text:
Does gross production (P) and biomass (B) mean the same?
From fundamentals of ecology, Odum 2005:

... autogenic succession usually begins with an unbalanced community metabolism, where gross production, P, is either greater than or less than community respiration, R, and proceeds towards a more balanced condition, where P=R. The rate of biomass production  (B/P ) increases during sucession until a stabilised system is achieved, in which a maximum of biomass (or high information content) and symbiosis between organisms are maintained per unit of available energy flow.

Isn't gross production (P) same as biomass (B) ? I can't tell them apart, given that Biomass is the amount of matter living organisms (usually of a specific trophic level) of a given area at a specific time is made up of.

Sanjuta, please provide a context in your title. As such hardly anyone would know what it is about without reading your post, and making them do that  is (1) impolite, (2) likely to make them ignore it in the first place.

@David I generally avoid making title too long, i.e. why I haven't put the full forms.

Titles are important for two reasons. 1. As a courtesy to list members so they don't waste their time on posts that are not of interest to them, 2. For indexing of SE Biology so users searching for a topic can find it. Certainly a title should not be longer than necessary, but writing good titles is a discipline a scientist needs to master.

Searching for context from what you wrote, I found this which seems to be an original article later introduced to the textbook you are using. I think this other version is more clear; P refers to photosynthesis, which is also gross production of biomass; B/P is the ratio of standing biomass to new photosynthetic product; rate of biomass production seems wrong unless you expand it to "existing biomass relative to rate of biomass production."
In summary, the correct interpretation should be that P is indeed the gross production, but B/P is simply the ratio of biomass to the gross production. If R is the loss of biomass through respiration and R < P, then both B and B/P will increase (i.e., you will accumulate biomass) until P=R. Probably in this process both P and R also increase, but what is important is that B/P is increasing, which means the new biomass isn't as efficient at new photosynthesis (presumably either because light is a limited resource or because more of the biomass is not held in photosynthetic organisms).
P is in units of mass/time; R is in units of mass/time; B is in units of mass. The equation would be dB/dT = P - R, or another way, B(t1) = B(t0) + (P-R) * (t1-t0), where t1 is some time after t0.

The website seems to quote from an older edition of the book I'm using. I can't agree to P being photosynthesis because in heterotrophic succession the early seres are dominanted by heterotrophs, so there's theoretically no photosynthesis there and also the equation P=R has been used in the broader sense applying to both types of succesion.

Considering autotrophic succession where as you said P= total primary production by plants, what does standing biomass/crop mean? Even when the water is removed the dried biomass will be same as primary produce.

@SanjuktaGhosh I think you are mostly just overthinking the details. By production the author means production in unit time - a great example would be a forest. P might be all the production of new foliage, etc, just this year - B, the total biomass, includes all of the tree trunks, old branches, everything produced in prior years. Maybe think about it like a warehouse storing boxes: P is the new boxes you made. B is the number of boxes in the warehouse. R is number of boxes you sell and remove from the warehouse.

In heterotrophic succession, you are starting with a lot of boxes, but not producing any. R is bigger than P: you are selling boxes faster than producing them. Eventually, one of two things will happen: either you start producing more boxes, so P increases until P = R and now your count of boxes stays steady, or R stays high but P doesn't increase, you sell all your boxes, and now you have no more boxes to sell, now R is 0, P is 0, and R=P.

In autotrophic succession, you start with a fairly empty warehouse, you are making boxes but not selling as many: P is large relative to R. But your warehouse has some carrying capacity, so P can't be large forever without you running out of space. As your B grows, you have to start selling some boxes to make room for all the P coming in, so your R increases. Maybe if you stack too many boxes, the older ones on the bottom get crushed under the weight and you have to remove those boxes as R. Eventually, P = R when you are producing as many boxes (P) as you are selling or crushing (R).

A very important point that you might be getting tripped up on is that neither source is saying that P = R always: they are saying that, over time, as an ecosystem matures after a disruption, P will eventually equal R. You could delay this from happening by constantly introducing new disruptions, but in that context if you just look over a longer period of time you will still see that P ~= R.

Last point - I am wondering, in your mind, what do you think is contributing to "gross production" of biomass if it isn't photosynthesis? What other processes produce biomass? I think the author changed P from photosynthesis to production to allow for more atypical ecosystems like ocean vents where chemical energy isn't coming from the sun.

Back then I had a bit of misconception about heterotrophic succession which lead me think that P is not Photosynthesis. Thank you for the answer.


text:
How do both autotrophic and heterotrophic successions end up having Gross Production = Respiration?
I was reading Information theory by Eleith, Odum and Golley  from different sources, one of which was Funfamentals of ecology by Odum:

... autogenic succession usually begins with an unbalanced community metabolism, where gross production, P, is either greater than or less than community respiration, R, and proceeds towards a more balanced condition, where P=R. The rate of biomass production (B/P ) increases during sucession until a stabilised system is achieved, in which a maximum of biomass (or high information content) and symbiosis between organisms are maintained per unit of available energy flow.
The succession begins with P>R in autotrophic sucession and P<R in heterotrophic sucession.

I have tried to find explanatory texts both in this and other books without any success so my question is how's this balanced state achieved in both types of successions (the answer is hinted in the first paragraph which I don't quite understand)?
Related to my last post.

The author is saying that 1) Mature ecosystems tend to have a balance between production (=P) and use (=R, respiration) of biomass. This is actually tautological because the author would probably define a mature ecosystem as one where this is true (P=R).
If it starts out P > R, the autotrophs are dominant: more biomass is being produced than used up. It is possible, for a time, that P will increase as, for example, plants grow more leaves, but R is growing too, and there is an eventual limit on P, which at maximum depends on the light available to the ecosystem. As biomass grows, so does the amount of biomass to potentially decay, so eventually R will always catch up to P, until there is balance.
If it starts out P < R, that means you are using up biomass faster than you are creating it. This case is even simpler: you will gradually run out of biomass, and R will decrease.
In either case, when the author is talking about P = R, this is going to be in relative terms; there might still be variations between them, for example seasonal variation, but on average over years or decades you would expect P = R in a mature, stable ecosystem.

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Worm found inside of wahoo
A fisherman from Hawaii wrote the following:

This Fat juicy worm lives inside of every Wahoo that I catch. Inside
  the stomach. Right at the junction to the intestines. Sometimes there
  are two.

What is this parasite?

It is Giant Stomach Worm (Hirudinella Ventricosa).
It is a platyhelmith parasitic to Wahoo fish, feeding on its blood and found inside the stomach. It makes 98% of Wahoo's parasitic infections.

