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Does the creation of memory involve mRNAs crossing the synaptic gap?
There is a diagram from a book titled "Teaching with the brain in mind". The diagram shows
The diagram appears to show that the "creation of memory" involves "messages coded by RNA" moving through an axon and being released into the synaptic gap, whereupon they presumably bind to the receptors on the other side of the synapse.
Unfortunately the book does not seem to provide any sources for this and I have not been able to find any sources corroborating this claim. Can anyone provide any references?

The diagram is garbage.  The book's author, Jensen, has a degree in English, not science, and the book is part of the promotion of his workshops on how to teach.

I have never heard of this pathway. Memory is usually assoiciated with synaptic plasticity by ‘Long-term potentiation’ (LTP), which has glutamate as a neurotransmitter. Neuroscience Exploring the brain (Bear, et al,. 2007), has a pretty good explanation of this process, if you're interrested. Motor patterns have more mechanisms than LTP, and are not as well understood.

Neurons have been shown to secrete exosomes (extracellular vesicles containing RNA) which may regulate neighbouring cells. However, this is mechanistically different from synaptic signalling by neurotransmitters. Moreover, I am not sure if exosome secretion is linked with synaptic activity and whether it plays a role in memory formation. Even if exosomal RNAs do have a role, their contribution is likely to be minor, compared to other pathways (such as NMDAR, mGluR, neuropeptides etc) involved in memory formation.

References:

Bahrini, Insaf, et al. "Neuronal exosomes facilitate synaptic pruning by up-regulating complement factors in microglia." Scientific reports 5 (2015).
Bellingham, Shayne A., Bradley M. Coleman, and Andrew F. Hill. "Small RNA deep sequencing reveals a distinct miRNA signature released in exosomes from prion-infected neuronal cells." Nucleic acids research (2012): gks832.
Chivet, Mathilde, et al. "Emerging role of neuronal exosomes in the central nervous system." Front. Physiol. 3 (2012): 145.


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What is inside IDL (intermediate density lipoproteïn)?
I am studying about the endogene lipidcycle in the human body and I know that VLDL (very low density lipoproteïn) is made in the liver and that it contains triglycerides and cholesterol from your food but also made in the body.
Next with that, I know that VLDL brings triglycerides to the adipose tissue (or fat tissue) and to the muscles with help of the LPL (lipoproteïnlipase) just as chylomicrons do.
Enclosed; VLDL will go over to IDL (intermediate density lipoproteïn).
But what is the definition then from IDL exactly?
Is IDL just a smaller lipoproteïn then VLDL and does it only contains a sort of 'leftover' of the triglycerides? Or does it also contains cholesterol?
And if VLDL brings the triglycerides to the muscles and fat tissue, does it only contains triglycerides then? Or does it also carry cholesterol with it? If yes, what happens with the cholesterol then?
Because my book is only telling me about the transport of triglycerides to the fat tissue and muscles, but in the beginning it also says that it carry's cholesterol, and a little further in my book it even tells it can also carry cholesterolesters from HDL...
It's getting confusing...
Hope somebody can tell me what is exactly in all the kinds of lipoproteïns, where the lipoproteïns are all made, and where the products they carry come from, and where they go to. Because my book is being very indistinct.

Which book did you  read...?

"Is IDL just a smaller lipoproteïn then VLDL and does it only contains a sort of 'leftover' of the triglycerides? Or does it also contains cholesterol?" Yes / yes  / yes.

"but in the beginning it also says that it carry's cholesterol, and a little further in my book it even tells it can also carry cholesterolesters from HDL... It's getting confusing..." - The latter emotion is "adequate". From memory I'd say:  IDL turns to LDL by shedding "even more" fatty acids (as it did when it still was VHDL (Berg/Stryer, Biochemistry), and it carries cholesterol, as it becomes LDL remnant, and as such is able to take over  chloesterolesters from HDL (the latter "confusing" in a stricter sense, I guess)

Taken from Fundamentals of Biochemistry (Voet et al. 2013). Note the differences in apolipoproteins between LDL and IDL, as well as the ratio triacylglycerol : cholesteryl esters between VLDL and IDL.

The question is not specific enough to elaborate? Does Voet et al. tell about different fate and function of cholesterol and triacylglyerol? What are the inferences that must be made from the numbers? I mean, any answer should not be restricted to referencing alone...sorry.

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What does vitamin B6 and B12 absorption depend upon?
I'm looking at my question about homocysteine metabolism and am doing a followup inquiry into vitamins B6(Pyroxidine) and B12(Cyanocobalamin). I've found this interesting bit about vitamin B12 and am looking at its implications:

Approximately 56% of a 1 mcg oral dose of vitamin B12 is absorbed, but absorption decreases drastically when the capacity of intrinsic factor is exceeded (at 1–2 mcg of vitamin B12)

Quote from vitamin B12 fact sheet
I'm trying to understand the implications of an intrinsic factor involved in B12 absorption. Lets say that a person gets vitamin B12 from both food and a single supplement pill. Will taking that pill "use up" the absorption factor and prevent food's vitamin B12 from being absorbed over time?
This is the first time I'm hearing of additional "factors" that may limit vitamin absorption in the human body. Is this common across vitamins, or is it B12 specific?
Thank you for your input!

Vitamin B12 (cobalamin) is a water-soluble vitamin required for homocysteine methyltransferase. In order to be absorbed, it must bind to intrinsic factor (IF), which is produced by the parietal cells of the stomach. The absorption of the vitamin B12-IF complex occurs in the terminal ileum (of the small intestine). The quote just means that if there isn't enough IF, then you can't absorb vitamin B12.
There are many things that limit absorption of vitamins, and even vitamin B12. Because vitamin B12 is found in animal products, vegetarians and vegans may need to supplement it. Pernicious anemia is an autoimmune disease that destroys IF or the parietal cells, Gastric bypass surgery can lead to vitamin B12 deficiency. Anything that affects vitamin B12 absorption in the terminal ileum, such as in Crohn's, celiac disease, or enteritis, can lead to deficiency.
To answer your question, no. Yes, it will use some IF (provided you have IF), but that would allow your body to absorb vitamin B12. For people who have diseases mentioned above, they can take vitamin B12 via injections, subligually (under the tongue), or intranasal gels, according to the fact sheet you cited.
Because all the B vitamins and vitamin C are water-soluble, they are easily absorbed through the intestinal wall. Excess amounts are usually excreted in urine. I believe vitamin B12 is the only vitamin that needs to be bound to a factor, due to its larger size. It can be stored in the liver for several years. Fat-soluble vitamins (A, D, E, K) are absorbed with lipids.

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Which eradicated viruses still have remaining stockpiles?
Other than smallpox, I'm curious to know if there are any other stockpiles of eradicated or nearly eradicated viruses, and if so where are they located?
Thank you.

I'm voting to close this question as off-topic because it is not about biology but about social policy.

If you ask this question on the history or politics stack exchange sites, I'll answer it for you ;)

again, I don't think this information would be publicly available in many cases because rogue nations involved in developing biological weapons would likely keep their research a closely guarded secret.

There are only two eradicated viruses, and one "nearly eradicated", and all have known stocks. For the purpose of this question, it's completely irrelevant to talk about "rogue nations"

Only two viruses have been eliminated in the wild to date: Smallpox (humans) and Rinderpeste (cattle). As the question notes, smallpox stocks still exist. So do Rinderpeste stocks; see Identifying and Reducing Remaining Stocks of Rinderpest Virus, which is from 2015, but has no indication that the stocks were to be destroyed in the near future.
The only virus that is "nearly eradicated" is poliovirus (human) and there are still many stocks of polio, although organizations are working on reducing their number ("Toward Eliminating Poliovirus—In the Lab).

Thank you so much for this information--it's exactly what I was looking for for my med school presentation.  Do you also know if there are any established stockpiles for other, non-viral infectious agents that are becoming progressively eradicated (e.g. Plasmodium falciparum, Dracunculus medinensis, Treponema pallidum pertenue)?


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Is the default kmer 25 value in Trinity still ok for assembly of 150bp reads from Illumina HiSeq 2500?
I will soon be receiving Illumina HiSeq 2500 data (150bp PE stranded reads). In the past we have been using Trinity as our assembler of choice, but it uses a default kmer value of 25. I believe this may have been optimal for GAIIx data (35bp) but is it still ok to use such a kmer for 150bp data?
All inputs will be greatly appreciated!
Thanks!

what sequencing are you doing- WGS/RNAseq/... ?

I am doing RNA-seq of multiplexed samples in order to determine differential expression between different samples

I have't used trinity.. I use cufflinks and for longer reads (>50nt) this is not really necessary (by default off in cufflinks for reads >50nt)..

As far as I know, Tophat-cufflinks require a reference, don't they? I am working on a non-model organism so will be doing de novo assembly, hence the use of Trinity. What do you mean is not necessary?

Oh okay.. In that case I cant say. I have some acquaintance with velvet but not trinity. In tophat (I am sorry I said cufflinks) that is used for enhanced prediction for splice junctions.
For de-novo assembly the choice of k-mers should be such that it maximizes your N50 but does't consume a lot of resources. You can see this post

Thanks for the link and your explanation. Yes, resources and N50 maximisation are definitely factors to consider, though probably not the only one. Using only a single kmer value Trinity may be a bit less greedy in resources, making it attractive to use whereas velvet is known to require lots of RAM, hence my initial question ;-)


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How does drug-induced photosensitivity work?
Some drugs (tetracyclines, for instance) can cause photosensitivity reactions—that is, some patients become extremely sensitive to the sun, developing rashes or inflammation after spending time in bright sunlight. Sources I've read describe this as an immune reaction similar to an allergy, but I've also heard that antihistamines are generally ineffective at treating such reactions.
So my question is, what are the biological processes behind this reaction, and how does it differ from a normal skin allergy that could be treated by antihistamines?

