is, why not? These spiders aren't eusocial, and they're not cooperating to catch prey that much more massive than the individual spider.

I would disagree on the point of eusociality as this study states http://rd.springer.com/article/10.1007%2FBF00300005. Can they bring down something which is a hundred or thousands to times larger than them? No I do not think so, but as the investigative group notes in the answer, they do not really catch the same number of prey. Rather, they catch a much smaller number of prey of increased biomass culminating ultimately towards more biomass per spider than they would have gotten individually.

Hmmm... still, I think my question could basically be summed up as: "Why don't ham-hornets exist?" Do you think the case of these spiders really seems like the same thing I was asking about? Or does it just seem similar in a few factors?

I mean, it's definitely not the answer: "Yes, actually, ham-hornets do exist", so how does it help to shed light on the question of why they don't?

It is similar in the fact that the creatures are as eusocial as a non-eusocial species can get. This species being the most social ones among spiders, an organism generally considered as a solitary animal. But to answer the question why don't they hoard food? I would have to say that because the needs of the few outweight the amount of food available. A leopard will never get caught in the web, it will generally be smaller animals which the entire colony can devour.

But as far as hoarding goes, this article documents hoarding in spiders

Hm, yeah, everyone knows that the stereotypical individual spider "wraps up flies for later", even. But still, do you really think this is actually a direct answer to my question? Or just interesting, potentially related information? It makes sense to me as the latter, but not the former.

While piranhas can take down very large prey, such as cattle, that is not their ordinary behavior by far, and actually quite unusual. Attacks on large animals and humans are typically non-fatal, with some nips and bites taken, but the victim usually can escape. Fatal attacks occur with children, impaired or disabled adults (such as drunkenness), and at the peak of the dry season when water levels are very low and food is scarce. Studies have actually shown that they are rather timid fish, using their teeth primarily for defense.

Your giant spider colony example completely misses the point. Yes, they exist in large colonies, and larger webs can catch somewhat larger prey "several times their body size" (from your link), but they do not hunt much larger species like the OP is looking for. I don't think s/he doubts cooperative hunting exists, they're just looking for examples of individual predators being orders of magnitude smaller than their intended prey.

Unfortunately for you, such animals do exist (O'Donnell et al. 2005).
This is a direct field observation of a swarm of army ants attacking and consuming a 60cm long earthworm, as well as consuming a 10cm long snake.
From the linked article:

We collected workers from two Cheliomyrmex andicola foraging raids.
  During raid 1 on 26 September 2003 at 1030 h, we encountered a large
  C. andicola raid column in primary terra firme forest, exiting from soil-covered foraging trails that the ants had constructed on a slope.
  The sky was clear, and ground surface temperature was 25.9°C. Beneath
  the raised tunnel of soil particles that the ants had constructed, we
  found the partially consumed carcass of a snake (1 cm in diameter and
  10 cm long). Most of the snake's scales and skin had been removed.
  Cheliomyrmex andicola workers were observed chewing on the snake and carrying away bits of flesh in their mandibles. As we dug near the
  carcass, the ant workers responded by biting and stinging our hands.
  The workers clung to our skin, and we noted that their stings were
  more painful than those of other army ants from the site (e.g.,
  Eciton burchellii and Eciton hamatum). We collected ant workers and samples of snake flesh into 70 percent ethanol. During raid 2 on 1
  October 2003 at 1205 h, during a brief rain shower, our attention was
  drawn by rustling sounds in the leaf litter on a slope in a partially
  cleared area of terra firme forest adjacent to the station buildings.
  A subterranean column of C. andicola workers erupted from the soil
  in pursuit of a fleeing giant earthworm (possibly a species in the
  genus Martiodrilus: Zicsi 1990). Several hundred ant workers emerged
  from the soil and ran over the leaf litter in the direction taken by
  the worm. Five C. andicola workers mounted the worm and were biting
  and apparently stinging its body. After the worm crawled for a
  distance of 3 m down slope from where it exited the soil, its body
  contracted from over 40 cm in length to approximately 20 cm in length.
  The worm abruptly stopped moving and became rigid on the soil surface
  within 10 sec of exiting the soil, and was then unresponsive to human
  touch. We assumed that the worm was either paralyzed or dead. We
  lifted the worm to examine it, and we collected ant workers from its
  body and from the raid column as it arrived where the worm came to
  rest. Workers collected from both raids had no prey (other than snake
  flesh at raid 1) in their mandibles.

However, most army ants are (fortunately) not predators of large animals. This appeared to be the only unambiguous literature reference of predation of large animals by eusocial insects that I could find in a brief literature search.

Sigh. Okay yeah, that sounds like what I was expecting. No hornet ham-hives, though? I guess the obvious follow-up question is: How can we kill them all? I guess we should really just migrate into space and then nuke the entire horrible planet to be sure.... Do we have enough nukes? Do we need more nukes? Maybe we could just fling it into the sun, to be sure...

@Owen_R Actually, despite the fact that they can prey on animals much larger than themselves, many army ants are themselves preyed upon. For example, driver ants are often eaten by chimpanzees

That joking aside, though, I still feel like it should be surprising that this isn't a more prevalent strategy. The lack of ham-hornets seems like it needs an explanation, ya know?

Also, I find myself focusing in more and more now on this idea of "ham-hornets", and I think there are actually good theoretical reasons to focus on it. Flying hornets would be particularly effective at attacking a rabbit~deer, since they can attack from all directions and are so individually manoeuvrable. That is, it's a lot easier to imagine escaping from a swarm of ants crawling up your leg than a swarm of hornets flying all around you. So it seems like it should be additionally surprising that we have reports of ants acting like that but not hornets. What might be preventing ham-hornets?