It is a fleshy worm that varies in size and shape; with extended worms the size of a mans finger and contracted ones about the size of a walnut.

It requires two hosts to complete its lifecycle; a snail and a wahoo fish.
A picture from National Geographic Society
Source: lahaina news
Note: A youtube video shows this worm moving.

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Separation of sister chromatids diring anaphase without Centrosomes in plant cell during mitosis
As in animal cell during mitosis sister chromatids are separated from each other during Anaphase by the pulling of kinetochore fibers toward their originating poles of centrosomes but as we know that Plant cells lack centrosome or centrioles then how sister chromatids are separated in plant cells from each other?


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What's the best wat to combine biological replicates in qPCR gene expression analysis? (2^(-∆∆Ct) method; one-way anova, turkey's test)
I am measuring the levels of gene x after transfection of cells with a plasmid and I want to compare them to the levels in mock-transfected cells. I did three different transfection experiments, in different days (three biological replicates). I then quantify expression through RT-qPCR.
How can I combine the data from the three biological replicates?
I was applying the ∆∆Ct method to each biological replicate separately, and then combining and analyzing the final fold change of the three replicates in a one-way anova, with turkey's test for significance calculation.
My supervisor suggested a different strategy: calculate the ∆Ct values (Ct mutant - Ct housekeeping) of the three biological replicates, then calculate the difference (∆∆Ct) of each ∆Ct with the average ∆Ct of the mock-transfected cells (∆Ct(transfected cells; replicate nr. x) - ∆Ct(mock; average of replicates)). Then, calculate the 2^(-∆∆Ct) of each ∆∆Ct obtained.
In both ways, at the end three fold change values are obtained (one for each biological replicate). However, the variance is much greater in the second method and, for example, there's no significative difference (one-way anova, turkey's test), while the significance is reached with the first method.
My question is: which method is the best? And, possibly, why?
p.s. I really hope I made myself clear, it's not easy to explain with words what I mean. Please tell me if you cannot understend some parts of the question.


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Can you help with insect identification? (Outback Australia)
This was in my child's shoe that was left outside. They got it out of the shoe and it went on the wall where they measured it. The body is approx 3 cm and from head to tail it's 6 cm. Any help would be greatly appreciated!
We are in central Australia in the Outback.

It is a cricket very similar to Potato bug found in North America and a female having a long ovipositor.

Wait until somebody else responds, you may get an answer with species level identification.

Could this be related to the "Weta" from
New Zealand ? It looks quite similar to https://en.wikipedia.org/wiki/File:Tree_weta.jpg

This is a member of the family Anostostomatidae, but given its sex is unlikely to be placed further (many Orthoptera are best identified on the basis of males, including this family).  There don't seem to be internet-based identification tools for the group (but the page http://bie.ala.org.au/species/urn:lsid:biodiversity.org.au:afd.taxon:a8042a0a-f34e-4ae3-ab86-5306b9176774#gallery shows a number of specimens and living examples, the latter usually taken only to family); Chapter 5, "Australian king crickets: distribution, habitats and biology (Orthoptera: Anostostomatidae)" in the book The biology of wetas, king crickets and their allies appears to be the best option I've seen that might allow a further identification.

I see that you are answering a lot of entomolgy species ID questions but never provide (internet) references and rarely elaborate much which makes it very hard to tell if your ID is correct or not - this probably is the reason you receive down-votes. To avoid that, please link to sources with images or include these images (depending on photo license) in your post. This will allow others to see the reasons for your ID and give them the opportunity for further reading. Thank you!

The insect you have is commonly known as a Weta. The Weta covers over 70 species, two superfamilies (Stenopelmatoidea, Rhaphidophoroidea) and two families (Anostostomatidae and Rhaphidophoridae).
I believe this is from the Superfamily Stenopelmatoidea and Family Anostostomatidae. Let me let me tell you why.
The two families are separated based in part of their anatomy of the ovipositor - to be non-technical: the stringer-looking projection on its butt. This is a tubular organ through which the female insect deposits its eggs.

Figure 1. Anatomy of Cricket
From “The Biology of Wetas, King Crickets, and their Allies” the main differences between Rhaphidophoridae and Anostostomatidae are as follows:

Anosto-stromatidae are characterized by dissimilar ovipositor - The
  lower part of the upper upper valae are inserted in special furrows of
  the lower valvae.
Rhaphidophoridae  Ovipositor - the lower valvae are covered with the lower parts of
  the upper valvae on the outside (a trait found in both
  Rhaphidophoridae and Stenopelmatidae).

If we take a look at your first picture again, you will notice that there is a furrow going around the ovipositer. This why I believe it is from the family Anostostomatidae.

Finding the correct genus is a little more difficult. Nearly all 70 species of Weta are located in New Zealand and Australia. Here is a pretty good summary of the different Weta Species. I would say this is a female tree Weta, more specifically the Hemideina femorata.

Interesting side note, the Giant Weta is considered to be one of the heaviest insect in the world, with one female weighing in at 2.5 oz!!

Graham Chiu had it right, he's just posted a picture of a male (they are highly sexually dimorphic) - the female is lighter in colour and has an ovipositor, while the male is dark with curved cerci. The book that has been mentioned a few times (The biology of wetas, king crickets and their allies) is a great resource, I have it on my desk at the moment actually. I am studying a close relative of these creatures, the Wellington tree weta (Hemideina crassidens) and the females look very similar to these ones - see my profile pic for one of my girls! We get weta in the city when they belong in the bush, they travel in vehicles, on clothes, on other animals, they're pretty good at getting around, so I wouldn't be surprised if one managed to make its way to the outback.

Please feel free to add some reffereces. :)

Looks like a king cricket, Anostostoma australasiae

http://www.qm.qld.gov.au/Find+out+about/Animals+of+Queensland/Insects/Grasshoppers+Crickets+and+Katydids/Common+species/Giant+King+Cricket#.WIs179XRU0M

Please explain why and how.

And especially explain why the spiny legs and dark color are missing. And how this rain-forest dweller of SE Queensland ended up in the outback...

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How is chewing gum processed?
There is the common belief that

Chewing gum takes 7 years to digest

But is this actually true? Does it really stick to your intestines for 7 years, or is it processed like all foods, except it isn't broken down and is excreted soon after digestion?

I think this question fits much better to skeptics.se.

Agreed with Chris that it doesn't belong here, but it is probably too simple for skeptics.se - you probably can't find a sufficient "notable claim" that this is true. Rather, if you just search for "chewing gum digestion myth" you will find many reputable sources that make it clear that, no, gum doesn't stick in your intestines for 7 years.