Drug induced photosensitivity (DIP) refers to the development of a cutaneous disease in response to the drug chemical in combination with light. Only the drug or light alone cannot cause the reaction and both are required to be present together. The underlying pathophysiology is important clinically to identify the type of cutaneous manifestation the drug-light combo has caused. There are majorly two types of reactions, phototoxic and photoallergic reactions.
Also, the kind of light required depends on the kind of drug and the the wavelength at which it gets photoexcited. Although UV-B is a mojor cause of sunburn, the wavelength required for DIP for most drugs falls in the UV-A part of the spectrum.
Phototoxic reaction
Phototoxic damage refers to the direct damage the photoactivated drug can cause to the tissue. Light leads to excitation of electrons and as they return, they can lead to formation of reactive oxygen species which damage the cell membranes and DNA. This tissue damage leads to activation of proinflammatory cell signal transduction pathways and leads to inflammation in the area. Clinically, it looks like an exaggerated sun burn.
Photoallergic reaction
This is similar to the same old hapten story. A drug which is otherwise non-antigenic turns antigenic after a photoreaction. Most probably, the reaction should have caused the modified drug to bind to cutaneous proteins leading to cell mediated immune reaction. This T-cell mediated inflammatory response usually has an eczematous morphology if the photoallergen is applied topically or the characteristics of a drug eruption if the photoallergen is administered systemically
It is important to differentiate the kind of reaction, a drug would cause.For example, the tetracyclines that you mention are phototoxic but not photoallergic. Photoallergic reactions have far lesser incidence than phototoxic ones.
Coming to the other part of your question, on the treatment, most important is to educate your patient for appropriate photoprotection. If severe, the drug could be withdrawn and switched to a safer one. Treatment includes topical corticosteroids to bring down the inflammation in either reactions. Oral antihistaminics are reported to have limited advantage. Why this is so,I'm afraid, I do not know. Hence your question remains partly answered.
Reference: http://emedicine.medscape.com/article/1049648-treatment

Thanks for the detailed answer. I admit I'm not familiar with some of the terms in your answer but it has shed a lot of light on the topic. It stops just shy of stating why oral antihistamines are not effective, but perhaps that aspect has not been studied thoroughly.


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Identify this Harvestman
I spotted this guy in Switzerland. It's clearly an Opilione (Harvestman), but I really know nearly enough about this diverse group to be able to identify the species.

Sorry, I didn't think to place any reference near it for scale. Can anyone tell me the species or at least the genus? (Bonus points if anyone can guess what it's feeding on)

you smashed the poor guy?

@DevashishDas No of course not; I didn't harm either one. I saw him, took the photo, then moved on.

Sorry, i was just kidding. Anyway, is this is the one? http://www.fcps.edu/islandcreekes/ecology/Arthropods/Harvestman/harvestman.jpg

It could be. The coloration is similar. Can you find another image that more shows back a bit more clearly and cite the species?

It is probably Daddy Longlegs (Leiobunum vittatum)

this invert color image show the resemblance.

Source:
http://www.insectidentification.org/insect-description.asp?identification=Eastern-Harvestman
http://bugguide.net/node/view/840130

Might be eating a cockroach:

UPDATE:
OR
It might be Mitopus morio(modern harvestman)

Thanks for the response. I'm a little skeptical of this identification though. First, in my image, there is a dark stripe down the back behind the eyes, but in yours, the body appears almost entirely dark with light fringes on the side and light joints. Second, several sources claim the distribution of Leiobunum vittatum is limited to North America, but my specimen was from Switzerland. I'll leave the question open for now, but I'll keep looking into it.

@p.s.w.g: I think you are right. But I am pretty sure genus is correct. Look for a species which have two parallel sets of dots on the back in that genus.

Age and sex may be a factor for body color.

Yes, I'm pretty sure it's a Mitopus morio. The coloration and patterning is correct, as well as the distribution.


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What are the main differences between lab-grown tissues and natural tissues from living animals?
What are the main differences between lab-grown tissues and natural tissues from living animals?
Using a biologist's classic "structure (anatomy) and function (physiology)" idea, I thought about the followings:
Structure:

It might be difficult to recreate the composition of different tissues / cells in living things precisely with artificial methods. This may lead to bad results when the tissue is used for tests of medicines and cosmetics.

Function:

Cells might not function and produce as expected (or is harder to make them function) in artificial compositions, as cells need strictly regulated environments to function correctly.

Also, I think using artificial tissues for drug tests helps researchers to avoid ethical issues which may arise if they use living animals instead. I think the cost is generally higher to make artificial tissues than to gather test animals; however I am not sure if this applies to every case - maybe some tissues are relatively cheap to grow in labs.
What are some other differences? The answer can be about the advantages and the disadvantages of making / using lab-grown tissues and using living animals as well.

Does Lab-meat fit in this?

@DevashishDas hmm... I guess yes.

Immortalized cell lines are often cancerous, which has large effects on their gene expression profiles. They also adapt to cell culture conditions after several hundred passages in culture. I've cultured both HepG2 cells and primary mouse hepatocytes. The HepG2 are a hepatocellular carcinoma line and grow fine in culture, while the primary hepatocytes don't really grow in culture and only live for a few days after you extract them from a mouse. We were doing gene transfer assays with both sets of cells. The quickly dividing HepG2 cells were easy to transform using PEI, and while primary hepatocytes could be transformed with PEI, they worked better with calcium phosphate, probably because it was less toxic. I noticed that HepG2 cells were smaller than primary hepatocytes, and the primaries were far more fragile, we could run HepG2 through a peristaltic pump with no problems, but had to handle all the primary cells by hand.
As far as cost goes, tissue culture is almost always cheaper. You can make a bottle of media for a few dollars worth of material and use it for several passages. The cost of running an incubator and biosafety cabinet are also minimal. So unless you're doing something unusual, cell culture is affordable. However, it's an incomplete model at best. Trying to create whole tissues in the lab counts as unusual.
Doing work with animals is far more accurate than cell culture, but much more expensive. Our mice are cheap, but still cost about a dollar each, and about 20 cents a day for housing. A typical biodistribution experiment will use 3 mice per time point and 8 - 10 time points, so 24 to 30 mice assuming no mistakes during dosing. On top of that, doing animal work has a lot more bureaucracy involved, with animal use protocols and approvals and inspections.
The question about whether to use animal models vs cell culture comes down to what you're trying to accomplish. If you're studying gene regulation or protein interactions, cell culture usually works better because it's more amenable to gene transfer and allows you to use techniques like fluorescent fusion proteins and bioconjugation. If you're studying drug metabolism and toxicity you should use whole animals because the interactions between metabolites and specific tissues are hard to reproduce in cell culture. In some far off future we may be able to totally replace animal models with cell culture or even computer models, but we're not even close.

Natural tissue are living at body temperature in homeostasic conditions. They are organized with other tissues and organs.
An incubator at 37 0C incubator, growth factors and medium is added in an artifical culture flask for tissue culture.
There are then primary lines which are derived from humans and cultured exvivo requires careful handling  and secondary cell lines which are established. Secondary cells and tissues can be engineered with addition and deletion of genes. Many labs use. Primary cells then have to authenticated senescence stop dividing if not cancerous. A characterisation  only if there is suspicion of contamination with other lines. Where characterisation of morphology of cells with lesser numbers are present can be visual may be sparse and also when establishing pure culture.


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Is there any relationship between heartbeat rate and life span of an animal?
Is there any relationship between heartbeat rate and life span of an animal?
Do they belong to a cause-and-effect relationship or are they both caused by some phenomenons or a common cause?

After reading a story of a man who was sentenced to hard labour, climbing the equivalent of a few miles of mountain every day on a victorian treadmill for many years, and the fact that he lived to 87 or 90, i think cardio is still a good idea:)

Interestingly there is a inverse negative correlation between heart rate and life span, meaning the faster your heart rate is, the shorter is your lifespan. See this figure (from the paper 2 cited below):

When the authors plotted the approximately total heartbeats vs. the lifespan, the amount of total heartbeats was in a pretty narrow corridor:

So it seems that at least the hearts in mammals have a maximum number of strokes they could do. The obvious question what causes this phenomenon is not really answered.
Since the metabolism of small animals is (compared to their weight) higher and also their oxygen consumption is higher because of that, it is hypothesized that this causes more reactive oxygen species and related damage which subsequently leads to an earlier death.
See the references for more details:

Rest heart rate and life expectancy.
Heart rate, lifespan, and mortality risk
Oxidative damage to DNA: relation to species metabolic rate and life
span

In the second plot, getting a "narrow corridor" on a log scale is hardly a surprise. Also, I'm pretty sure that either or both plots must have some of the species labels mixed up (and they both consistently misspell "hamster"). Of course, neither of those issues necessarily invalidate the general claim that short-lived species tend to have faster heart rates (which, given that both traits correlate with body size, is hardly surprising either), but those are the kind of mistakes that proper peer review and competent editors ought to catch. Honestly, I expected more from an Elsevier journal.

So they are both effects of a faster / slower rate of oxygen intake, am I correct?

I wonder if this is more of secondary correlation with size? In other words both life expectancy and heart rate correlate with animal size.  The human influence can't be ignored for the domestic animals on the chart (dog in particular).

@AtlLED Thats the other thing which can be correlated, see here.

Just to emphasise the point about the "narrow corridor", the entire variation in lifespan shown is covered by just over 1 log (with man pushing that up to maybe 1.5 log), and the variation in heartbeat by around 2 logs. Thus, even with no correlation at all, the metric heart beats per lifespan would be bounded by around a 3 log range, only just less than is shown on that figure.

@AtlLED Yes it could easily be. Both scale allometrically with body mass: heart rate with a negative quarter power ($R \propto W^{-1/4}$), and lifespan with a positive quarter power ($E \propto M^{1/4}$); their product  ($R \cdot E$) therefore scales with $W^0=1$, ie. is approximately invariant. You could attempt to explain these allometries in different ways that don't causally relate them to each other.