Army ants have been reported to kill and butcher animals that were unable to get away - babies in cradles, tied up goats, etc. Speed of killing really does seem to be the issue here.
Japanese tiger hornets are huge, have a potent venom, and inject a lot of it, which kills dozens of humans every year... eventually. But because it's slow-acting, they don't use their sting for hunting, just for defense. For hunting, they use their mandibles, and bite the heads off stuff.
Some hunter wasps can paralyze smaller prey, which would give more time for killing, but they can't paralyze anything big.


text:
Why are sight and sound prerequisites for intelligence?
Edward O. Wilson, in The Diversity of Life wrote (emphasis mine):

Ninety-nine percent of the animals find their way by chemical trails.  […]
Animals are masters of this chemical channel, where we are
idiots. But we are geniuses of the audiovisual channel, equaled in
this modality only by a few odd groups (whales, monkeys, birds). So we
wait for dawn, while they wait for the fall of darkness; and because
sight and sound are the evolutionary prerequisites of intelligence, we
alone have come to reflect on such matters […]

I'm getting this from an anthology (Dawkins' "Modern Science Writing") so I don't see how Wilson supports this statement, and my google-fu is bringin up nothing relevant-seeming.
My question is: why are sight and sound prerequisites for a species to evolve intelligence?

To answer your question, we must first ask the question What is defined as intelligence?
A googling will tell you that most people believe intelligence to be something related to apes or even more conservatively to humans. But, I find this to be a bit unpragmatic. The closest level of abstraction I find towards defining intelligence is this wiki on Animal Cognition. Having said so, I personally would define intelligence on a much more abstract level.
Intelligence can be broadly defined as a learned response towards an external stimulus, providing the organism with an increased fitness/survival within it's ecosystem.
So Intelligence can be broken down into two parts

Memory of a stimulus
A programmed response towards that stimulus

This is a very famous video showcasing intelligence in the animal world; Crow Intelligence test
But My objective is to state that sight and sound are are not at all prerequisites of intelligence.
This paper from way back in 2014 is I think the best that I can state
Memory and Fitness Optimization of Bacteria under Fluctuating Environments
In this particular paper the authors test the capacity of E coli to produce a response within fluctuating environments, and they find that as the generations progress the later generations take lesser time to produce a response towards the stimulus. They also note that what happens if the prior external environmental state is restored. In such a case later generations become optimised for that particular state.
This is a very good example of memory which is stored at the level of DNA, and a level of intelligence is manifested in a microbial system. So therefore, can you really state that "sight- and sound" are pre-requisites of intelligence. I would say No They are not, that would be an over-simplistic way of what intelligence really is.

He may be referring to the fact that many nocturnal animals wait for the cover of darkness to be able to get their food safely or in order to cloak themselves to approach their prey better. However, this seems to be a matter of personal opinion. He wants you to think that we are smarter because we have to hide and hunt in broad daylight. I haven't been able to support his theory as bats can be considered very intelligent - and they primarily hunt at night.
In fact, we also consider dogs - and their wolf counterparts - to be intelligent as well, and you typically only see wolves at night.
Also, studies are showing that humans who are "Night Owls" are smarter than people who are "Morning Larks" according to a study in Psychology.
If you're interested in different kinds of behaviours and how intelligent they are you can look at BBC Animal Adaptations, which has a really cool list of what abilities each animal has split into categories. Particularly, they have an "Animal Intelligence" section which goes into detail about particular behaviours humans consider to be signs of intelligence. Personally, I think their list is a little out of date - where it is missing a few animals - but by their standards, many of the nocturnal animals have not made it onto the list.
A reason that hearing could be a prerequisite for intelligence is that communication is considered to be a HUGE part of intelligent behaviour. Tool use could be a reason that sight is considered a prerequisite for being intelligent. Really, the five senses (sight, hearing, touch, taste and smell) allow us to really take in the world and adapt to it properly. Sight, hearing and smell typically allow us to be warned of dangers but the fact is that we have to be intelligent enough to know what to do with the information.

Summary: Intelligence can be measured in many different ways. Edward O. Wilson could have been looking at a number of different things when he came to his conclusion (where sight and sound were required for intelligent beings). The truth is that it is all speculative.

If you judge a fish's intelligence by its ability to climb a tree, it will grow up thinking that it's stupid.

Subsequently if you judge my intelligence by my ability to spell, I will also go on thinking I'm stupid ;)

I have not judged you by your ability to spell English words, I have merely corrected them.

With all due respect to Dr. Wilson, this is just an anthropocentric, post hoc ergo propter hoc logical fallacy. Dr. Wilson looked around the world we live in, saw that most intelligent creatures navigate by sight and/or sound and concluded that those sense are a prerequisite for intelligence. I see absolutely no evidence to support this theory.
First of all, that is a classic fallacy. It is the equivalent of a 17th century European going to Africa and concluding that having pinkish skin is a prerequisite for the development of technology. Or if I were to go to Japan and conclude that having an epicanthic fold is a prerequisite for making good sushi.
The fact that the paths chosen by the evolutionary process on this planet are skewed towards sight and sound for more intelligent species does not in any way imply that those senses are needed for intelligence. What is needed are ways of detecting and reacting to the environment as quickly as possible. Light and sound are indeed particularly well suited for this since they travel several orders of magnitude faster than chemical diffusion. That's a good reason to conclude they might have given a selective advantage to the species relying on those two waves to detect their predators or prey.
There are, however, other options. Radar (bats) and sonar (dolphins) can be thought of as sight (or hearing) but are quite different. They both involve the emission of a wave and analysis of what is reflected back. Sight involves the analysis of light emitted by the sun and reflected by the environment. Being able to use your own body to emit the energy needed for your perception would seem to be a huge advantage. Our wonderful sight only works half of the time.
You could also, conceivably, have very fast perception based on things like:

Quantum entanglement; actually faster than light.
Magnetoception;
Electrolocation;
Gravity;

Some of the above already exist in species on this planet, others do not. Admittedly, using quantum entanglement would be kind of tricky. On the other hand, I see no reason why tiny disturbances in the gravitic field could not be detected just as tiny disturbances in the electromagnetic fields are by animals like sharks and cockroaches.
The main point of all this is that the fact that intelligent animals on this planet tend to do X does not in any way imply that X is a prerequisite for intelligence. Quite frankly, I expected better of someone like Dr. Wilson than such baseless speculation presented as fact.


text:
How long does conception take?
I know that conception is a multi-step process. A sperm fuses with an egg. Its contents diffuse into the cytoplasm.
Dad's DNA is transported to the nucleus. Proteins are gradually made from Dad's DNA. Do we know how long that process takes?
I'm most curious about conception in humans, but information about other species is welcome too.
EDIT:  The time I'm interested in is between the fusing of sperm and egg, and the first transcription of the newly incorporated paternal DNA within the zygote's nucleus. However, if conception is better defined by different events, feel free to correct me. I'm far from a specialist in the subject.