If I changed to 'how are indegestible foods like chewing gum processed?' wold that be on topic?

Close voter - how is this primarily opinion-based? It's not like we choose whether or not it takes 7 years

@BeastlyGerbil we can't answer unless you provide a breakdown of the composition of the specific type of chewing gum you are thinking about. We're biologists, not industrial chemists and have no idea what chewing gum is made of. And are they all made of the same thing? That said, I very much doubt anything takes years to digest, but this is another question.

Although I agree that this could go on Skeptics.SE, this question is relevant on Bio.SE b/c the OP is asking a straightforward question about how non-digestible food is digested. @terdon, I think you're being  unfair as those details are really irrelevant and could even be addressed further in a biologically-focused answer. (Also, a quick google search will inform you about general ingredients of chewing gum). Beastly Gerbil, edit a bit more and provide a bit of evidence demonstrating your own research and people should leave you alone.

Purportedly White House Spokesman Sean Spicer consumes (chews and swallows) at least 35 pieces of gum every day.
Mastication breaks down the components and carbs, oils and alcohols are digested accordingly, but the rubber is pushed through by your intestinal muscles. You might enjoy this article which goes into detail about the breakdown and digestion of "gum" constituents. For the most part tho the rubber in gum passes through like corn, peanuts and such.
So, no - no "seven years" to digest. I remember hearing that as a kid. I think it is the kind of thing kids are told to discourage them from swallowing outright instead of chewing gum.


text:
Mg in bacteriochlorophyll
In the figure 1A of http://photobiology.info/Jones.html
the Mg is not belong to other structure.
Is that because something is omitted or is it indeed like a pearl in a mussel's mouth? In the later case could we replace the Mg by some other atoms (and the bacteriochlorophyll still live well)?

The Mg atom is not bound in the porphyrin ring, it is coordinated there.

http://photobiology.info/Jones.html
The author of the above page told me              The magnesium (purple sphere) is bonded to the four pyrrole nitrogens (the four blue atoms pointing towards it.

I checked chemistry books "coordinate" means the shared electron all came from one party ? So,what is the difference between bounded and coordinated?

When the atom is bound, chemical bounds are formed. If it is coordinated, it is kept in place by interaction between the atoms (for example by van der Waals force).

So, both Mg in chlorophyll and Fe in RC are coordinated? Will a coordinated atom have a fixed orientation with other atoms?


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Why are most mutations recessive?
Why are most of deleterious mutations recessive in nature? I understood that if it's recessive then one reason may be that the mutant gene doesn't code for a functional protein and so there is no  phenotype to express.  But why is it recessive in the first place?

It is a bit ironic that you phrase your question with 'in the first place'. There is a parsimonious explanation for the effect: Dominant deleterious variants are quickly removed by purifying selection whereas recessive deleterious variants can "hide" in individuals that carry a dominant neutral/advantageous variant.
You can think about it this way: In heterozygous carriers (in which the other variant has a neutral or positive fitness effect), a recessive deleterious variant has no (strong, depending on the dominance coefficient) negative effect on fitness and therefore, in those heterozygotes, purifying selection will not remove the variant (efficiently, again depending on the degree of dominance) - it can only act on homozygous carriers of the recessive variant. A consequence of that is that the recessive deleterious allele usually segregates at low frequency with most carriers being heterozygous.
In short: This probably has little to do with there being more recessive deleterious variants per se (even though that might also be the case due to the mechanisms you described in your question). In the snapshot we are looking at when we investigate genetic data, the likelihood of finding dominant deleterious alleles is way lower than finding recessive deleterious alleles as the latter usually just persist for a way longer period of time.

@JewelJohnson: You are welcome. If the post answers your question, I'd be glad if you'd accept it. ;) Cheers!

How do I accept it?


text:
What makes delayed onset muscle soreness stop occurring?
If someone lifts weights or takes a long jog after not doing it for a while, they can experience delayed onset muscle soreness (DOMS).
However, when they return to the same exercise days afterwards, the chance of a new DOMS episode occurring diminishes.
I used to think that it was partly due to muscle getting larger. However, an individual who trains themselves to lift 100kg, stops for 2 months and still manages to lift the same 100kg can experience DOMS (assuming that little has changed in the muscle size and force it can exert).
This leads me to ask: are there other biological phenomena involved, rather than just muscle size?

Stopping for two months would result in muscle atrophy — are you trying to propose a hypothetical scenario in which muscle size wouldn't decrease?

I'm not sure what you are asking? When you stop training for two months your muscle size would decrease.


text:
Is blood donation risky for patients with MGUS?
Monoclonal gammopathy of unknown significance (MGUS) is often considered a pre-cancerous condition.
Blood donors with MGUS are typically advised to discontinue blood donation as their blood may be risky for blood recipients.
This paradigm has been recently challenged (e.g. La Raia 2015), but also reinforced (e.g. Felldin 2016).
It is also possible that blood donation may be risky for donors with MGUS as well, as it leads to an overall boost and stimulation in hematopoiesis which may indirectly favor prograssion from MGUS to myeloma.
Is it true?

People in the UK are prohibited from donating with MGUS.


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Is it possible to synthesize chiral version of an organism (incompatible with our pathogens)?
In theory, it should be possible to synthesize chiral (mirror image) version of some organism: with all molecules replaced with their enantiomers, e.g. L-sugars in place of our D-sugars.
Direct application of such chiral life could be production of enantiomers of proteins in e.g. chiral E. Coli, what might be useful for example as new drugs.
However, the most interesting is that such chiral life would be incompatible with our pathogens, for example allowing to design really sterile ecosystems for harsh environments like Mars. Finally, such chiral human would be immune to most of our diseases.
Nice article: http://wikibin.org/articles/chiral-life-concept.html
The question is if it is technologically possible to synthesize e.g. a chiral version of E. Coli?
Update: Wikipedia https://en.wikipedia.org/wiki/Chiral_life_concept