There is a relationship: they are negatively correlated. Shorter-lived animals tend to have faster heartbeats, and longer-lived animals tend to have slower heartbeats. It gets more striking than that, however: they aren't just negatively correlated, they're approximately inversely proportional. A mouse, and an elephant, will both have around 1.5 billion heart beats before they die.
Poetic as this is, the relationship probably isn't causal. It's not that you have a given number of heartbeats, and when you use up your last one your heart dies of exhaustion. That would be silly.
It is illuminating to view the invariance as emerging from how both heart rate and lifespan scale allometrically with body size ($mass=W$).$^1$ Larger animals tend to have slower heart rates, and also tend to live longer; both relationships are in the form of power functions, whose exponents are multiples of $1/4$.

Heart rate ($R$) scales with a negative quarter power exponent: $R \propto W^{-1/4}$
Lifespan ($E$) scales with a positive quarter power exponent: $E \propto W^{1/4}$

"Total number of heartbeats in a lifetime" is just the product of heart rate and lifespan. As such, it should scale as
$R \cdot E \propto W^{-1/4} \cdot W^{1/4}$
$R \cdot E \propto W^{-1/4+1/4}$
$R \cdot E \propto W^0$
$R \cdot E \propto 1$
That is: if $R$ and $E$ scale in these ways - which they do, approximately, within many taxa - then their product $R \cdot E$, the total number of heartbeats in a lifetime, will be approximately invariant.
The question is why they scale in this way; and, beyond that, why the exponents in rate and time allometries are so ubiquitously multiples of $1/4$.

Does lifespan scale with $M^{1/4}$ because (for whatever reason) heart rate scales with $M^{-1/4}$; and your heart dies of exhaustion after a billion beats? (Call this the Heartbeat hypothesis.)
Does heart rate scale with $M^{-1/4}$ because (for whatever reason) lifespan scales with $M^{1/4}$; and, at the pearly gates, if the ledger says your heart beat 1.5 billion times before dying, you get a free t-shirt; and the heart likes t-shirts, but is also economical, beating as fast as necessary but no faster? (Call this the T-Shirt hypothesis; in my opinion it's barely sillier than the Heartbeat hypothesis.)
Does lifespan scale with $M^{1/4}$ because (for whatever reason) something else, like mass-specific metabolic rate, also scales with $M^{-1/4}$; and that something has damaging and life-shortening effects? (This was the once-popular Rate of Living theory.$^2$)
Does lifespan scale with $M^{1/4}$ because longer life causes selection for larger body size, in such a way that gets you the appropriate scaling? (Long-lived animals can afford to sexually mature later; maturing later means they have more time to grow, and will be bigger when they finally do mature. Apparently this can get you $M^{1/4}$ lifespan allometry if you combine it with certain assumptions about growth and fecundity, you model selection as happening in a stationary population, etc. This is sometimes called the Charnov model.$^3$)
Does heart rate scale with $M^{-1/4}$ because mass-specific metabolic rate does? Does mass-specific metabolic rate scale with $M^{-1/4}$ because heart rate does? (I dunno, these sound plausible? A cell's metabolism is fueled by stuff delivered to it by the blood stream, so it'd make sense for them to be proportional, right?)
Does mass-specific metabolic rate scale with $M^{-1/4}$ because that's how the optimum scales for efficient resource delivery through fractally branching networks like the bloodstream? (The proof is too math-y for me. This idea is the current mainstream explanation for why biological times and rates ubiquitously scale with exponents that are multiples of $1/4$, instead of eg. $1/3$ as you might expect if it were just to do with surface area / volume ratios. This is called the West, Brown & Enquist model.$^{1,4,5}$)

tl;dr: There is a striking negative correlation - specifically, an inverse proportionality - between heart rate and lifespan. But there's no particular reason to think it's causal, and both also correlate strikingly with a million other things. A lot of this has to do with how things scale with body size. Such scaling is called allometry; allometries are often power functions; for biological rates and times, the exponents of these power functions are often multiples of $1/4$ (as opposed to eg. $1/3$ or $1$). This quarter-power ubiquity in biology used to be mysterious, but now has been given an explanation (at least for the scaling of metabolic rate, which intuitively could do part of the explaining for other rates) by the West, Brown & Enquist model as being the result of optimally efficient resource delivery in fractally branching transportation networks.$^1$
The Heartbeat hypothesis is silly; presumably the approximate invariance of "1.5 billion heartbeats in a lifetime" comes from the $M^{-1/4}$ and $M^{1/4}$ scaling of heart rate and lifespan, themselves occurring for some other reason. I don't know but I assume the fractally-branching bloodstream explains the heart rate allometry. The lifespan allometry is more mysterious. It was once commonly thought to follow directly from the mass-specific metabolic rate allometry (Rate of Living theory), but that theory has fallen on hard times.$^2$ It has been given other potential explanations, notably the Charnov model which suggests that low mortality rates result in selection for a later age of maturity, giving animals more time to grow large.$^3$

West, G. B. "The Origin of Universal Scaling Laws in Biology". Physica A, 1999.
Austad, S. N. "Cats, 'Rats,' and Bats: The Comparative Biology of Aging in the 21st Century". Integrative and Comparative Biology, 2010.
Charnov, E. L. "Evolution of Life History Variation Among Female Mammals". Proceedings of the National Academy of Sciences, 1991.
West, G. B., Brown, J. H. and Enquist, B. J. "A General Model for the Origin of Allometric Scaling Laws in Biology". Science, 1997.
Dawkins, R. and Wong, Y. "The Cauliflower's Tale" in The Ancestor's Tale, 2004.


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Where do lost membrane proteins go after exocytosis?
Exocytotic vesicles take away membrane proteins and glycocalyx on the cell's plasma membrane surface. When those vesicles are released into the interstitial fluid and wherever else, where do they go?
Do they stick to the vesicle everywhere? Or do they get removed from the vesicle? If the vesicle fuses into another cell, do those proteins and carbohydrate attachments stick to the new cell?

In the process of exocytosis materials which are about to be released are transported in small vesicles to the plasma membrane. The plasma membrane fuses with these vesicles and this sets the substances free on the outside of the cell. See the figure (from here):
The other possibility for transport vesicles is that they arrive at their target cell and either fuse with the membrane and release the transported substance into the cell or that they are taken up in another vesicle which is then targeted towards the endosome/lysosome. See the figure (from here):

It doesn't matter which way is chosen, the membrane of the vesicle is recycled either by integration into another membrane of by going through the lysosome.

I see. I must have confused the 2nd way with exocytosis


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Long term effects of "brain freeze" on the cerebral vasculature
According to one theory, ice cream headaches are caused by an increase in blood volume of the anterior cerebral artery:

Another theory into the cause of ice-cream headaches is explained by increased blood flow to the brain through the anterior cerebral artery, which supplies oxygenated blood to most medial portions of the frontal lobes and superior medial parietal lobes. This increase in blood volume and resulting increase in size in this artery is thought to bring on the pain associated with an ice-cream headache.
(from Wikipedia)

Does repeatedly experiencing this phenomenon put someone at higher risk for some sort of cerebral vascular accident, or is it not any more harmful than a small increase in blood pressure that one might experience under exertion, despite the painful nature of the headache?

I do not have a source for the following as it was taught to me in neuroanatomy classes, the explanation given for brain freeze is that it is  referred pain through the trigeminal nerve. The  meninges (the tissue lining the central nervous system) is innervated by the trigeminal nerve in the head. Therefore the pain feels as though it is like a headache from meningeal irritation but is in fact benign.
Given that the mechanism is through referred pain rather than any vascular event it should not put you at any increased risk.
This being said if you experience repeated headaches and are unsure of the cause it would be wise to consult your doctor.


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Is sexual reproduction outside the same biological family possible? Has it ever occured successfully?
Are there any examples of two species taxonomically classified in different biological families that have successfully hybridized and produced viable offspring? If not, is there an example of where reproduction occured with non-viable offspring?
To be clear, I mean regular sexual reproduction that could occur in the natural world outside a lab. Even so, I'd be curious to know if it could even occur in a lab without direct genetic manipulation.
For example, grolar bears which are ursid hybrids between different species in the Ursus genus are known to exist. Also ursid hybrids between bear species in different genuses have been produced in captivity (sloth bear Melursus ursinus x Malayan sun bear Ursus malayanus and sloth bear x Asiatic black bear Ursus thibetanus). Would an extra-familial hybridisation be possible? Would this be more likely in the plant kingdom?
This question is inspired by a separate question on the Gardening SE which hints at a general lack of understanding of the genetic similarity required for cross-pollination in plants. It made me wonder whether there are any exceptions to the general assumption that extra-familial hybridisation is impossible.

Following the definitions of hybrid and of sexual reproduction, one could consider Horizontal Gene Transfer and answer YES to your question with the case of the photosynthetic sea slug for example.

I should have been more specific to limit this to gene transfer/recombination occurring by sexual reproduction (i.e. vertical gene transfer) but thanks for the point.

One of the problems is that "Family" and really any taxonomic designation are fuzzy. We often don't even really know where to draw the line between two species, even in animals, where such things are relatively easy. Since none of the taxonomic designations tell us anything about genetic distance except "the two taxa are genetically different from each other", any examples of inter-familial hybridization won't tell you anything about the general likelihood of such an occurrence...

A more valuable question might be "What is the maximum genetic distance at which hybridization by sexual reproduction has been observed?" And of course, the answer to that is, "I don't know" :P. Which is why this is a comment and not an answer.

@ChinmayKanchi As stated, there is a practical purpose behind the question, not merely a completely idle wondering. A new gardener without much backgrounding in biology wants to avoid hybridisation in her vegetable patch. How do you give simple instructions on avoiding it? For the lay-person the problems of taxonomic fuzziness are of zero interest. She just has labels with the species written on. Based on the single answer, I'd tell her first only be concerned about inter-genus and inter-species hybrids and then on how to prevent such cross pollination.

Yes, and as I said, single examples don't allow you to draw any conclusions about the general case. Will species x hybridise with species y is the appropriate question to ask in this case.

@Lisa My point is that even when you say hybrid via sexual reproduction you do not exclude Horizontal gene transfer. There are so many different way of reproducing sexually that our definitions are usually quite broad. But your question is interesting, I just thought it was worth stating horizontal gene transfer as this process fits in the definitions of sexual reproduction.