Can you define exactly which timespan you're interested in? Ejaculation to DNA entering nucleus? Sperm contacting egg to DNA nuclear entry? Some point until the first cell division? Please [edit] your question to clarify it, otherwise it is rather unclear.

Done. I figured there might be a research project somewhere that dealt with early embryonic growth, so I guess I was pretty general.

There is research showing that spermatozoa contain a number of RNA species, including mRNA, so theoretically translation could begin almost immediately. The Wikipedia articles on human fertilization and fertilization in general contain lots of other information, if you haven't read them already. Unfortunately, there's nothing in them about timing that I could find. I'm sure it's out there, though.


text:
Can the liver prioritize it's metabolizing potential?
Let's assume we have two toxins - one of which is routinely metabolized by the liver, and the other is new to the organism (consider for example alcohol in a heavy drinker and any other drug that is taken for the first time) and they are administered at once.
Does the liver have any way to prioritize metabolizing either of these substances or does it happen simultaneously for both?

Liver contains thousands of enzymes, thus you should be more specific about the substances you want to compare. If the substances have similar affinity to the specific enzymes their interaction will be equally competitive, otherwise the winner will be the substance with the greater affinity to the most of "receptors" and enzymes.

Aside from "toxins", the liver metabolizes a host of endogenous and exogenous compounds. Endogenous compounds are compounds that are normally present and produced within the body like ammonia and estrogens for example. Exogenous compounds are those like ethanol/alcohol, acetaminophen, and other drugs/etc that are not normally in the body but rather we take a mediations or recreational drugs, etc. Most of the compounds that the liver metabolizes are through a set of enzymes called the cytochrome P450 system, which includes numerous enzymes (too many to list here) that catalyze a number of reactions that help detoxify a substance and/or make it more likely to be excreted in the urine by the kidneys.
If the liver "sees" old and new compounds it doesn't differentiate between which it might metabolize first - that is based on concentrations within the liver. In fact, only if the compounds are metabolized by the same liver enzymes will they compete with one another. If they are metabolized by the same exact P450 enzymes, then the concentrations of each of these substances within the hepatocytes (liver cells) will determine which one gets metabolized more frequently. For example, if the concentration of substance A is much, much higher than substance B, then substance A is going to outcompete the other substance for the enzymes that metabolize it (similar to competitive inhibition in biochemistry). Most of the time, endogenous and exogenous compounds do not necessarily compete at the same P450 enzymes because there are so many different P450 enzymes within the liver.
The liver does not have any way of prioritizing different compounds, however, if the liver is exposed to a particular substance over a long amount of time then it may express more of a particular cytochrome P450 enzyme that metabolizes that particular substance. This is similar to alcoholics being able to metabolize a lot more alcohol than someone who has never drank alcohol previously.


text:
Are low-intensity radio-waves carcinogenic?
A recent review article, Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation reached a surprising conclusion

our analysis demonstrates that low-intensity RFR [Radio Frequency Radiation] is an expressive oxidative agent for living cells with a high pathogenic potential and that the oxidative stress induced by RFR exposure should be recognized as one of the primary mechanisms of the biological activity of this kind of radiation.

They suggest the oxidative stress can cause cancer and non-cancer pathologies.
This study has received next to no media coverage. With RFR impacting so many people it makes me wonder, is this study valid? I would expect this to be front page news given the large number of studies reviewed.
Are low-intensity radio-waves carcinogenic?

I seriously doubt it, and there are a number of meta studies which support this. However, I will take a look at this study next week, when I have access to it.

A lot of processes generate oxidative stress: infection, digestion (metabolism), etc which are fairly common. The free radicals generated by ionizing radiations are different from the usual ROS.

This study has received next to no media coverage. With RFR impacting so many people it makes me wonder, is this study valid?

Well first of all, lets be clear: that is not a study.  Its a review article, basically a paper that summarizes a series of studies published.  The review itself isn't valid or invalid necessarily, it simply takes a series of papers (which may or may not be correct or relevant) and then summarizes them.
As for validity, that is a summary of a lot of obscure papers on mechanisms by which RF fields could interact with cells, rats or in a few cases plants.  Its hard to say if the conclusions are valid, but selecting a few papers at random, they are mostly very obscure journals and many report very specialized measurements that are far removed from demonstrating carcinogenic effects in humans.  Its difficult to draw conclusions that are relevant to human health from that, although it does seem plausible that low frequency fields could have a measureable effect on cells or even rats.

Are low-intensity radio-waves carcinogenic?

Assuming you mean in people, that is a hard question to answer, and not the right question given a review article that does not address effects in people.  A better place to look may be this review article:
Carcinogenicity of radiofrequency electromagnetic fields
published in The Lancet and addressing evidence of carcinogenicity in humans.  To summarize:

The Working Group concluded that there is “limited evidence in humans” for the carcinogenicity of RF-EMF, based on positive associations between glioma and acoustic neuroma and exposure to RF-EMF from wireless phones. A few members of the Working Group considered the current evidence in humans “inadequate”. In their opinion there was inconsistency between the two case-control studies and a lack of an exposure-response relationship in the INTERPHONE study results; no increase in rates of glioma or acoustic neuroma was seen in the Danish cohort study,4 and up to now, reported time trends in incidence rates of glioma have not shown a parallel to temporal trends in mobile phone use.
The Working Group reviewed more than 40 studies that assessed the carcinogenicity of RF-EMF in rodents, including seven 2-year cancer bioassays. Exposures included 2450 MHz RF-EMF and various RF-EMF that simulated emissions from mobile phones. None of the chronic bioassays showed an increased incidence of any tumour type in tissues or organs of animals exposed to RF-EMF for 2 years. An increased total number of malignant tumours was found in RF-EMF-exposed animals in one of the seven chronic bioassays. Increased cancer incidence in exposed animals was noted in two of 12 studies with tumour-prone animals12 and 13 and in one of 18 studies using initiation-promotion protocols.14 Four of six co-carcinogenesis studies showed increased cancer incidence after exposure to RF-EMF in combination with a known carcinogen; however, the predictive value of this type of study for human cancer is unknown. Overall, the Working Group concluded that there is “limited evidence” in experimental animals for the carcinogenicity of RF-EMF.