First off, quick clarification: "chiral" simply means distinct from its mirror image. All current life is chiral, in that it is made up of molecules  which have a "handedness". What you're asking about is life which is made up of molecules of the opposite handedness (which I'll term "mirror chiral").
Such a lifeform is theoretically possible - chemical and biological reactions and reaction rates are entirely the same between the two handednesses - presuming that all participants (substrates, products, catalysts, etc.) are flipped to the opposite chirality. A mirror chiral Jarek would look and function exactly like the normal chirality Jarek, although he would need to eat mirror chiral food instead of normal chirality food.
So what difficulties would you have to synthesize a mirror chiral organism?  The biggest one is the bootstrapping issue. There's a large suite of molecules in the cell which are all needed in order to replicate the cell, or even just maintain it. All of these need to be present in order for the organism to work. The organism can make all these components from scratch, but to do so it already needs to have these components.
Synthetic organisms - that is, organisms with a genome assembled in a computer and synthesized abiologically - have been made. The trick, though, was that the synthetic DNA was then placed into already existing organisms to be replicated and to have its genes expressed. There's no limitation (besides perhaps cost) to synthesizing mirror-chirality DNA - the same machines which synthesize normal chirality DNA can do it if you swap out the reagent bottles. But what do you do with it once you have it? There's no existing mirror-chiral organisms you can place it in to replicate and express the genes.
If one was to make mirror-chiral organisms, you would need to synthesize all of the necessary cellular components in their mirror-image form. So you would need mirror RNA polymerase, mirror ribosomes, mirror t-RNA, mirror ...  If you do things right you can skip most of the cellular components, but you still need a large number of them.
This is not necessarily a pipe dream. Last I knew, the J. Craig Venter Institute, the people who made the first synthetic DNA organism, are actively looking into it. The trick is to trim things down to the bare minimal number of chiral components needed to bootstrap the system. That's (more-or-less) where their current efforts are focused, from what I understand: what's the minimal number of genes needed for a viable cell? Which of these are needed to "bootstrap" a cell from bare DNA?
Personally, I'm pretty confident that a mirror-chiral organism will be created one day. The time frame for this is a little unclear, but there's nothing theoretically limiting it. The biggest issue is our current technical limits in synthesizing sufficient quantities of (non-DNA) biomolecules in a chemical (abiological) fashion. But those are constantly improving, and with additional research into what's needed for bootstrapping a synthetic cell, we'll push down the requirements even further.
Of course, the first mirror-chiral organism will be pretty simple. It's going to be less complex than even E. coli. It will also need to be fed a diet of (expensive) mirror-chiral food (amino acids, sugars), so its use will be limited as well.

I see you agree that it is only a matter of time (20 years?) when first mirror-chiral organisms will be created, maybe just because we can. We need to have in mind that it can also be very dangerous, for example mirror-chiral photosynthesizing cyanobacteria would have nearly no natural enemies - could dominate our planet, disturbing the bottom of our food chains: producing L-sugars instead. This seems a really important possibility we should well understand before it (inevitably?) becomes a reality - why there is no public discussion on this topic?

I have decided to restore the Wikipedia article - please help improving it: https://en.wikipedia.org/wiki/Chiral_life_concept

It is already starting: mirror-image polymerase in 2016 http://www.nature.com/news/mirror-image-enzyme-copies-looking-glass-dna-1.19918

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text:
Effect of 2,3-bisphophoglycerate (2,3-BPG) on haemoglobin
When 2,3-bisphophoglycerate (2,3-BPG) binds to haemoglobin, a higher partial pressure of oxygen is needed to bring about 50% saturation of with oxygen.
What is the physiological significance of this and its molecular basis?
How would this affect the oxygen dissociation curve of  haemoglobin and would it alter the Bohr effect?
Note regarding editing
In its original form this was a multiple choice question that had remained unanswered for a year, possibly because the detractors are very bad. Because the topic it covers is thought to be of general interest it has been reformulated as a standard question. For the record, the original question asked which of the following were correct: (1) 2,3-BPG in red blood cells causes the oxygen dissociation curve to shift to the left. (2) The binding of 2,3-BPG to haemoglobin lowers the affinity of the haemoglobin for oxygen. (3) Binding of 2,3-BPG to haemoglobin reduces the Bohr effect. (4) When 2,3-BPG is absent, oxy-haemoglobin is less likely to unload oxygen. The ‘correct’ answer was given as (2), but the poster thought that (4) was also correct.

What research have you done before asking it here?

I've studied oxygen dissociation curves and the Bohr effect; it's just this one question that I don't understand. 2,3BPG obviously shifts the curve to the right and this means that haemoglobin associates with oxygen less easily but dissociates from it more easily. It basically reduces haemoglobin's affinity for oxygen. So if you remove 2,3BPG, the affinity for oxygen should increase and this means that haemoglobin dissociates from the oxygen less easily. I feel that I am missing some very obvious point here so could you please help me.

I think you're correct.

No I checked the mark scheme and statement 4 is definitely wrong but I don't know why.

I have formulated this as a standard question for the reasons explained. I have removed the "homework" tag for this reason and because the original poster will have progressed to other things. I think that although this question overlaps two others, it is unique in addressing the interaction between the Bohr Effect and that of 2,3-BPG,

The oxygen dissociation curve for haemoglobin (Hb) in the absence and presence of 2,3-BPG is shown in (i) below:

It can seen that the curve has shifted to the right (MC-1 incorrect) and the oxygen affinity is obviously decreased, as it takes a higher concentration (pressure) of oxygen to achieve the same percentage saturation (MC-2 correct — and so is option MC-4 as far as I and @JM97 can see, agreeing with the poster. MCQs are an educational abomination!).
The physiological significance of this is  considered in detail in my answer to another question, but, in short, it ensures that an adequate proportion of the (smaller) amount oxygen taken up at the lower pressure in the lungs is released in the tissues (3 minus 4, cf. 1ʹ minus 2).
To address the interaction between the effect of 2,3-BPG and the Bohr Effect one needs to consider the corresponding curves for the effect of hydrogen ions (falling pH), shown in (ii), above (see also my detailed answer to this question).
It can be seen that the effect of hydrogen ions is similar to that of  2,3-BPG. Can these two have independent (additive) effects? It is known from molecular studies that they both interact with and stabilize deoxy-haemoglobin at different positions (see ii, below), and in one model of the allosteric mechanism they can be considered as shifting the equilibrium from the tense (deoxy-) to the relaxed (oxy-) state of haemoglobin:

(i) Generalized diagram of allosteric equilibrium of tetrameric protein between relaxed state (where it can bind substrate/ligand) and tense state. Negative effectors favour the tense state. (ii) Illustration of this for haemoglobin, where H+ ions protonate His-146 of the β-subunits and 2,3-BPG forms ionic bridges between the two β-subunits.
So it would appear that Bohr effect can still augment the 2,3-BPG effect, but I would imagine that the extent of this augmentation would depend on the initial position of equilibrium, and I would not expect it to be additive — I may be wrong. (Is MC-3 correct or not? A school student can hardly be expected to know unless he had been fed the ‘correct’ answer. Perhaps he is intended to interpret the option as meaning “does the 2,3-BPG effect work in the opposite direction to the Bohr effect”. You may now understand why I loath MCQs.)
Bibliography
The diagrams are my own, based on various sources I have used over the years. To check whether what I have written is correct, the reader may wish to check any of the many accounts online, including the following which have references to original material:

Wikipedia article on haemoglobin
Proteopedia article on
haemoglobin

I would welcome comments on the question of the additive nature (or otherwise) of the effects of hydrogen ions and 2,3-BPG. There are better enzymologist/protein chemists on this list than me.