Interfamilial hybrids have never, to my knowledge, been recorded occurring naturally (without human intervention).
In plants, somatic inter-familial hybrids have been produced for a wide variety of species pairs in the lab (e.g. between carrot and barley; Kisaka et al. 1997).
In animals, there are some historical reports of hybrids between chickens (Mathis & MacDougald 1987) or peafowl (Serebrovsky 1929), both in Phasianidae, and guineafowl (in Numididae). The animal example meets your condition of being outside the lab, although they were produced by breeders.
Refs

Kisaka, H., Kisaka, M., Kanno, A. & Kameya, T. (1997) Production and analysis of plants that are somatic hybrids of barley (Hordeum vulgare L.) and carrot (Daucus carota L.). TAG Theoretical and Applied Genetics. 94 (2), 221–226.
Mathis, G.F. & McDougald, L.R. (1987) Evaluation of interspecific hybrids of the chicken, guinea fowl, and Japanese quail for innate resistance to coccidia. Avian Diseases. 31 (4), 740–745.
Serebrovsky, A. (1929) Observations on interspecific hybrids of the fowl. Journal of Genetics. 21 (3), 327–340.


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Why are human titin and mice titin considered the same protein?
I have a book that says:

In humans titin is a chain of 34,350 amino acids, but in mice it is even longer with 35,213 amino acids.

If two polypeptides had different amino acid sequence lengths, how can they be considered the same protein? Or is it because they share in common one or more amino acid sequences - which, if a polypeptide contains, biologists consider it a particular type of protein - that they are both considered the same protein?

Plenty of proteins have different isoforms that are produced from the same gene (for example by alternative splicing). They can be different in size and function and we'll still call them by the same name.

If they perform the exact same function, they can be considered the same functionally.
Hemoglobin in most humans is the same, down to the amino acid sequence; the hemoglobin in sickle cell anemia, Hemoglobin C, Hemoglobin SC, thalassemia, and others are all different by at least one amino acid, yet they are all hemoglobins, and all do the same job: they carry and release oxygen. Insulin in humans and pigs are not identical (human insulin differs from porcine insulin by a single amino acid - Thr instead of Ala - at the C-terminal residue of the B-chain - but they are both insulin, have an identical function in each animal.
Clearly two proteins of different lengths are not identical. (Did the book claim that they were identical? If it did, it was an error.) If they perform the exact function, they can both be called by the same name and be considered functionally the same protein.

Human and mouse titin are orthologs, and can be confirmed through an NCBI query for TTN.
Orthologous proteins are not the same, per se. They retain the same function, and basically result from speciation: the common ancestral gene got divided between two species. However, the sequence may potentially differ because obviously the species have diverged.
Homology between the two can be confirmed computationally, through phylogenetic and alignment analyses, but I believe the naming convention Titin for both mouse and Human stems largely from the function of the protein in either organism.
Naming convention and explanations of homology are nicely outlined in this Bio.SE post.


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How do detergents get in hydrophobic membrane interior?
According to Molecular And Cellular Biology (Stephen L. Wolfe),

Membranes disperse almost instantaneously if exposed to a nonpolar environment or to detergents, which are amphipathic molecules that can form a hydrophilic coat around the hydrophobic portions of membrane lipids and proteins in water solutions.

This might be a stupid question but... if detergents can 'form coats around hydrophobic portions' of membrane-suspended molecules, they must, somehow get in the hydrophobic membrane interior... right?
How do they get in the membrane interior? Do they form clusters like endocytic vesicles? What happens after they form hydrophilic coats around hydrophobic molecule regions?

It depends on the concentration, but at higher concentration the detergent molecules build so called micelles, where the hydrophobic "tail" is orientation into the inner part and the hydrophilic "head" is orientated to the outside. This allows the micelle also to fuse with the membrane and then to desintegrate it.
This illustration from the Wikipedia shows the schematically:

Its from the surfactant article, which has more details.

The membrane is dispersed by detergents.  But the detergents, under the right concentrations and conditions (salt, pH, et) form micelles with smaller curvature than the lipids that compose cell membranes.  With some luck, they can form a small hydrophobic micelle bubble around the protein.
This figure is depicts detergent micelles around a membrane protein's membrane bound regions, hopefully without distorting the shape of the protein!

Since you asked in the comments, here is a picture of the electron density of the detergent micelle in ompF Porin crystals - the detergent density is blue the protein is red.  For a while in the mid 90s through maybe a few years ago there were a reasonable number of simulations including detergent molecules.  The mobility of the chains in the micelles means that no specific model structure would be accurate, but it can help understand the electromagnetic environment of the solvent in cases which are important like charge transfer in a photoreaction center or the dynamics of transport through an import/export protein.

Thats a great image.

thanks. If you want to see a more true to life one, many membrane proteins have visualized detergent micelles in simulations and in the crystal unit cell.  I'll add another image above.

sorry... haven't been in SE for months; and DO please show me that image! @shigeta

actually the last image there is a good example... the blue density is all micelle in a porin unit cell.  protein is red


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How does regurgitated food go to the 3rd stomach chamber instead of going to the 1st?
Ruminants are known for their regurgitation of food; the food goes through the 1st and 2nd stomach chambers, then returns to the oral cavity in cuds. The cuds then come back into the stomach, but this time they go through the 3rd and 4th chambers, instead of going to the 1st and 2nd again.
How is it ensured that the regurgitated food doesn't go through the 1st and 2nd chamber by a mistake?

Your question supposes a very linear version of the flow of stomach contents of:
1->2->mouth->3->4
In reality, it is not so linear. Firstly some background: The rumen and reticulum form the first two parts of the four, and are in fact a single chamber/organ (collectively known as the reticulorumen). They have different wall structures, and perform initial digestion of different particles (mostly heavier particles in the rumen such as grain and more digested hay). This reticulorumen chamber is where the initial microbial fermentation of the feed occurs. Matter passes from rumen to reticulum and back regularly by means of two distinct muscle contractions.
To aid in the breakdown of the feed, the cud is regularly regurgitated, chewed and then re-ingested. The re-ingested cud returns to the reticulorumen. From there, in order to advance down into the later stages of the digestive tract, it must pass through the reticulorumen orifice into the third compartment - the omasum. The orifice allows particles up to 4mm in size in cattle.
The omasum chamber removes water and some nutrients. The contractions of the omasum remove water and move solids through the system, and the contractions are speculated to filter out any larger particles and return them to the reticulorumen. Matter that has been processed by the omasum is passed along to the fourth chamber, the abomasum.
So to answer your question in brief, after mastication the cud returns to chambers one and two, potentially going round this loop several times until it is sufficiently broken down by chewing, saliva and bacterial action, and then it can proceed from there to the third chamber.
The "digesta circulation and reticulo rumen motility in the ruminent" paper (C. Poncet, C.H. Malbert, R. Baumont) has this to say:

The outflow of digesta, allowed by the opening of the ROO [reticulorumen orifice] during the second phase of the reticular contraction, is highly selective. The effluent does not contain particles greater than 2mm in sheep and 4mm in cattle. This is due to the buoyancy of the large particles in the reticulum, to the self filtration of the digesta during the passage through the ROO and perhaps to backflows from the omasum to the reticulum.

You may find it useful to get a copy of this collection of papers (quote from p.366): http://books.google.co.uk/books?id=Bcsa8Z4u-E4C&printsec=frontcover#v=onepage&q&f=false

Thanks. Just to make sure I understand, do you mean that the large pieces of food simply cannot get through the passage to the 3rd chamber, and only the ingested, chewed-into-small-pieces food manages to get through?

In the main yes, although all digestion will be a little inexact - the odd larger particle could in theory get through I would guess. The size of the reticulorumen orifice would place an upper limit on the size of particle that could pass, and it is believed that the omasum will pass back some larger particles - the omasum contracts to expel water and move matter, and this may work in both directions.


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What do viruses do during incubation period?
For example, there is an incubation period of around 1 to 3 days for common cold, and that of AIDS can range over to decades.
What do viruses do actually do during the incubation period?
What triggers them to turn active again?

In the incubation period the virus replicates, infects more cells and prepare for the outbreak.

during the incubation period the virus is typically increasing in numbers and spreading between cells. It takes a while for symptoms to become obvious because it takes time for enough damage to be built up in the tissue to become noticeable.
Take for instance the Rhinovirus which causes the common cold, once you become infected it is a day or so before enough damage has been caused to the tissue at at the back of the throat to give you a cough.
In addition some of the symptoms of infection are caused by your own immune system as a way of fighting the infection. For instance inflammation is often a sign of infection but is typically caused by the immune system to allow the movement of plasma and leukocytes into the infected tissue. As the immune system requires time to recognise and respond to a pathogen this leads to the delayed onset in symptoms.
AIDS is actually a syndrome caused by the HIV virus. the HIV lifecycle occurs CD4+ T-Cells, after infection occurs the immune system tries to cope by destroying the infected cells but over long time the infected population increases. The immune system becomes more and more compromised until the CD4+ cell count drops to a level where the patient is diagnosed with AIDS. At this point the immune system is compromised and the chance of a secondary infection by a different organism increases which the patient can no longer fight off. The actual cause of death for someone infected with HIV is rarely the HIV itself but is quite often a different agent.

Some of the viruses also stay as proviruses..

Very good practical examples to answer this question! I like the way you use acute inflammation. AIDS is well explained from the general to the specific.


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Hydrophilicity and polarity
If any given molecule is polar, and is capable of hydrogen bonding, I can be sure that it's hydrophilic.
However, are those two the only conditions that make a molecule hydrophilic?

Is this a biology/biochemistry question?

its a common term used in biochemistry

As phrased right now it's a chemistry question.  Maybe if it asked about specific biological molecules instead?