Note that cancers that people theorize to be associated with exposure to nonionizing EM fields tend to be extremely rare, meaning that studying them is very difficult.  This leads to a lot of uncertainty, because one must try to correlate very rare events with environmental effects. Therefore "limited evidence" does not mean "no", it just means that the effect is hard to measure and may or may not be significant given what we know.


text:
Do the enzymes and compounds in saliva help with stain removal?
Does spitting on stains help with removal?
Saliva is high in amylase that should help with the breakdown of protein rich stains like blood and semen. It also contains antimicrobial enzymes and antibacterial compounds. Does semen contain any kind of surfactant agents?
So, my questions are:
Does spitting on a semen stain aid in or add to the cleanup?
On which stains are saliva beneficial and how long does it have to sit?

Why spit when you could just use soap and water?

Amylase doesn't break down proteins. It breaks down amylopectin -- a type of starch (sugar) molecule. Proteins are broken down by proteases (not found in saliva or semen), and many available stain removers use proteases.

@MCM Why don't you make this into a real answer?

As a chemist, I understand the amylase enzyme comment. Amylase in our mouth does help break down sugar compounds. However, there are other components in our saliva such as acids that could help in the removal of stains as well as water or sodium. I found that saliva helps with grease stains due to the sodium component within saliva, as saliva contains more than just the enzyme amylase.

It would depend on the stain - and more specifically the material and staining agent. Saliva contains blood clotting agents so I doubt it would help with removing blood stains. The enzymes in saliva are unlikely to help with the stain removal.
The water in saliva would be more likely to help, dissolving the stain. So your probably better off with water.

I've been spitting on anything red (
of biological origin (blood, wine, ketchup) for decades and seeing the stains dissolve and disappear like magic.
Spit on it generously, let it soak for a few seconds, rub it in with your fingernails; see it disappear.

do you have any biological explanation for your observation? Can you add any credible sources to back up what you're saying?

@Chris Observation is senior to theory. Not the other way around. You can easily perform the test and reproduce the results.
Having a somewhat bad case of psoriasis, I regularly deal with dried blood stains in bed sheets (the plaques break during the night, smearing blood on the sheets, which then dries by the morning). The saliva trick does work to a remarkable extent, pure water doesn't. The phenomenon is easy to observe and replicate.
I always assumed this was a well understood issue, but if not, it could be one of those "oh, that's funny..." observations that science thrives on.

Just did this and it worked. On a fresh curry stain which is notoriously difficult to remove. The guys acting like experts in the previous posts are just wrong. Not sure if it's the enzymes, the water or some other substance contained in our saliva, but it works like magic. Apply generous amount of saliva, let it soak for a couple mins and scrap vigorously with your fingernail. Stain disappears like magic.

Do you have any biological explanation for your observation? Can you add any credible sources to back up what you're saying?


text:
Does your iris color have an effect on your vision?
I've always wondered if having different iris colors, (eye colors) may have any advantages or disadvantages on ones vision. Specifically regarding the effects of light.
Personally, I have troubles being out in the bright sun without sunglasses. My girlfriend on the other hand does not share this issue. Coincedentally my eyes are a light blue and hers are brown. After realizing this, I began to notice a trend when it comes to blue eyed people having this same issue.
So, on a bright day, does a person with blue eyes have a higher sensitivity to the light than their darker counterparts?  Thank you.

I don't have time to do proper research and give a nice answer, but here is an answer from an unverified source. By unverified I mean I didn't check the credentials. It seems like a pretty good answer though.

@SolarLunix "when melanin develops, it creates a protective filter that reflects the light back out of the eye"??? REFLECTS?

@Ilan it's the same principle that makes the sky look blue from what I understand.

Firstly, note that "eye color" is actually iris color.
The person with a lighter iris will have more straylight compared to person with brown iris:

The graph represents Intraocular straylight of the age-matched groups. Participants with light-blue-colored iris showed significantly higher values for intraocular straylight than those of the other groups.

Persons with light-blue-colored eyes have significant higher IOSL
  (intraocular straylight)
  values than persons with darker-colored irises (blue-grey,
  green-hazel, and brown). Light-blue-colored eyes had 0.07 to 0.08 log
  units higher IOSL values, which is an increase by a factor of 1.2. In
  regard to CS (contrast sensitivity), subjects with light-blue iris color showed also lower CS
  values than subjects with other iris color.

Edit: The study concluded that in people with blue irises, IOSL was significantly higher. Although IOSL did not affect best-corrected visual acuity (e.g. visual function based on a standard letter chart test at the optometrist), it did affect contrast acuity, meaning that folks with blue eyes had more difficulty assessing contrast differences (e.g., telling apart two grays with a slightly different brightness).
Christian Nischler & al. Iris color and visual functions. Graefes Arch Clin Exp Ophthalmol (2013) 251:195–202.

Thanks for the answer!  Seems like a fair study aswell. All european participants but other than that I would say pretty unbiased. Also, appreciate the iris tip aswell, not always on my "A" game when it comes to adding proper jargon.

Too bad though... kinda wish the study would have come to a more neutral conclusion. Guess light blue eyes aren't so great after all...

I added the functional consequence of straylight. +1


text:
What is variation in Speciation
I read a lot about speciation. To my knowledge, a species is often defined as a group of individuals that actually or potentially interbreed in nature and produce fertile offspring. Speciation is a lineage-splitting event that produces two or more separate species.
Now, some creationists claim that there is no speciation, rather variation in the same species. As in "fruit fly experiment", I read that two groups of fruit flies don't interbreed after the evolution and speciation takes place. As per the definition of species (biological concept of species), they are supposed to be two separate species (reproductive isolation). Nevertheless, creationist claim they are still fruit flies and there is no speciation. They say that's just a variation in fruit flies, not speciation. I can't understand their claim.