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RNA seq: Should non-infected units be used for RNA-seq?
I am designing a RNA-seq experiment to study transcriptomic profile changes upon parasite exposure. Some papers I read, mostly extract RNA from the entire treatment group (organisms exposed to parasite), without (seemingly) bothering if all the organisms were indeed affected. Doesn't this practice bias results? Are there any studies on how this could affect results?

It will dilute your signal if you have a pool of samples +/- the parasite prepared as one library prep. It is always better to maximize the number sequencing libraries (usually cost prohibitive) and extract RNA from samples you are confident exemplify the condition of interest, and an equal number of control samples to maximize your statistical power.


text:
Does any lifeforms can make a haploid cell from any other cell without meiosis?
Like the title says, is it possible to produce haploid cells without meiosis?

I don't think so, but it is possible to transfer the nucleus of a haploid cell to the body of a diploid cell and vice versa

The question is a bit unclear

Can you produce haploid cells without meiosis?

The question is a bit unclear. for two reasons

What do you mean by "you". You mean can we do such thing with modern technology or do you mean does it ever happen or do you does it ever happen in human cells.
It is also unclear what from. Are you implicitly asking whether "you" (whatever 'you' mean in your sentence) can make a haploid cell from a diploid cell or form anything?

Answer
In this answer, I will assume that the question is

Does any lifeforms can make a haploid cell from any other cell without meiosis?

The answer is yes. Many organisms have a long haploid stage during which many mitosis occur. Haploid cells undergoing mitosis results into two haploid cells.
You might want to read more about life-cycle (wikipedia), especially the sections on haplontic life-cycles and haplo-diplontic life cycles.

I think these are great answers that will cover OP's curiosity, but the question isn't really up to our standards - can you edit the original question to fit your answer?

Thanks for your answer. English isn't my mother-tongue, but you assumed the question correct Remi. I had a lecture about Saccharomyces cerevisiae, and wasn't sure if the budding generates haploid cells. But if I understood it correct, an "a" mating type spore can generate a haploid "alpha" cell without meisosis, right?


text:
Why don't all male animals kill a rejecting female?
If a male animal is sure that the female animal will not reproduce with it, wouldn't it be mathematically optimal for the male to kill the female? (To ensure that no alleles of the "overreact-to-rejection" gene in other males can make use of the female as a reproductive resource)
I might be missing something very obvious here, but I can't seem to see why a gene for "kill-rejecting-potential-mate" wouldn't spread through the gene-pool.

I think you are missing many possible explanations. For example, females fight back - combat is risky and would be just as likely to prevent success with future potential mates. Additionally, in many species females are on average stronger or larger than males. It also seems to me that reducing the number of potential mates, even after a rejection, is a poor strategy. While a male is busy battling with the rejecting females, the other males are busy mating with all the others. I also don't know what you mean by "overreact-to-rejection" gene...

Evolution isn't just about an individual passing its genes on, it's about a population surviving and adapting through time. Limiting your numbers does not appear a good survival strategy on the population level. You are possibly eliminating alleles that are, or would be in the future, of selective advantage.

Why do you think all females don't kill males they reject?

Combat is risk. Rejecting female may kill rejected male.. thereby removing gene for male who over react to rejection. Females may move in groups, so injuring one female member may result in all females in herd to reject said male. Combat take time. While rejected male is spending time killing rejecting female. Other males are mating with non rejecting females. Males do produce daughters. Murderous rejected male, may produce murderous rejecting daughters.

I asked moderators to delete this question, but:
1: Everyone seem to assume that I am misogynist. I'm not. In fact, I am glad to see the "outrage" against apparent misogyny 2: @swbarnes2: because male animals often give very little contribution to reproduction. 3: @ bpedit: a gene that result in the death of a whole population would still spread through the gene pool, even if only in the local gene pool before the latter's destruction.

@bedit: This is in fact wrong. Selection does neither work on populations (it works on individual phenotypes and maybe ... maybe on groups with close kin - that is at least debatable) nor does it generally favour survival (and by no means survival of a population), unless survival is necessary for reproduction. It actually is about individuals passing on genes that lead to selected phenotypes.

A "kill-rejecting-potential-mate" gene??? This quite frankly is utterly absurd! I mean come on, please acquaint yourself with the concept of a gene first before broadcasting such theories.

The simple answer is most animals females can fight back. Its similar to the reason male to male fighting often evolves to become more and more ritualized. Fighting is risky, and the closer in size and capabilities the fighters are, the riskier it becomes. Behavior that tends to get you injured for little to no benefit tend not to get passed on. and there is little to no benefit in killing females for a male. Plus a female who is alive can change her mind later, so there is a direct benefit to the male for not harming her.
Now there are animals where a female will be bullied into mating to the point of risking injury or death. Those animals are very rare and have high dimorphism, they have males that are MUCH larger and more dangerous than the females, to the point the female is incapable of being a significant threat to the male. It is most common in animals that express harem polygyny. It also tends to carry the risk of inbreeding.
One horrifying example is hamadryas baboons. Males maintain a harem and threaten any female that even strays too far from the male. They even bite disobedient females.

There's natural selection for males that do what ever they can to stop a female mate they already have from having an affair because if she has an affair, she might produce an offspring that's not his own so they can't get as much food to rear as many of his own offspring. Although killing her makes her unable to have an affair, it's not selected for because she can't produce a kid that is his own either if she's killed. If she deserts him in addition to rejecting him, there's no evolutionary advantage in him killing her because she won't stop him from finding another mate that will produce a kid with him. It would however be an evolutionary advantage for a male to reduce his options and do something to make it so that he will be unable to not kill his mate if she rejects him. Females who did not reject males that reduced their options in that way would be selected for and then in response to that change, males that reduce their options in that way would be selected for. If after that, a mutant male that could make it look like they reduced their options when they didn't arose, it would outcompete the males who actually reduced their options and then females who rejected a male would stop being selected against and maybe it some cases be selected for.

You need to reread the question more carefully.  It is about killing non-receptive females not killing promiscuous ones.