I think the answer is no.
The definition of polarity is basically that a molecule has a dipole, and as water has a very large dipole, if a molecule will mix with water readily, its usually pretty polar.
Water also can share its hydrogens in hydrogen bonding, which is an actual shared covalent bond where a hydrogen atom is shared between two acceptors.  The hydrogen bond is fairly weak (~ 0.5 kcal/mol) but water does a lot of hydrogen bonding.
So hydrogen bonding and polarity are often a shared characteristic of an molecule, but are not the same thing.
Ions are quite hydrophilic but do not need to be hydrogen bond donors or acceptors.   Chloride  (Cl - ) is not a hydrogen bonding atom - its so acidic that it exists nearly entirely in the Cl- form in water solution. But its definitely electro negative and really soluable in water. Are Ions polar though?  Chloride is symmetrical and so its not really polar.
Still is there a polar molecule which is neither a hydrogen bond donor or acceptor?  Acetone and the cyanide ion (CN-) are a polar molecules which have no hydrogen bond donor, but can accept them.
I think sulfate is an example of a polar molecule which does not form hydrogen bonds.
Sulfate (SO4 -- )  has four S-O bonds arranged in a tetrahedron but each of them is highly polar - with 90% of the negative charge on the oxygen.  But like the Chloride ion its so acidic that it much prefers its free ionic state.  It would have very little hydrogen bonding character even when its in water.  Sulfate can form hydrogen bonds, but I think they will only be stable when there are several of them at once.  Sulfate binding protein has seven hydrogen bonds when it binds sulfate, using the chelation effect to make the binding strong enough to be stable.


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Why don't amino acids get linked in the functional groups of acidic and basic amino acids?
There are 'acidic' and 'basic' amino acids like aspartate and histidine.
When protein is synthesized with those amino acids, what ensures that the to-be-assembled amino acids will not bond to the amine groups or acidic groups in the functional groups of the amino acids in the polypeptide?

When the amino acid comes to the ribosome it is in the form of an aminoacyl tRNA in which the carboxyl group of the amino acid is esterified with the 3' OH group of the ribose moiety at the 3' end of the tRNA.
There is already a growing peptide bound in the P site of the ribosome with a free -COOH group which will react with the -NH2 group of the incoming amino acid in the A site to form the next peptide bond. This reaction takes place in the context of what is essentially an enzymic active site. The reactants will be held in the correct positions for catalysis to take place (in this case the catalysis is carried out by the ribozyme activity of the small ribosomal RNA).
So the answer is that the selectivity of this reaction is just another example of the way in which enzymes are able to carry out highly-specific reactions. So, for example, the enzyme hexokinase, which phosphorylates glucose at the 6 position has, potentially, four other -OH groups that, chemically speaking, could be phosphorylated.

I think it does happen that peptide linkages can happen to side chains.  For the reasons that @AlanBoyd lays out, this won't happen in conventional peptide synthesis and is in principle the answer to the question here.
To add a note though:
Non ribosomal peptide synthases can produce peptides with many subsequent unorthodox modifications.   If you look at the structure of bacitracin, I believe the large ring is closed by condensation between a lysine amine and the carboxylate of the amino acid on the other end of the ring.   There should be plenty of other examples.

So called secondary metabolism pathways create many diverse compounds - nearly anything seems to be possible.

Yes, agreed. A classic example of this is the tripeptide glutathione, a key molecule in controlling redox potential in cells. Glutathione is gamma-glutamyl-cysteinyl-methionine. The bond between the Cys and the Met is a classical peptide bond, but the one between the Glu and the Cys involves the side chain (gamma) carboxyl group of the Glu. This is referred to as an isopeptide bond. But glutathione isn't made by ribosomes, it's made by specific enzymes, so it's the exception that proves the rule.

thanks @AlanBoyd secondary metabolites are a corner case for sure but hopefully useful.

@TomD thanks - was doing the answer from memory. Can't edit the original comment however.


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Which hydroxyl from either the phosphate or the glycerol is taken during synthesis of a phospholipid head?
The oxygen anion in the phosphate group is likely to be bonded with a hydrogen cation and thus forming a hydroxyl.
When the phosphate group is condensed with glycerol to make a phospholipid, is the hydroxyl from the glycerol molecule taken or the hydroxyl from the phosphate group taken?
I believe it's related to the difference of electronegativity of oxygen and phosphorus which causes unequal sharing of electrons between atoms, thus making a hydroxyl from one side easier to get taken off than the hydroxyl from the other side is.

I'm trying to figure out where in the process you are talking about.  Are you asking about the creation of Glucose 6-phosphate, phosphatidic acid, or phospholipids down stream of DAG?  I was originally thinking the creation of phosphatidic acid, but I'm not sure.

In all phosphorylation reactions, the oxygen of the hydroxyl group in the substrate attacks P of phosphate. This is because of high partial positive charge on P which is bonded to four highly electronegative oxygen atoms. When the bond forms between the substrate oxygen atom and phosphorus of terminal phosphate, electrons are transferred to the O that bridges the ester bond between 2nd and 3rd phosphate. Therefore the O of the substrate is retained and that of the terminal phosphate (of ATP) becomes the part of the 2nd phosphate (now terminal phosphate of ADP).

See this

My recollection is that the formation of a phospholipid normally involves acylation of glycerol 3-phosphate. Glycerol 3-phosphate is a glycolytic intermediate, and so there is no actual phosphorylation of a glycerol; the phosphate on the glycerol will have come from the phosphorylation of glucose or of fructose 6-phosphate.
In a kinase reaction the oxygen of the -OH in the acceptor acts as a nucleophile at the P of the phosphate, so in terms of your question the O atom comes from the acceptor, not the donor. Presumably if there was a glycerol kinase (I expect there is) it would have the same mechanism so the O would come from the glycerol.


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Any food crops that could grow in a desert provided that they get fertilizer and water
I am working on an idea to provide nearly unlimited amounts of water in desert regions. To make this commercially viable. I would use the water to irrigate desert sand and grow crops. Given my extremely limited understanding of biology, I cannot find an answer to the following question:
Are there any food crops (preferably high valuable/low maintenance ones), that can grow in a desert, given that I can just provide the seed, water and fertilizer and stop sandstorms.
My motivation for investigating this is the following map showing regions that are either already deserts or at risk of becoming deserts:

Source: http://en.wikipedia.org/wiki/Desertification

I think the people behind seawater greenhouses have been exploring this very question

Just look at whatever grows in hot areas. If you can provide unlimited water and protect from the elements, then it is no longer a desert and desert plants will probably not even survive.

With respect to nutrients, there is a big difference between pure sand deserts and ones with higher contents of clay and organic matter, and this will affect which plants can growth there.

@fileunderwater I am considering pure sand deserts mainly. If that is not viable, then I have to go for especially suited areas.

I think many projects have shown that desert is self-reinforcing (so deserts expand b/c plants have trouble surviving at the margins), but also that non-desert is self-reinforcing (so if you're able to get a patch of forest that survives in the desert, it can also naturally expand to convert desert to forest). So it seems like a first step might be focussing your water/shelter/fertiliser etc. on giving an initial boost to a robust plant community that once established will work for you (ie. not need more external inputs). Cf. http://en.wikipedia.org/wiki/Gaviotas.

You might want to check what food crops grow easily in hydroponics. Those crops require little soil nutrition as long as they are fertilized and watered. Also perhaps what grows in sandy soils(Watermelon, I infer coconuts,etc)

Following up on Jeremy Kemball, does your idea even require that the plants be planted in the desert soil? Or can they just be grown hydroponically above the water or in, say, keyhole gardens (which are becoming common in some sub-Saharan countries).

Even if you have unlimited water available to the plants you'd still have to worry about the high temperatures and light levels of these areas. In the hot periods I would look into any plant that uses c4 carbon fixation like millet, sorghum, corn, sugar cane... In the cooler periods maybe look into rotating to a cool season legume crop like the cowpea that would help fix nitrogen. Another really important thing to do would be to find cover crops that will hold down the soil and build up some life in the otherwise sterile sands of the desert.


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Do scouting bees get to pass their genes to offspring?
Let's say the food-scouting behavior of scouting bees are enhanced when some particular alleles are expressed. By natural selection, the allele frequency for that "good" allele should increase because more of the scouting bees with that allele get to pass the allele to offspring generations, as more of them survive in the ecosystem.
But considering that only male bees get to produce offspring with the queen bee, do scouting bees (I assume to be females) ever get a chance to pass their genes to future generations? Or are they males? If they are males, do they get to produce offspring?

I think this question has a fundamental problem: You are using the term their genes as in regular sexual selection. In highly social collectives such as bees you better not think of the individual, but see the whole collective as one big evolving complex. The worker bee cannot reproduce itself, but here this is not a severe evolutionary problem. By raising offspring it will help the genes of her hive (and therefore also her genes to some extend) to prosper.


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Statistics on energy consumption breakdown per biological functions across organisms?
Are there any statistics available on how much energy organisms use for each biological functions (i.e. something similar to the line of "Bacteria spend X% of energy on information processing, Y% for tissue maintenance and Z% for locomotion. Mammals spend..."). I'm particularly interested on how much energy is spent on information processing.
I vaguely remember seeing such stats somewhere, but for the love of god I can't remember where...

Out of curiosity, what do you mean by information processing? I can see this being used in several ways in biology: transcription/translation, signal transduction, you might even make an argument that some forms of enzyme binding kinetics are information processing (identifying the correct input from a sea of possible inputs). Of course also these numbers would only be meaningful in very specified and constrained environments.

In bacteria this has been studied in great detail for cells growing in steady balanced exponential growth. The classic reference work for this is Physiology of the Bacterial Cell by Neidhardt, Ingraham, and Schaechter: http://www.amazon.com/Physiology-Bacterial-Cell-Molecular-Approach/dp/0878936084 . Over the course of a few chapters they painstakingly identify how many ATP molecules are consumed for each process, from replication, transcription, translation, cell wall synthesis, etc, over the course of a single cell cycle. Not sure if this has been done in eukaryotes.

@A.Kennard: I mean the energy spent on sensing external stimuli (light, sound, pressure, smell...) and making decisions based on it. I realize making such categorization would be very hard and error prone (just like in real economies, I guess), but I imagine it could still yield interesting insight, like parasitic insects can get away with only x% while mammals typically have to spend y% etc.