Voting to close because this is a question of semantics. You both observe the same phenomenon and are arguing over which word to describe it. Whether you call it speciation or variation, the event still happened.

you should probably go to reddit with this question - they are more focused on handling such questions and dealing with the interface of the general public with science there.

@canadianer variation and speciation have different meanings. Tanvir, you should clarify where you have actually seen this usage; it would be easy for us to check the authenticity of the reference. Basically, variation is a general term to describe genetic and phenotypic variability whereas speciation, as you have indicated, has additional constraints.

@WYSIWYG Even after re-reading the question, I can't quite remember what point I was trying to make, but you've certainly missed it ;)

You are asking explanations about a creationist argument. One could provide explanations about some hypothesis that you may found in a science paper but not explanations for a creationist argument just because, by definition, a creationist argument is not supported by any evidence and logical thoughts. However, you may want to link to a creationist website making a specific claim of interest and we may eventually talk about whether the claim is wrong/misleading. It would be very handy to have the claim in quotes rather than an explanation of what the claim is.
You say

[..] after the evolution and speciation [..]

This piece of sentence sounds weird. You could say after the evolution of something (meaning the appearance of this something through evolutionary processes that are mutations, natural selection, drift and eventually others) but just "after the evolution" sounds as if evolution may not exist during some periods of time.
Talking about speciation in fruit flies, you will likely be interested in reading this post.
UPDATE
In general, when talking about fruit flies we talk about the Tephriditae. Tephriditae is a family of flies which contain about 5000 described species (including the model organism Drosophila melanogaster).
So, there is definitely different species of fruit flies. Of course, within any population (to the exception of populations of exact clones by definition), you have variation. This variation is a key concept in evolutionary biology. If this is unclear to you you may want to learn a bit more about evolutionary biology, including the concept of heritability ($h_N=\frac{V_A}{V_P}$).
Speciation took place in Tephriditae (otherwise we wouldn't have the species we have today) and is still taking place. The post I linked above gives an example of speciation between lineages of Drosophila melanogaster that has been directly observed in the labs.
Your issue seems to likely be a semantic one. As there is variation within a lineage and this variation is associated with groups that are in reproductive isolation, then the two lineages you consider do not belong to the same species anymore. Therefore, there was a speciation event.

Actually, I do belive in evolution and I m an atheist. When I raised the fruit flies case to a creationist , he said, they are still fruit flies and there is no speciation. He said thats just a VARIATION in fruit flies, not speciation. But I cant find any logic there. IS IT SO ? He alwasy links VARIATION to SPECIATION case. HE says there is never SPECIATION taking place, its just a VARIATION in the same species.

I added an UPDATE to my answer. Let me know if this answers your question.

Thnk u very much. I m grateful. I got the same understanding as u mentioned. But I think creationists dont know the meaning of species.
One more thing, he said, he doesnt want to talk about insects in this context, since it creates some problems , such as- 1.Anachronism 2. Grandfather Paradox . What are they, How on earth are they related to speciation ?

I never heard of the concept of anachronism in evolutionary biology and the grandfather paradox is related to time travel, so it definitely has nothing to do with evolutionary biology.

He said- The slow changes in traits in organisms taking tens of thousands of years to yield a visible change in variation as you suggest, does eventually trap yourself in to a problem of "Time Riddle" - you just dont have enormous enough of time at hand for all these species to come into being. A quick average time calculation suggests that you should have a new species come into being every 15-20 yrs [just rough average time estimation suggests that in about 1 billion yrs ~50 million distinct species evolved]. Don't just start with punctured equilibrium now. You just cannot have it both ways.


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Can plants feel pain?
I was wondering whether plants could feel pain, for example, does grass feel pain when you mow the lawn? Or do the plants and trees that grow vegetables and fruits feel pain when you harvest them?
The internet is very vague about it. There are several articles on the internet, but they just say that plants do not feel pain, they only send out a chemical substance. Others say that almost all multicellular organisms feel pain, because pain is defined as any signal of having impaired tissue.
I think that plants can't feel pain because they have no nerves or central nervous system. However I'm not sure whether this means that plants can't feel pain.
Since the question is clear when pain is defined as any signal of having impaired tissue, I think it would be more interesting in the case that pain is defined as actual discomfort, like humans and animals (maybe it should be restricted to Eumetazoa) feel it.

You'll have to define what you mean by "pain". If you define it as "a signal informing the organism of damage", then yes, they do. If you refer to pain as your or I would feel it, that's a different matter.

Welcome to Biology.SE. The whole issue is around the definition of pain. Tell us what pain is and we'll tell whether plants do have this sensation. I am voting to close as primarily-opinion based.

@terdon I have added the definition.

@Remi.b I've added a definition of pain, but I'm unsure what you mean by primarily-opinion based. Can you clarify?

@wythagoras the Stack Exchange network of sites (to which this site belongs) doesn't do opinion. We're "just the facts, ma'am". A question where multiple answers are valid ("What's your favorite flower") is a bad fit for this site and will be closed as "primarily opinion based". For more on the type of question we deal with, see http://biology.stackexchange.com/help/dont-ask

@terdon No, I mean: Why is this question primarily-opinion based?

I think @Remi.b meant that it was, when it lacked a definition of pain. Now, it's just virtually impossible to answer :). Can anything with no CNS feel pain? Perhaps not but everything alive (just about, and including plants) will try to move away from harm. Does that mean they feel pain?

see here for some more: http://biology.stackexchange.com/questions/29776/how-can-we-know-or-measure-pain-in-animals/29803#29803

I am not quite sure the close vote "primarily-opinion based" is a good fit to this specific case. I definitely meant that the whole question circles around what you mean by pain. It is like asking "is a squirrel a big animal?", it depends on what you mean by big.