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Eating possibly spoiled food in the fasted state - is it considered protective against the potential harm?
It is a known fact that the acidic environment in the stomach serves several purposes, such as providing suitable conditions for primary chemical digestion of food molecules and protection from certain kinds of infections which may be caused by bacteria taken in with the food - I'm not giving any specific reference, any basic gastrointestinal system physiology text will give this information and more.
My question relates to the latter role I mentioned above: about the stomach being most acidic when in the fasted state (i.e. the period between about 2 hours after eating and eating again).

This article describes a stomach pH of 1.7 in the fasted state and a pH level of 6.7 shortly after eating

My question:  If I'm about to eat food that is potentially contaminated by bacteria, would it be better if I wait until I'm well into the fasted state (i.e., very hungry) in order to minimize the risk of indigestion or any other adverse outcome of eating spoiled food? If so, would the reason be because my stomach is as acidic as possible in that state?


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Why are fearful stimuli more powerful at night?
For example, horror movies appear to be scarier when viewed at night than during broad day light.
Does light have any role in this phenomenon?
Are there changes in hormones at night versus during the day that makes fear stronger?

I think this is a really awesome question, I might try to edit it a bit if you don't mind, I'll try not to change the meaning. I might also write up a quick answer based on rodents, though something you may or may not realize is that "fear of the dark" is certainly not universal - if you were a mouse asking the question, you might wonder why the daytime is so scary.

I don't have time right now for a full response, but I'll just dump a couple starters out there. The hormonal side I'll have to do a little research on, there are certainly hormones that change throughout the day but I don't have detailed knowledge of this specific effect. There is also a direct projection from certain cells of the retina directly to the amygdala, an important brain structure in fear. The topic is actually of high interest because similar circuitry is implicated in anxiety disorders and PTSD and belongs in the broader category of "what makes 'normally' not-scary things scary."

@Bryan Krause: Indeed, fear of the dark is not universal even among humans.  I've always liked the night myself, and can't really understand why people use nightlights & such.  Nor have I ever noticed any change in intensity of 'fearful' stimuli that wouldn't be explained by not being able to clearly see the source.  E.g. that growl might be a bear, or your neighbor's friendly dog.  In the day, you would know (unless it's in the bushes) and react accordingly.  In the night, you assume the worst case and prepare.

I think it would be necessary to report references that this is actually the case (fear response is activated more easily at night), otherwise it is just an opinion.

here:  http://cogsci.stackexchange.com/questions/16751/why-do-we-fear-more-in-the-night

I suspect that it's a combination of uncertainty and expectation, and there might some related neuromodulatory effect, but I don't know any relevant literature.

Maybe it is psychosomatic; we as children grew up fearing the dark. We are let to believe that ghosts haunt at night. It can be considered similar to Triskaidekaphobia (fear of 13) or Hexakosioihexekontahexaphobia (fear of 666).

Short answer
The increased fear responses during the night are believed to be mediated by elevated corticotropin-releasing hormone (CRH) levels in the brain that drive the fear responses in the amygdala.
Background
Fear responses can be experimentally assessed by recording the startle reflex. For example, loud noises can evoke gross startle responses in rodents (whole-body startles) and more subtle responses in humans (eye blinks).
In nocturnal animals, it has been shown that startles are facilitated by bright light. In contrast, fear responses in humans, a diurnal species, have been shown to be stronger in the dark (Grillon et al., 2007).
In the rat, the light-enhanced startle has been associated with the hypothalamic–pituitary–adrenal axis (Fig. 1). Specifically, light exposure has been shown fear mediated by corticotropin-releasing hormone (CRH) (Grillon et al., 2007).

Fig. 1. HPA axis. source: Wikipedia
The HPA-axis is affected by the circadian clock and therefore exhibits a pronounced daily rhythmicity. The HPA axis is activated by hypothalamic release of CRH, which stimulates the secretion of adrenocorticotropic hormone (ACH) from the anterior pituitary. ACH triggers the production of cortisol by the adrenal glands. Cortisol, in turn, provides negative feedback and shuts down HPA-axis activity by binding to corticosteroid receptors in various HPA-axis structures, e.g.the hypothalamus (Fig. 1). As a result, cortisol levels show a robust diurnal rhythm that runs in opposite phase with CRH. Cortisol in humans peaks at the time of awakening and drops to its lowest levels around bedtime, whereas the opposite is true for CRH (Miller & Gronfier, 2001).
The startle reflex shows a diurnal variation roughly opposite to the rhythm of corticosterone and in phase with CRH. Specifically, startle responses in nocturnal animals such as rats are highest during daytime (their passive phase) when CRH is peaking, and corticosterone is at its lowest. Conversely, startles are lowest during the night (their active phase) when CRH levels are lowest, and corticosterone levels are high. In man, a diurnal species, exactly the opposite pattern is observed. Hence, startle responses are thought to be endogenously modulated by the circadian system, most likely via effectors of the central pacemaker such as the HPA-axis (Miller & Gronfier, 2001).
In rats, administration of exogenous CRH enhances the startle reflex and blocking of the glucocorticoid receptors which produces a blockade of negative feedback, also increases startles. Conversely, blocking CRH receptors decreases the startle response, as does corticosterone administration (Miller & Gronfier, 2001).
CRH receptors are expressed at various brain centers, including the amygdala. The amygdala is a key structure in the limbic system, the emotional control center of the brain. The amygdala is specifically associated with anxiety and fear responses. Indeed, it is thought that CRH receptors in the amygdala are responsible for the fear-promoting actions of CRH (Grillon et al., 2015).
Hence, it is not darkness or light per se that mediate fear responses. Instead, it is the circadian control of the HPA axis that controls the daily variations in fear responses.
References
- Grillon et al., Biol Psych (2007); 62(10): 1183–6
- Grillon et al., Neuropsychopharmacol (2015); 40: 1064–71
- Miller & Gronfier, Psychophysiol (2006); 43(3): 297–301

@Mesentery - no rush :-) Apologies for the delay, but complex questions like this one need some careful preparation :-) It took me a while to gather the appropriate references and get the story right. Especially because most research has been done in nocturnal species the subject is quite complex

Great answer. Of course this is almost certainly only part of the story - I would expect there could also be learned and instinctual associative learning related to darkness and fear - the strength of which no doubt displays a lot of situational and inter-individual variability. And great find on that Grillon paper - I was searching for something similar when I initially commented and wasn't immediately successful, finding mostly the rodent work in the light instead.


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What is the best way to make a phylogeny from a list of genera?
All I have is a list of about 500 eukaryotic genera, and I need a neighbor-joining tree to show their relationship.  I want to cast on top of this tree the loss of a particular enzyme.  Is the best way to do this to make a 16S phylogeny?

Do you have any information besides their names? Like 16S sequence data?