Awesome. You're right that the categorization may be difficult, but I absolutely see the potential interest. Narrowing down the question like this to the fraction of energy consumption in signal transduction already makes it more tractable.
Complementary to your question about energy consumption, are you aware of the bioinformatic research on genome reduction in parasites? I think interesting trends can be observed comparing the loss of signal transduction proteins compared to other protein groups. An example of this type of analysis: http://ijsb.sgmjournals.org/content/54/6/1937.full

This is not a proper answer. Bear with me. I'm in a hurry; will edit the answer to a decent form when I find time.
From the abstract of this paper:

Of the 80% of oxygen consumption coupled to ATP synthesis,
  approximately 25-30% is used by protein synthesis, 19-28% by the
  Na+-K+-ATPase, 4-8% by the Ca2+-ATPase, 2-8% by the actinomyosin
  ATPase, 7-10% by gluconeogenesis, and 3% by ureagenesis, with mRNA
  synthesis and substrate cycling also making significant contributions.

Also check this out.


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Is it possible to make humans extinct artificially?
Verging on the realm of science fiction, my question is that is there any theoretically possible way, biologically/chemically, with which the entire human race can be killed without affecting the rest of the biosphere at all? I am only curious about theoretically possible no matter how unlikely. If we encounter a sufficiently advanced alien civilization bent on our destruction, would it be possible for them to make sure all humans die without harming any other living organism on our planet?
Is there anything biological/chemical which makes us unique or different than other lifeforms on Earth? Something which can be used against us? Or are we just so similar with a bunch of other species that we cannot be wiped out without other lifeforms getting harmed or our destruction cannot be ensured? Is it possible to artificially make humans extinct?
Thanks you.

This question appears to be off-topic because it is not about biology as defined in the FAQ. It would be much better suited to scifi.stackexchange.com

@BrandonInvergo Actually I would be okay with either one. I prefer an external mechanism but just for the sake of intellectual curiosity, internal mechanisms will also be interesting.

@MattDMo I though about this very carefully and decided to put the question here instead of at scifi.stackexchange.com because I am looking for scientifically theoretically possible methods. This is specifically related to human biology and I don't think scifi.stackexchange.com is the proper place to ask bio questions. This is a "question about biological concept". Is there anything biologically different about us which makes us different enough from other species on this planet?

In 50 years time, if you had a 20 billion dollars and a space program, you could probably make a fleet of 1 ton sattelites which can track the entire planet using 1cm resolutions and that uses a 20 kilowatt laser to destroy all vehicles except tanks and then to destroy humans, including all agriculture vehicles, and visible crops, so humans would be decimated by hunger. It would need to take out human space launching first, and then it could at least prevent humans from using cars or walking without 3 inches of steel over them. The sattelite would aim for all non-plant/animal structures.

Infectious diseases is probably the only way I can think of. Viruses for example may have tropisms based on receptors to which they attach. These receptors may be and often are unique to a species, and thus an infection could target humans very specifically. Differences between humans and animals present the weaknesses and resistances we would have to such an infection. As an international species, spread of the disease can be quite rapid. However, our increased intelligence means we could given time, understand the threat and combat it.
If an infectious disease killed rapidly enough that development of a cure or administration of one was not easily possible, the disease itself would be wiped out by quarantine measures (theoretically). For an infection it is not wise to kill the host too quickly as this prevents survival of the infection which is dependent on its host.
Thus we want an infection that is non-pathological at first then rapidly pathological but affected the whole world as a whole. This infection would need to spread to every individual so would have to be incredibly infectious and for no individuals to have any resistance to it and also ideally to kill everyone at roughly the same time or at least quickly enough to prevent us having time to come up with a cure. The only way I can think of that would fulfil all of those conditions is if the infection on it's own was non-pathological but then a novel secondary universal factor made this infection pathological. This factor would have to be in low levels prior to infection but then rapidly escalate to worldwide distribution.
Disclaimer: Obviously this is theoretical and probably not at all possible.

Thanks, +1 and accepted. A virus specifically engineered is the only way I could think of as well but wasn't sure. I was thinking of something which would lay dormant for a long time to make sure everyone is infected and then all of a sudden become active and just wipe out everyone very fast. Not sure if this is even theoretically possible or not.

This answer is building on the answer by @BrandonInvergo and focusing on the "..possible way...the entire human race can be killed without affecting the rest of the biosphere..." part of your question.
No, it is impossible to remove humans without affecting the biosphere (barring some extremely made-up scifi scenario) because many species are adapted to us. It doesn't stop with the parasites and pathogens in Brandon's answer. Most obviously, the majority of all domesticated animals and plants will go extinct, and these number ~750 species (Duarte et al 2007). A large number of other species (e.g. plants, insects, birds) are also adapted to man-made environments and many are likely to go extinct if humans disappear, and these effects will cascade into their respective ecosystems. Just look at what is happening to species adapted to traditional low-intensive pasturelands in e.g. Europe.

Really? All of those species would go extinct as well? Wouldn't they all just adapt back, meaning adapt to live without man-made environments? That's how they were living before.

@FixedPoint For domesticated species most will go extinct since they have been so heavily modified and cannot compete successfully in the wild. For other species dependent on man-made environments the outcome depends on how rapidly their living environment changes, but many are likely to go extinct. Some are likely to find refuge in their native habitats, e.g. natural grasslands. However, the original habitats are sometimes lost or the species is extinct from their original range, and some have evolved adaptations to their current antropogenic environments.


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Why do our eyes "wrap" hue from UV to IR?
On the high-wavelength side of things, we see almost-infrared as reddish, with a slight tinge of magenta. On the low side, we see violet fading into the same magenta color. Why is that?
You can see it clearly on any hue chart. There's an unbroken flow from one to the other, even though the wavelengths are literally as far apart as they can be while still remaining visible.
I understand that color vision is limited due to several biological factors(cone receptivity, absorption, etc), but why do the colors on both side fade into each other? Is it just our brain making things "neat" and continuous?

Basically.  You are most likely looking at the electromagnetic spectrum, which is linear and conveniently makes sense... except for magenta.
Colors as we perceive them are additive and made up of Red, Green, and Blue; this is opposed to subtractive color we learned about while finger-painting in kindergarten (Red, Yellow, Blue).  The three types of cones in our eyes each are sensitive to one of these colors, and it is from the combinations of Red, Green, and Blue that we see all the colors we see.  Yellow, for example, is when the red and green cones are both stimulated.  Purple/violet is from red and blue stimulated together.  This is the single special case, as you point out, because red and blue are at opposite sides of the spectrum from each other.  Our brain has two options:

Use the color smack-dab in the middle aka Green
Make a new one as if they wrapped around

Green is far away and already taken, so our brain intelligently invents Magenta.  This produces, instead of a linear EM spectra, a circular color wheel that looks very intuitive.

I understand RGB(software developer), and I see what you mean about a red/blue mix needing an invented color, but what about (almost) pure infrared? With a (strong) very-near IR laser, you'd expect it to appear as red, but it still gets closer to magenta as wavelength increases, even though there shouldn't be any blue/violet light to mix. For example, in a very dark room, I can see my TV remote IR led, and it is definitely not just "red".

TV remotes are often not pure IR.  At that level, the long tail of the faint visible colors can be enough to stimulate a color; you are not seeing the IR being rapidly sent.  Some cameras (my laptop does it) will show IR, often as a neat little purple.  That's a good test to see what you're not seeing.

Yes, playing with my camera is what led me to the question, since even there they pick it up as some shade of purple, depending on hardware. I think the bit about the faint visible colors is the primary answer.

this is really easy to answer.
this is a chart of the light activation of the light sensitive cells in the human eye.

see that little blip up on the tail end of the red cone, that minor ranges means the extreme blue end of the spectrum activates blue cones but also has a chance to activate red cones. That is why you can sometimes see magenta tinges in bluest of blue light. There is also a sensitive issue as blue cones are the least sensitive of our cones so it requires a stronger blue light source to activate it than the equivalent light on other cones, since red is more sensitive a strong blue and a weak red source will blend to about equal as far as our eyes are concerned so at the bluest end of the spectrum, where the blue activation is at its weakest it does not take much to activate the blue and red "blip" equally meaning all sources at that extreme end blend into magenta.
Also magenta itself is not actually part of the spectrum, it can be produced in two ways, the first I discussed above, hitting the far end of that little blip perfectly. The second and most common requires light from two disparate and different parts of the spectrum in other words not a single wavelength. It is blue light and red light without green light, it is not a real color but an artifact of how our eyes see light. Your cones can't tell how they are activated just that they are. Yellow and cyan (and every other common human color)on the other hand can be produced by a single wavelength, which may or may not activate multiple types of cones.
You can find more information here

The question has an invalid premise. Namely, that the UV light looks like magenta/purple. It is not the case. While it it true that approaching UV end the perceived color becomes more purple (because the red protoreceptors have a second maximum there), moving further to the UV area (which is possible if the eye has the lens removed), makes the perceived color more whitish/light blue because the green receptor also has a second maximum there (somewhat further than the red one).
I do not know why the IR has magenta color though. It could be because of not pure source. Try using a hot piece of metal to see if it becomes more purple as it cools, I think it does not.

The photo-detectors of the eye don't detect a linear spectrum... they detect three colors. The amplitudes of the three colors are mixed a bit similar to a color wheel.


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What is coffee effect on muscles ? On sport performances?
Since coffee is a vaso-restrictor does it have any impact on sport performances ?
I mean does it go against natural way the body works (sending more blood to muscles due to the increasing needs) or does the body easily bypass this effect ?
Edit : I leanred that coffee has a great impact on sport performances but what realy interests me is to learn more about its vaso-restrictive effect , how doesn't it reduces performances ?

Did you do any research on the subject prior to posing the question here?  To my understanding, If information is easily accessible by a google-search, the moderators and other users here will ask you to do research in advance and possible rephrase the question to be more specific.