You suggest to define pain as any signal of having impaired tissue. This seems like a perfectly valid definition to me. It seems a bit counter-intuitive but it is valid. I'd suggest to restrict your last paragraph to this specific discussion instead and to get rid of the term pain to say "sensing impaired tissue" instead. It might interest you to open a post on Philosophy.SE to ask for definitions of pain that would be easily apply to any living things.

I think before discussing "pain", we'd probably have to discuss whether plants actually can "feel".
This is also down to how one wants to define this (hence "opinion based"), but I assume most people (?) would equal the lack of a brain/neurons with the lack of the capability to feel. And I presume so do you, as you show by using the tag "neuroscience".
In which case the answer to your question "Can plants feel pain?" is "no", regardless of whether plants react to damage through the release of chemicals or not, and whether one would like to classify this as "pain" or not.


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How does being afraid or nervous affect mental performance?
It's known that when somebody is not relaxed (nervous,worried....) , they can't concentrate , what exactly in being nervous is the problem?

I will try using logic, but that might only just get you on a lead:

Concentration means being focused on a specific task.
Consciously, you want to focus on a specific task, but there are other process that may want to claim ressources and that you cannot repress.
Anxiety, but also fear or worriness are symptoms that basically translate an unconscious (or conscious) proccess that requires your attention.
Therefore, two concurrent psychological process require focus from your conscious mind. Ergo, you cannot concentrate on either on them. Usually, the emotional part will win since it involves brain structure (such as the amygdala) that are specialized in shunting more evolved brain structures. That is when you are afraid of something, it is very hard to repress that feeling with logical thinking.
In psychoanalysis, Freud introduced something called as "The pleasure principle" (I hope that's a good translation). This principle is one of the few basic principles that rule human behavior. Now, anxiety is an indicator of displeasure. Your mind will try its best to settle that issue before settling anything else. That is why usually you cannot isolate anxiety.

Here's an example:
You hate spiders. You need to measure the surface of an old mannor. You've seen some spider webs. Odds are you will have much trouble to concentrate on measuring any room's surface, because one task your brain will perform for you is checking in every corner whether a spider can be seen, so you'll be able to identify a potential threath as soon as possible and react appropriatly (usually, get the hell out of there if you're really affraid of spiders.
Here's another example that doesn't use fear:
Your girlfriend texted you before an exam, and she said "We need to talk". Since you are emotionnaly bound to your girlfriend, you might get anxious: what does she want to talk about ? Your mind will begin scanning for every possibility, emphasizing on the worse ones (the ones that will disturb the "Pleasure principle" the most for instance). Now that you identified that she might break up with you, this thought will just keep popping up, even if you manage to think for a minute about the exam you should be thinking about right now.
Fact is this is a matter of autoconservation for your psychee. A breakup will certainly harm you more than a failed exam. Your brain is very smart about processing important stuff before, and any attempt from your conscious mind to shunt this will most probably fail.
By the way, there is a psychology stackoverflow. I guess you should have posted this question there.
Hope this helped !


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Is nuclear DNA immuno-privileged?
It is well known that if DNA occurs in the cytoplasm of eukaryotic cells, an immune response may be triggered through a myriad of DNA receptors and pathways as part of the immuno response. Yet, apparently the nuclear DNA does not induce any type of such response. Is it known why this happens? Is it just due to the fact that the nuclear DNA is immuno-privileged?

comment on the edit: exogenous DNA its not restricted to viral origin alone, it can occur by prokaryotic invasion as well, for example.

Was just trying to improve wording - please feel free to roll back. You mentioned the viral stuff in your original question.

Also - isn't it so that eukaryotic DNA released from cells is immunogenic in its original host? I.e., is your question valid?

I dont get the point. "eukaryotic DNA that comes from the nucleus is immunogenic", is it? lets assume it is, why would that make my question ilegitimable?, genomic fragmented DNA pieces will be retained in the cytopalsm after nuclear envelope breakdown in mitosis, so thus the nucleus would be cleaned and we are thereby talking again about cytoplasmc DNA response, which I already introduced in the question. I really dont see your point. Do you maybe refer that this putative immuno response happens already in the nucleus even before nuclear env. breakdown? I think thats a key point if so

do viral DNA INSIDE the nucleus induce any response? if so, why not genomic DNA?

You introduced "cytoplasmic DNA response" in your question. Would the following  somehow reformulate your question:  "How does the cell know whether DNA/RNA in the cytoplasm must be translated for binding and immunogenic presentation by MHCl or, alternatively, be bound by Pattern Recognition Receptors (PRR, see answer given) to trigger some inflammatory pathway?"?

Pattern recognition receptors (PRRs) can potentially discriminate between endogenous and exogenous DNA:

Microbial nucleic acids can be discriminated from self nucleic acids using various parameters, such as their sequence, their tertiary structure, their molecular modifications and their localization. In addition, mislocalized DNA and RNA can be an indicator of cellular damage and infection. [1]

and

Microbial nucleic acids are discriminated from self nucleic acids based on different parameters, such as their sequence, structure, molecular modifications and localization. On the other hand, mislocalized self nucleic acids — such as extranuclear DNA or extracellular RNA — can be recognized as DAMPs, probably because they are reliable indicators of cellular damage. [2]

Somewhat suspect is the similarity of those quotes; I only link to both reviews so as to include both in the references for further reading.
Distinguishing by sequence and structure are self-explanatory. Molecular modifications could include unmethylated CpG sites which are more common in bacterial and viral genomes and are recognized by TLR9. [3] Mislocalized DNA means any that is found outside the nucleus, which is a sign of damage or infection. Most of the well-studied nucleic-acid-recognizing PRRs are found outside the nucleus: TLRs are constrained to endosomes and the extracellular environment while RLRs are found in the cytoplasm. The as of yet identified DNA sensors like DAI also seem to localize to the cytoplasm. Extranuclear PRRs do not necessarily need to discriminate between endogenous and exogenous DNA: any that they sense is mislocalized. However, at least one dsDNA-recognizing PRR, IFI16, localizes to the nucleus as well as the cytoplasm, where it can recognize viral dsDNA. [4]

It has been assumed that cells distinguish viral from cellular DNA due to the former's presence in the cytosol. However, … Kerur et al. (2011) propose that the DNA genome of Kaposi's sarcoma-associated herpesvirus (KSHV) is recognized inside the nucleus by the DNA sensor IFI16, leading [to] inflammasome activation. [5]

IFI16 apparently distinguishes exogenous from endogenous DNA by its length. [6]

Endogenous DNA is present in vivo as chromatin and the amount of exposed linker DNA between histones is too short to promote the cooperative binding and oligomerization that IFI16 requires for signalling (B). An older model, where IFI16 binds independently, is also shown (A), but it suggests that IFI16 should bind self-DNA and doesn't fit with experimental results.
That is just one specific example of how a PRR can distinguish self from non-self. DNA sensors actually seem to be on the cutting edge of research into the innate immune system and, as such, the complete picture has yet to be determined.