16S phylogeny would only work for bacteria and archaea unless you are talking about mitochondrial or chloroplast 16S rRNA. Your phylogenetic marker choice should depend on which phyla you are looking at. I suggest you try using Ef-tu if your genera are highly diverse
http://www.scs.illinois.edu/schulten/tutorials/ef-tu/eftu_tutorial.pdf
Once you have a tree in Newick format, iTOL has some nice web tools for overlaying data on trees
http://itol.embl.de/itol.cgi


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Designing degenerate primers using alignment of protein sequences from other species
I am trying to design a PCR primer for a gene whose sequence is not known. Even the whole transcriptome sequencing done in our lab did not identify that particular gene. Hence, I guess I am left with only one option: to design the degenerate primers for this gene by performing sequence alignment of the given protein from several related species and designing primers based on conserved region. Could you please explain the process of primer design by this method. I know some steps which I have described below stepwise:
step 1: download sequence of protein in question from related species from NCBI in FASTA format
step 2: perform alignment using clustal omega
step 3: identify the conserved domains
I am not sure how to move forward from here. I tried J-codehop for next steps but it is asking many parameters for which I have no clue.
Thanks

Try going through this tutorial: http://www.scs.illinois.edu/schulten/tutorials/ef-tu/eftu_tutorial.pdf
It is a nice introduction on how to use multiseq and identify conserved domains from AA or nt sequences across many taxa.
Also check out http://fungene.cme.msu.edu/
The RDP staff at Michigan State University are the masters of doing exactly what you're trying to do.


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How did parasitoid wasps evolve their life cycle?
I know there are a variety of wasps with various strategies for acquiring and controlling hosts. Do these form a rough picture of how these life cycles could have developed in the first place? What is the most recent speculation?

This is similar to the seahorse problem, in that it requires a distinctly non-mammalian perspective. Parasitoid Wasps, Natural Enemies of Insects provides a more in-depth explanation.
Existing wasp strategies may illustrate the possible transitional forms. It is not a linear transition: all of these have branched off and there are multiple parasitic strategies.

Solitary wasp, captures prey to feed to its larvae
Ectoparasitoid wasp, which lays its egg directly on prey that is paralyzed or otherwise unable to resist as the larvae eats it alive
Endoparasitoid wasp, which has formed a symbiotic relationship with a virus that disables the prey's immune system thus allowing eggs to be laid inside the prey
Hyperparasitoid wasp, which preys on other parasitoid wasps

This has the beginnings of a great answer, but needs a bit more detail before it answers the question fully.

@arboviral: Thank you for your comment. I was becoming peeved that my question would never be answered and all my google searches revealed expensive textbooks and papers behind paywalls.

No problem! If you need to get paywalled articles and are on Twitter you could try #icanhazpdf (https://en.wikipedia.org/wiki/ICanHazPDF).


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Feet size correlated with testosterone in women?
Do females with bigger feet have more testosterone? Examples:
1.Regular-sized women with larger than average shoe size
2.Taller women who tend to wear larger shoe sizes more often than not
I ask because some people say that when women feet get bigger they resemble men's feet more. I ask if this such resemblance is indicative of testosterone higher naturally in these women vs. women with smaller feets. I hope someone can understand and apply these methods to an answer.
For example my sister have bigger feet (size 10 in women's Canada) and people have always told her, especially family, that her feet look like a guy's feet/structure more because they are bigger.
Like the genes that mold the bone structure and design of the foot could having higher test. impact the feet and give the women with larger types feet that people say are more masculine more natural test?

can you add any scholarly publication to support asking this question? this sounds unfounded... also, how does testosterone affect bone growth? you suggest that bone length is somehow increased by increasing concentrations of testosterone in the blood - is there any evidence for that at all?


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How does vitamin A deficiency arise?
How does vitamin A deficiency arise?
I am living in a "developed" country, so excuse me if I miss some facts
that are real, and threatening, in other parts of our world.
I heard about https://en.wikipedia.org/wiki/Vitamin_A_deficiency ,
but looking at what foodstuff contains vitamin A or precursors,
I'm at loss how anyone can suffer from vitamin A deficiency.
Obviously, I'm lacking some information here.
One thing that looks particularly misleading is when you are
presented with vitamin A contents of foods, neglecting precursors
like carotenoids that can be easily converted to vitamin A as needed.
As a (sometimes misleading) rule of thumb, I was thinking that most
yellow or orange looking food was prone to contain vitamin A or some
of its precursors.

The WHO report "Global
 prevalence of
vitamin A deficiency
in populations
 at risk
1995–2005" (page 12 of 68) puts it like this:

Where animal source or fortified foods are minimally consumed, dietary
  adequacy must rely heavily on foods providing beta-carotene. However,
  while nutritious in many ways, a diet with modest amounts of
  vegetables and fruits as the sole source of vitamin A may not deliver
  adequate amounts, based on an intestinal carotenoid-to-retinol
  conversion ratio of 12:1 (2)  This ratio reflects a conversion
  efficiency that is about half that previously thought, leading to
  greater appreciation for why VAD may coexist in cultures that heavily
  depend on vegetables and fruits as their sole or main dietary source
  of vitamin A.
Usually, VAD develops in an environment of ecological, social and
  economical deprivation, in which a chronically deficient dietary
  intake of vitamin A coexists with severe infections, such as measles,
  and frequent infections causing diarrhoea and respiratory diseases
  that can lower intake through depressed appetite and absorption, and
  deplete body stores of vitamin A through excessive metabolism and
  excretion (3, 4). The consequent “synergism” can result in the body’s
  liver stores becoming depleted and peripheral tissue and serum retinol
  concentrations decreasing to deficient levels, raising the risks of
  xerophthalmia, further infection, other VADD and mortality.

Just as a side note: green leaves contain heaps of beta-carotenes as well!


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Difference between clonal and subclonal mutations
I'm a physicist writing a proposal that has to do with cancer as a disease driven by evolutionary selection. As far as I understand, all tumors start with a single precursor (single cell or group of cells), and the other cells derive from this precursor by cycles of alterations and selection processes.
Reading recent articles, such as this, I learned that the derived cells include both clones and subclones. Since I'm not sure I understood things correctly, I have a few questions on the difference between the two words:

Is it OK to call clones the cells derived from the precursors?
When should I use subclones?
In the case of heterogeneity, is it fine to call clonal population a group of clones with the same characteristics?

clones means when a cell has the same DNA characteristics as his predecessor so in that case of yours you could say that those cells are clones while for sub-clones I am not that sure, the difference of clone and sub-clone is that a sub-clone is basically a clone who is then remade with a different characteristic(an upgrade if you will) , since cancer are mutated cells you could call them like that but only if you study its DNA, meaning you have to study deep to find out if there are sub-clones in there. AS for the 3 question I didn't quite understood what you meant cuz you just used 2 words with opposite meaning because heterogeneity means a group of organismes with different characteristics and clonal population means organismes with same DNA ( much like a colony of bacteria).