I learned that coffee increases performances but i don't find a lot to learn on it's vaso-restrictor effects which is what realy interests me

I would advise you to then clarify in your question that you have done prior research and now search for answers regarding a specific area. I am no expert on the subject you are asking about, so I apologize if my comments seem unnecessary. I am merely trying to improve your chances for finding a useful answer.

Ty for this comment , i'll edit the question ! :)


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How is the Force of Contraction Applied to the Tendons by the Muscle's Individual Fibers?

Image and question have been updated for clarity!
The image above is a side view of a semi-transparent skeletal muscle. The dark red lines represent individual fibers, the blue lines represent tendons. The pink area also consists of muscle fibers, but it is made transparent for the purpose of the demonstration. Please assume the fibers are properly encased in fascicles and fascia. Tendons connect the muscle to the bones. The bones can move towards the center of the image if pulled. The arrows show the flow of force during contraction along each fiber.
The muscle has grown large enough that the outer fibers protrude around the tendon (where they connect). During contraction, do the protruding outer fibers help pull the tendon towards the center of the muscle like the internal fibers in the middle of the muscle do? If so, how is the force controlled and directed to accomplish this?
It seems there exists athletes with this type of anatomy (such as very large bodybuilders) but the bio-mechanics of this type of anatomy completely confuse me. It would seem the flow of force of the outer fibers would pull the tendon away, unless the force is somehow redirected. Thank you so much for your insight on this!!!

Could you try to clarify this? Is your drawing of a muscle fiber showing a cross section or a side view? My guess based on your quesiton is that it's a side view (meaning contraction is in the same plane as the tendon) -- is that right? If that's the case, knowing that muscles only contract (meaning they are unidirectional in their "tugging" ability), I would suspect your tendon would move in the same direction as the muscle fiber. However, without knowing where your muscle is attaching (i.e., which side is the origin vs insertion) it's difficult to say which direction this muscle is moving.

I recommend thinking about this a little more and then trying to clarify both your picture and what you're asking. Perhaps also provide a reference for your athlete example to help clarify. Thanks.

Sorry about the confusion, I went back and edited the question and image to try and clarify things! I hope the question makes more sense now!


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Does the fossil record disprove Evolution?
It is said by people opposed to Evolution, that the fossil record contradicts and disproves it. They say all the animals suddenly appeared, exploded everywhere, were fully formed, had no transitions, no gradualism, no change, and no sign of an evolutionary trend by which they could have emerged from an earlier type.
They then use these quotes to back this up from Evolutionists themselves:
"All the larger groups of animals, e.g. fishes, amphibians, reptiles, mammals seem to have appeared suddenly on the earth, spreading themselves, so to speak, in an explosive manner in their various shapes and forms. Nowhere is one able to observe or prove the transition of one species into another, variation only being possible within the species themselves" Evolutionist, Max Westenhofer as quoted in Dewar's More Difficulties, p. 94
"The evidence of Geology today is that species seem to come into existence suddenly and in full perfection, remain substantially unchanged during the terms of their existence, and pass away in full perfection. Other species take their place, apparently by substitution, not by transmutation" Geologist, Joseph Le Conte
"The extreme rarity of transitional forms in the fossil record persists as the trade secret of paleontology (study of fossils). In any local area, a species does not arise gradually by the steady transformation of its ancestors, it appears all at once and fully formed." -- Dr. Stephen J. Gould, Prof of Geology and Paleontology, Harvard University. Mentioned in one of his regular columns in Natural History Magazine (1977) and also in The Panda's Thumb, 1980, p. 181-182
"different species usually appear and disappear from the record without showing the transitions that Darwin postulated -- we are now about 120 years after Darwin and the knowledge of the fossil record has been greatly expanded. We now have a quarter of a million fossil species but the situation hasn't changed much -- We have fewer examples of evolutionary transitions than we had in Darwins' time" Dr. David Raup, a paleontologist at the Field Museum of Natural History in Chicago. Field Museum Natural History Bulletin 50:22- 29
"Evolution requires intermediate forms between species and paleontology does not provide them" Dr. David B. Kitts, Paleontologist
"The known fossil record fails to document a single example of phyletic evolution accomplishing a major morphologic transition" Evolutionist, Dr. Steven M. Stanley
"The record certainly did not reveal gradual transformations of structure in the course of time. On the contrary, it showed that species generally remained constant throughout their history. New types or classes seemed to appear fully formed, with no sign of an evolutionary trend by which they could have emerged from an earlier type." Bowler, 'Evolution: The History of an Idea', 1984, p. 187
"We are still in the dark about the origin of most major groups of organisms. They appear in the fossil record as Athena did from the head of Zeus -- full-blown and raring to go, in contradiction to Darwin's depiction of evolution as resulting from the gradual accumulation of countless infinitesimally minute variations, which, in turn, demands that the fossil record preserve an unbroken chain of transitional forms." Jeffrey H. Schwartz, Sudden Origins: Fossils, Genes, and the Emergence of Species (New York: John Wiley & Sons, 1999)
Is this true? If not, why not? Does the fossil record prove or disprove Evolution?

This related question is relevant: http://biology.stackexchange.com/questions/5138/fossils-of-intermediate-stages?rq=1

It also seems to be pretty directly answered on Skeptics here http://skeptics.stackexchange.com/questions/101/does-the-fossil-record-evidence-sufficiently-support-evolution and here: http://skeptics.stackexchange.com/questions/3481/have-any-transitional-fossils-missing-links-been-found

Questions about creationist arguments are off-topic here. Specific questions about evolution are certainly welcome, creationist talking points not so much.

The fossil record is spotty, very few organisms are ever fossilized upon death, so we see a small sampling of evolution. If you had a digital image of the mona lisa and removed 99% of the pixels, it would hard to recognize, especially if you looked at 1 pixel at a time. Might be doable from far away.

Fossil records are fossil records. The people who use them to attempt to prove or disprove evolution use them to represent their causes in different ways, gleaning sometimes completely contradictory facts from the same bodies of information, sometimes even the same samples.
It is my personal belief that evolution isn't ever entirely phyletic, I like to imagine that once in a while a pup would be born or an egg would crack open and there'd be a malformed creature in there the likes of which the world has never seen, if only because its deformity has made it more adaptable or stronger to its environment, not the opposite which is usually the case with birth defects. And then yes this prototype would survive and find a mate and have offspring with its varied genes dominating, some same, some different, and begin the phyletic process.
But that's not the answer to your question. Your question isn't really answerable. Fossil records only prove that a creature once lived at that time period, and its bone structure and posture can reveal certain things to any observer, but they dont prove or disprove anything. A great deal of the works you quote speak on the topic with great finality, yet they are decades old.

Well, at least the fossil record is completely compatible with the predictions made by evolutionary theory. In so far, it definitely does not disprove evolution.

While I agree with you completely, I try to be as objective as possible. There are people out there who have attempted to use the fossil record to disprove evolution and I know at least a few souls who are proof of their success.


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What is the name of this small black insect?
Location: South India
Size: 1-2 cm

Did you see it recently?  Time of year would be useful.  More useful would be the habitat in where you saw it:  woodland?  Swamp?  Metropolitan?

Metropolitan, 2017, Night Time, Its on my front door, may be it is new invented species found by me, may be who knows.

+0. Your photo isn't of such good quality. Try to use the best camera you have available — preferably an SLR camera — and forcing the flash setting to "on". It might help to boost your camera's ISO setting.

Precise identification of insects requires use of microscopic lens and an immobile specimen.
I have neither of those here; also, my reference material is focused on North American species.  Nevertheless, with what I have available to me, it is most likely a member of order Hemiptera, family Alydidae:

Alydidae are mostly active during the day, so your specimen was probably resting and saw a nearby artificial source of light.  They use their piercing mouth-parts to suck the juices out of herbaceous seeds.  Unless yours was discovered in a heavily urbanized area, I would venture that this one feeds off nearby grasses and trees.


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Can improper/inadequate exhalation in humans trigger migraines?
Is there any relation between  one's breathing pattern and occurrence of headaches? How does inadequate exhalation affect humans?

I'm voting to close this question as off-topic because it seems a better fit for Health.SE

I meant it in a general sense, was not seeking a personalized answer.

If so then please remove any reference to self and try to make the question interesting for the community at large.

I have reworded my question. Can it be re-opened?

It's still too broad for the format here. I would opt for Health. SE, another stack in the SE network


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Can the characteristics of an offspring depend on the locality of its conception also?
Transfer of characteristics from a parent to its offspring is explained in biology. When an adult male and female (of humans) who are displaced from their local environment to another (say, a different continent)for a considerable period of time, conceive and give birth to a baby, the newborn also shows some traits related to the people of the new locality . How is this explained?

Do you have a reference of this actually happening ? Which traits are we talking about here ?

Kindly add little more specifics into the question, such as

What do you mean by considerable period of time?
What kind of organism are you referring to?

Off-springs are defined by the genes of their parents. Not the country they live in. Your claim (unless you can show a very good reference for it) is primarily opinion based.

Are those human offspring and parents ? Can you give examples of traits that a child of Asian parents would get from being conceived in Africa ?

maternal effects do exist (where offspring characteristics are partly determined by the phenotype of the mother, which in turn might be affected by the environment during pregnancy), but that doesn't sound like what you have in mind ...

I meant visible traits like skin and hair colour, their texture, even facial features (the bone structure) to an extent. This is just a personal observation, no references.

@beena benny if you observe a child who has traits of a local as well as the parents, keep in mind that marriage is a legal concept, not a biological one.

@beenabenny In that case it seems like the first question ought to be "DOES a child's traits depend on where they were conceived", and you ought to know that as far as current knowledge in biology and genetics go, for traits such as hair colour, texture and bone structure the answer is "they don't". If you have more details on your personal observations that could be useful; maybe we could find out how the conclusions you drew from those observations are wrong, or they could point us to a phenomenon we hadn't thought about or weren't aware of and thus help answer the question better.