References:

Broz P, Monack DM. 2013. Newly described pattern recognition receptors team up against intracellular pathogens. Nat Rev Immunol 13(8):551-565.
Desmet CJ, Ishii KJ. 2012. Nucleic acid sensing at the interface between innate and adaptive immunity in vaccination. Nat Rev Immunol 12(7):479-491.
Yoneyama M, Fujita T. 2010. Recognition of viral nucleic acids in innate immunity. Rev Med Virol 20(1):4-22.
Kerur N, Veettil MV, Sharma-Walia N, Bottero V, Sadagopan S, Otageri P, Chandran B. 2011. IFI16 Acts as a Nuclear Pathogen Sensor to Induce the Inflammasome in Response to Kaposi Sarcoma-Associated Herpesvirus Infection. Cell Host Microbe 9(5):363-375.
Unterholzner L, Bowie AG. 2011. Innate DNA Sensing Moves to the Nucleus (comment on Kerur et al., 2011). Cell Host Microbe 9(5):351-353.
Morrone SR, Wang T, Constantoulakis LM, Hooy RM, Delannoy MJ, Sohn J. 2014. Cooperative assembly of IFI16 filaments on dsDNA provides insights into host defense strategy. PNAS 111(1):62-67.

+1 But what about eukaryotic microbes? They have nucleosome wrapped DNA

@WYSIWYG Thanks. That's a good point, but IFI16 is just one example that I happened to find; there are apparently other ways to distinguish between self and non-self DNA. Also, while DNA viruses and retroviruses necessarily spend part of their life cycle in the nucleus, I don't know that cellular microbes do. Are they just constrained to endosomes?

@canadianer badass answer

@Katz I thought so too…


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What is the spacing between stop codon and transcription terminator?
When one tries to express a protein from a synthetic plasmid in E. coli, how many base pairs should there be between stop codon and the transcription terminator site?

A related post

In general, there is no need for a spacing between stop codon and terminator. They can be right next to each other.
When transcribed, transcription terminator forms a hairpin-like structure which interacts with the RNA polymerase to stop the transcription. Usually, the upstream sequence will not interact with the terminator and it will be transcribed normally. In a rare case the coding sequence might contain sequences that extend the hairpin and might result in interrupted translation. This can be avoided by doing a thermodynamical inspection of the secondary mRNA structure, but this is usually unnecessary.


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What bacteria do unborn babies contain?
This Scientific American article states that "[human] infestation [by bacteria] begins at birth". This would suggest that unborn babies are free from any bacteria. However, if the mother catches a bacterial infection, her unborn baby risks catching it, too. This would seem to contradict the Scientific American article.
Presumably, when a human egg is fertilized by a sperm, the resulting cell may be free of any bacteria. At some point, bacteria begin to colonize the growing human body. Which bacteria are the earliest to colonize, and at what point in the development cycle does this occur?
In particular: does the health of the foetus depend on the presence of certain bacteria?

"However, if the mother catches a bacterial infection, her unborn baby risks catching it, too." Sorry, I just caught this; I thought you meant perinatal infections. In general, this applies to viruses and a few bacteria/protozoa: Listeria, spirochetes, toxoplasma, etc. However, these are the exception. Your statement makes it sound commonplace. It's not.

related:http://biology.stackexchange.com/questions/44457/do-the-bacteria-from-unborn-babies-have-benifits-on-health?noredirect=1#comment77482_44457

Babies are bacteria-free at birth. The meconium (the first stool) contains no bacteria if secured early enough.

Meconium is a sterile mucilaginous material that accumulates in the fetal intestine and is expelled soon after birth. It contains secretions of intestinal glands, gut constituents (proteins, bile acids, fatty acids, and steroids), and components of amniotic fluid and vernix caseosa.

Bacterial colonization of infants begins at birth - literally. They pick up bacteria from the mother's vaginal canal in passing, which they swallow. This is not seen in infants delivered by C-section. The importance of colonization picked up through normal birth is such, that some hospitals are swabbing the vagina of mothers delivering by CS and colonizing the oropharynx that way.  Breast-milk also contains lactobacilli and bifidobacteria that probably contribute to the initial establishment of the gut flora of newborns.
And, yes, an infection the mother has while delivering must be taken into account. Herpes and Group B strep are both dangerous for a neonate.

The first microbes to colonize the intestines of newborn babies are the aerobic bacteria Escherichia coli and Streptococci. Later, the gut is colonized with anaerobic bacteria, e.g. Bacteroides, Bifidobacteria, and Clostridia. In 1–2 y, the gastrointestinal tract of infants has developed a natural microflora, which resembles the microflora of adults.

The infant continues to pick up bacteria from all people they come into regular contact with, including nurses.

The effect of the maternal flora on the initial gut colonization may be less than expected as the fecal flora of infants started to resemble both the fecal flora of the mother as well as that of the first nurse.
  Breast milk may contain bacteria which colonizes the gut as well

Infants aren't overwhelmed by infection due to the presence of  antimicrobial peptides found on their skin, GI tract, and immunity is conferred via breast milk.

Several AMP have been characterized in vernix and skin of the newborn, indicating a well-developed innate immune system, which may play a pivotal role at the time of postnatal colonization.

Antimicrobial Components of the Neonatal Gut Affected Upon Colonization
Dynamics of gut colonization and source of intestinal flora in healthy newborn infants
Protection of the Neonate by the Innate Immune System of Developing Gut and of Human Milk
Establishment and development of lactic acid bacteria and bifidobacteria microbiota in breast-milk and the infant gut

I have found these articles which contradict what you write: https://www.sciencenews.org/blog/growth-curve/baby%E2%80%99s-first-bacteria-arrive-sooner-we-thought http://symbionticism.blogspot.ca/2013/08/got-moms-bacteria-breaking-silence-on.html http://directorsblog.nih.gov/2014/05/28/not-sterile-after-all-the-placentas-microbiome/

@JamesNewton - I've seen contradictory studies (few) as well. Frankly, I don't think they're enough yet. I read the umbilical cord blood study (not a report of it). I also could cite animal studies. If mammals were born with some bacteria, germ-free mammal lines would be impossible. While I agree that the uterus is not necessarily germ free (and therefor the placenta is also at risk), right now this is a bit new, like Helicobacter pylori as causative of ulcers was. Time (and more research) will tell.

@JamesNewton - Also, I have a lot of contradictory seeming-evidence: The two people born aseptically who survived SCID in an aseptic environment (they had sterile feces), germ-free animal models (as mentioned earlier), and the results of many studies linking bacterial colonization of the uterus with infertility, miscarriages, etc., as well as the results of studies of anmiotic fluid and PROM (premature rupture of membranes) in neonates. Maybe coincidental, but not ready to throw the baby out with the bathwater yet.

@JamesNewton - Finally, there are some who feel the science in that study was poor, and that this aspect was underreported.

In medicine, there's a saying: Be neither first nor last. I've taken that to heart for 30+ years. I don't jump on bandwagons, but am not the last one to try something new. The health of my patients - not my ego - are my primary concern. My favorite role models in medicine (I have a bunch) are Barry Marshall and Robin Warren. That should say something. (P.S. If you have a better answer, please post it.)

Just a note: I have read that baby earthworms inherit the gut microflora (Verminephrobacter sp.) from the mother before they are born.

@WYSIWYG - I cannot speak to earthworm placental function at all. Lots of crazy stuff happens in other kinds of mammals, let alone invertebrates.


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Is there a schema for how human behavior is genetically determined?
It seem one can distinguish three different kinds of genetic determinism of common patterns of human behavior:

behavior that is directly wired into our nervous system, e.g. face-related mirror neurons and chewing,
behavior that is within reach of operand conditioning, i.e. that is predisposed by certain features of our bodies (and environment) and relatively easily discoverable by exploration, e.g. how to throw something,
behavior that is passed on culturally, e.g. tool use.

Does there exist something like this in the literature?

The standard is to group any phenotypic variance such as variance in behaviour in a population as being caused by environmental or genetic variance. I don't have a good understanding about the difference between your two first points. Brain is a predisposed feature of our bodies causing a behaviour.

I think the nature-nurture issue of human behavior is one on which libraries can be filled. Moreover, this question, if 'schema' refers to "organized pattern of thought or behavior that organizes categories of information and the relationships among them" https://en.wikipedia.org/wiki/Schema_(psychology) this Q is better suited for CogSci.SE. However, even there it will likely be closed given the vastness of the topic. I vote to close here. You may, or may have more luck at CogSci.

We can only observe correlations
Let's just talk about statistics. You can see a correlation between two things only if there is variation for these two things. It therefore, make no sense to look at a single trait that has no variance and ask "is it genetically coded?". The only thing that makes sense is to understand what variables explain the observed variance for the trait of interest. Here, in your question, you are interested in behavioural traits. This answer stands for behavioural traits as it stands for any other phenotypic traits.
What variables could explain variance in a given trait?
To make it easy, let's consider only two variables, genetics and environment. In reality, one should consider other variables such as epigenetic for example. The total variance in phenotype that you observe is the result of the addition of the variance of this phenotype that is due to genetics variance ($V_G$) and the variance of this phenotype that is due to environmental variance ($V_E$) and their covariance ($COV_{GE}$). In other words:
$$V_P≈V_E+V_G+COV_{GE}$$
It is very common to express the phenotypic variance as being the sum of the genetic and environmental variances (and some others such as epigenetic variance). However, you are free to make this partitioning as you feel it useful for you.
Let's investigate those variables a bit further
Of course, $V_E$ and $V_G$ can be further decoupled into a sum of variances (and covariances). And you are free to do the decoupling exactly as you want to. For example $V_E$ could be defined as the sum of the phenotypic variance that is due to variance in temperature ($V_T$), the phenotypic variance that is due to variance in water availability ($V_W$) and the phenotypic variance that is due to variance in the culture of the parents ($V_P$) (and all the covariance). $V_E = V_T + V_W + V_P + ... $
Similarly, the genetic variance $V_G$ can be further decoupled. It is standard to decouple this variance in dominance vs additive effects (relating to the genetic architecture underlying the trait) but this won't be of great help to you. How about talking about variance in the genes affecting brain morphology $V_B$ and variance in the genes affecting hormones concentration $V_H$ and their covariance (epistasis and pleiotropy) $V_G = V_B + V_H + ...$.
Common schema
To my knowledge there is no common schema in how to partition those variances for the specific study of the mechanistic of behaviour. I don't really understand what is the partitioning that you're suggesting in your post but I am hoping that this answer can help you to think further and eventually come up with a satisfying schema.

Thank you for this beautiful answer; it helped me to grasp some key concepts. It's quite difficult to understand my schema in terms of generic variance. It seems that it successively plays a less immediate role: Behaviors in (1) are presumably highly correlated with certain genes, in (2) there is more a dependence on the environment and in (3) the behavior depends on embodiment and situatedness.

The code for a fit phenotype is successively outsourced from genetics to memetics. The genetic code still facilitates the common behavioral patterns, but doesn't fully specify those in the latter groups since they require both an environmental and even a sociocultural context in the case of (3). Behaviors in this category are rather developed over generations, while those in (2) are discoverable within a lifetime (mostly before adulthood).