Nurture vs. Nature

Genetic makeup can not vary with the place of conception, but certainly the way genes are expressed can change with change in place of conception. Such changes are called epigenetical changes. Epigenetic change is switching on or off of genes which can be achieved by various method:-
1)  DNA methylation
2)  Histone modification and
3) RNA associated gene silencing
In theory, change in place of conception, can result in silencing or activation of differential genes in foetus. In fact there is this nice article which discusses how maternal nutrition switches on or off six genes in foetus 1 and [2]. Even stress can cause such epigenetic changes [3]. These environment triggered changes may also result in change of phenotype. For example in mice, the agouti viable yellow (Avy) gene which is a retrotransposon and is found in upstream of the agouti gene. The Avy elements are generally methylated and hence are shut off but in Agouti mouse, they are unmethylated and therefore switched on, which leads to a yellow coat.Though this methylation or unmethylation in agouti mice has not been proved to be a result of environmental factor, but in a strict theoretical sense this can happen (with some or other phenotypic trait)

1] Painter R.C., Roseboom T.J., Bleker O.P. Prenatal exposure to the Dutch famine and disease in later life: an overview. Reproductive Toxicology 20, 345-52 (2005).
2] Maternal nutrition at conception modulate DNA methylation of human metastatic epialleles(NCBI)
3] Exposure to stress even before conception cause genetic changes to offspring(science daily)

Your answer is a good one, but keep in mind OP's clarification in comments - they're talking about "visible traits like skin and hair colour, their texture, even facial features (the bone structure) to an extent." Do epigenetic modifications typically lead to changes in that kind of trait ?

I probably missed out the comment section while answering the question. I will edit my question to include the aspect of visible traits.


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Is there any alternative to x-gal white/blue screening for the monitoring of pseudomonas aeruginosa beta-galactosidase activity on agar plate?
I want to screen a pseudomonas aeruginosa mutant library carrying a lacZ transcriptional fusion for dysregulating mutations. I tried to do it on xgal plates but the accumulation of the blue color makes the screening difficult. I saw that people are using macconkey or endo agar media for two-hybrid beta-gal screening in E. coli for instance. I wonder if it would be something to try even with pseudomonas (which would only possess the lacZ gene, so no permease etc...) and if someone here ever tried it ? Or if other beta-gal substrates could be used for this application ?
thanks
Julian

I think your problem will be even worse when you'd use MacConkey or Endo plates. You can see differences between different kinds of bacteria / expression of certain enzymes on those plates, but the coloring / decoloring is based on soluble compounds that easily diffuse.
Hydrolysis of xgal creates an insoluble product that's staying more or less at your colony. Of course it's not perfect and after a while you have a completely blue plate, but this would happen much faster with a soluble compound.
Try adjusting your conditions so you can look at the plate before it's completely blue. Things you could try: look earlier, plate them a little bit more dilute so colonies are further apart, use less xgal so your final coloring is less intense, look for some papers that use xgal for screening and steal their tricks.


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Connectivity of the Superior Colliculus
Does anyone know anything about the connectivity of the superior colliculus? Or know of any straightforward published literature?
I've got that the superficial layers receive input from the visual system and the deep layers have multi-sensory inputs, but I'm finding conflicting information about the specifics.
I've read one source that suggests inputs are from magno and konio cellular retinal ganglion cells. But as I understand it, these are cell types in the lateral geniculate nucleus, so it's not clear if the inputs are from the LGN, or the retina.
Edit: Figure 2  here, shows "koniocellular" ganglion cells. Which I can't tell if they're meant to come from the LGN, or retina.
This article discusses some of the connectivity, but only with regards to eye fixation, rather than a general overview.

Please cite the sources.

Edited to add a couple of the sources.

(About the tectospinal tract) the tectospinales fibers originate in the superior colliculus, its axons pass ventromedially by the central gray matter and cross in the posterior tegmental decussation. The upper colliculus receives visual information, and the tectospinal tract is believed to act as a mediator of reflex eye movements in response to visual stimuli (Neuroanatomy of Crossman and Neary pg 81).
A relatively small number of fibers leave the optic tract, before reaching the dorsal nucleus of the lateral geniculate body, to terminate in the pretectal area and superior colliculus (fibers involved in pupillary reflex mediation) (Neuroanatomy of Crossman and Neary pg 157).


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Yew seed dormancy reduction
Yew seeds have very long dormancy when artificially planted.
They are also adapted to passage through digestive systems of animals that eat/transport them.
But could the dormancy be shorter (or the viability higher) if the seed passes through a birds digestive tract first? (An explanation: the seed's outer layers can get worn down that way, signalling that it is ready to start the process leading to germination.)
That would imply that the dormancy could also be artificially shortened by eg. dipping the seeds in acid and then alkaline solutions, which would be great.


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Seasonal fur shedding
How does an animal's (specifically dogs and cats) body "know" to shed fur in the spring and retain fur in the autumn?
Google just tells me that it happens, not the biological process of turning off the follicles and then turning them back on.

Their seasonal (colour) moulting is controlled by pituitary hormones, including prolactin, melatonin and alpha-melanocyte stimulating hormone (α-MSH), together with glucocorticoids, gonadal steroids and thyroid hormones (Zimova et al., 2018).
From the link:

We found that across species, ... photoperiod is the main driver of the moult phenology

In other words, daylight getting longer is a signal of spring/summer; daylight getting shorter is a signal of fall/winter.

Thanks for the editing from Bryan and Ron. I'm not experienced in this field and I learned from your contribution :-)

@BryanKrause but my indoor cats shed in the summer.

@RonJohn Do your indoor cats see daylight?

@BryanKrause much less than they see indoor light at night, or a dark room during the day.

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


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What is the name of this black-ochre striped snake?
I've seen the following snake (?) near Calvi (on Corsica):

I guess it was about 50cm long.
What is the name of this type of snake?

Great find!  Based on the picture and location, I believe this is the Corsican grass snake (Natrix natrix corsa).  It is a pretty rare subspecies, and is listed on Annex IV of the European Union Habitat and Species Directive.  Worth mentioning that it's nonvenomous.

Photo cred to Frank Deschandol/Philippe Sabine
Unfortunately, I was not able to find too much more info on this subspecies.  I know Natrix natrix are pretty widespread throughout Eurasia, but this subspecies is much more restricted.


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What is the name of this brown, "flat hat", fungus?
I've seen this in October 2016 on Corsica (Island of France):

See https://commons.wikimedia.org/wiki/File:Gr-20-petra-piana-to-onda-08.jpg for more images and higher resolutions.

feels like it could be some sort of Amanita. i only see that one image in your link, are there more from other angles?

Pretty sure (but not 100% certain) that it is a Amanita porphyria bk9845, which in german is called a "Porphyrbrauner Wulstling"

Cap: 3-12 cm; convex, becoming broadly convex, often with a central bump; sticky at first or when wet; bald; appearing streaked radially; the margin not prominently lined; grayish brown to brown or purplish brown; often with scattered gray to purplish gray warts or patches.

Source:

amanita porphyria


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Which ORF will be translated
I've a question about ORF and translation into protein. Say I have an RNA transcript that contains two ORFs, one in phase 1 ; one in phase2 ; as:

ORF number 1 in reading frame 1 on the direct strand extends from base 529 to base 759.
ORF number 2 in reading frame 3 on the direct strand extends from base 849 to base 1223.

So ORF number 1 comes earlier in the transcript, but ORF number 3 is longer ..
Is it always the first ORF that is translated ?
Edit >

It's in an eukaryoytic organism and same gene (it's the same transcript)

I use ORF finder (http://www.bioinformatics.org/sms2/orf_find.html) on my transcript sequence and it gives me two potential ORFs (ORF 1 and ORF 2 within two different frames)

Thanks

This is impossible to answer. Are you talking about bacteria or eukaryotic cells? Are these different genes?

There are several parameters such as presence of proximal Ribosome Binding Site in prokaryotes or Kozak sequence in eukaryotes, secondary structures etc.

Please [edit] your question and clarify. The answer could be ORF1, ORF2 or both or neither depending on the details. Is this in a species that has introns? Is the RNA spliced? Mature? Are these the same gene? What exactly do you mean by ORF? Are they both terminated by a STOP codon?

Making this even worse, is this a viral RNA that separates ORFs by IRES?

An open reading frame is one that extends for some distance without containing one of the three translational termination codons. This has nothing to do with translation initiation. Translation in both prokaryotes and eukaryotes requires an AUG initiation codon. You don't mention if there are any in-frame AUG codons in your hypothetical transcript. Without this information nobody would be able to provide a meaningful answer.

In addition, there are alternate start codons.

If both of the ORFs that the web tool predicted start with an AUG initiation codon, then the textbook answer is that the 5' cap on eukaryotic mRNAs is the first feature that is recognized by the translational apparatus, and the ribosome scans along until it finds the first AUG (it is a simplified description). However, if there are several AUGs near each other then the one that matches the best to the Kozak PWM (position weight matrix) will be preferred. The Kozak sequence can be approximated by: CCATGG which is also recognized by the restriction enzyme NcoI. Highly expressed genes tend to match most closely to the Kozak consensus.

The most common case like this is a prokaryotic mRNA, where polycistronic genes show up regularly.  In that case the ribosomes are free to attach to the RNA and both genes are usually co-translated.

The proportion of translation between the two genes does vary depending on the affinity of the ribosome to the mRNA, which is partially determined by the ribosome binding site sequence.
If there is a lot of transcription activity on the mRNA, many ribosomes at once can translate any single ORF, as you can see in the micrograph above.


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Software to calculate Fst from sequence data
I'm looking for a software to calculate Fst from 3 loci DNA data of individuals from a metapopulation. I don't have any prior on the population structure (have no idea of the number of subpopulations for example)
I've been looking at FSTAT but it doesn't run on MAC.
Do you have any easy alternative?

it should be pretty easily implementable in perl or python.

If You are familiar with R, try package adegenet. It contains very nice tutorials explaining its usage, including the very R basics. If You require graphical interface, install RStudio - very nice front-end for R. There are more possibilities how to calculate Fst in R, but adegenet is one of the most powerful genetic packages there.