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Fe in bacteria light-harvesting system Reaction Center
Is the Fe in the reaction center of bacteria light-harvesting system bounded or free atom?

After reading the comments in the first answer, I believe OP's question is this:

What kind of bond occurs in the Fe of the reaction center of bacteria light-harvesting system?

Before continuing, it's worth mentioning that an ionic bond is a kind of bond, and that atom would not be considered free (whatever that means) even if its bonds were only ionic ones.
However, to make things here even more unequivocal, the bonds of that Fe are covalent bonds (thus, that atom is not free under any definition...).
According to the Protein Data Bank in Europe, this is the x-ray high resolution structure of the photosynthetic reaction center from Rhodobacter sphaeroides at pH 10, zoomed at the portion that contains the Fe (link here):

You can see that the Fe has 5 bonds, thus summarised:

[SQUARE_PYRAMIDAL] - HIS 190L - HIS 219M - HIS 230L - GLU 234M - HIS 266M

And what kind of bond are those?
According to the same PDBE entry, they are covalent. Have a look at the color code in this page: http://www.ebi.ac.uk/pdbe-site/pdbemotif/?tab=boundmolecule&pdb=2uxj&ligandCode3letter=FE
Here is a screenshot, in case the link above doesn't work. Have a look at the 5 red bonds (red represents covalent... not very legible, I know):

Source: Protein Data Bank in Europe

I would argue that the Fe is bound as a (coordination) complex, as is the case with most metal ions in porteins. This bond is not strictly a covalent bond (the actual physics are actually quite complicated) as none of the electrons forming the bond come from the metal/iron atom itself.

I know what is a coordinate bond, I used to teach that. However, a coordinate bond is a kind of covalent bond (I would like a reference to "this bond is not strictly a covalent bond"). Thus, it seems to me that the answer remains the same.

On top of that, PDBE explicitly says covalent bond.

I guess it's mostly a matter of definition, if you classify a coordination bond as a subtype of covalent bond or as it's own type. My chemistry professor from university was arguing for latter version, so that's how I see it. Also wikipedia does not list a coordination bond as a type of covalent bond.

I see. Indeed, it depends on the definition. However, the same wikipedia lists the coordinate as coordinate covalent bond

I know no examples of free iron atoms serving active physiological functions within living organisms. Iron, as with other metals, are generally in their ionic state. As such, they are attracted and held in position by negative, or partial negative, charges on nearby atoms. Sometimes these are from the sidegroups of proteins but often the negative charges bonding the metals are on specialized molecules such as the poryphrin ring in hemoglobin whic contains an iron ion in the center, held in place by four nitrogen atoms like a gem in a ring.
The principal metal ion in photosynthesis is magnesium. Just as with the iron in hemoglobin, it is centered in a poryphrin ring. This is also true of the chlorophyl in bacteria. But there is also an iron ion associated with the reaction center. Apparently this is "connected" to the P870 bacteriochlorophyl molecule. Here is the article: http://photobiology.info/Jones.html
You can view this for yourself. Here's a link to the molecule in question at the Protein Data Bank (instructions follow): http://www.rcsb.org/pdb/explore.do?structureId=2BOZ
On the left side is a viewing window where you can see various representations of the protein and any associated molecules (ligands). This won't help because the Fe will be hard to pick out. Scroll near the bottom of the page and you will see iron (FE) listed as one of the ligands. In that row, in the far right column, click on "NGL". In case you got lost, here's the direct link: http://www.rcsb.org/pdb/ngl/ngl.do?pdbid=2BOZ&preset=ligandInteraction&sele=[FE]
That's the Fe with the big orange glow. Notice how it's held in place by 4 nitrogens plus a carboxyl group. Click on any "stick" making up one of those nitrogen containing structures. Notice, in the window's upper left, the label for this begins with "HIS". This stands for histidine, an amino acid. Indeed, every one of these goups surrounding the Fe is an amino acid belonging to the chlorophyll protein.
So, unlike the Fe in hemoglobin, this Fe is attached to the protein directly.

Thank you for the reply. But a few days ago a professor in Germany told me it is not bounded? What follows is her reply, did I miss interpreted her words? =================The non-heme iron can be exchanged, eg. against zinc. It is like a pearl in a shell. In contrast to this, the iron in the cytb556 protein subunit is bound by two subunits (alpha and beta) and coordinated by two
histidines.

You said "The principal metal ion in photosynthesis is magnesium"? Is it so? Ion is not the principal metal? Then, what is its function?

So, the Fe is bounded? Has it a fixed orientation with the RC and the LH1? I think the answer is yes? My question is, what is its orientation?

I checked the NGL link you provided. I agree the Fe is "held in place by 4 nitrogens plus a carboxyl group" (quoted as you said) But it does not seems to belong to other structure? But you said it is BOUNDED? Sorry if my question is naive. I do not understand chemistry. I did not studied chemistry after university. I understand only high-school chemistry.

So, is the magnesium in chlorophyll bounded or not?

@latra. The image showing the Fe is only an isolated portion of the complete molecule, the rest is not shown. There are ways to display it all but require use of a viewer and a bit of practice at using it.

@latra. I didn't read the entire article I referenced. I'm not experienced in bacterial photosynthesis but in plants there are "accessory pigments" which also capture light and shuttle the energy to the principal chlorophyll molecule (containing the Mg). Perhaps the Fe containing P870 is an accessory pigment in bacteria.

If the Mg in bacterial chlorophyll is like that in plants, it is bonded to a poryphrin ring within the protein comprising the chlorophyll. From an evolutionary standpoint I suspect that is true but can't guarantee it.

To your first comment. Perhaps what the professor means is that it is not PERMANENTLY bonded. The "bonding" of ions in cells is not covalent. That Fe in the image is only held there by electrical attractions to the negative groups surrounding it, no sharing of electrons. In fact the prof Is implying this by stating it can be exchanged. Maybe this is semantics. But The Fe is not just freely floating around. It it held, if temporarily, by an ionic association as shown in the image. I call that bonded.

Your prof refers to yet another Fe containing protein. So maybe the one I referenced is not the one you ask about?


text:
Do pregnancy and breast feeding increase basal metabolic rate?
Since pregnant or breastfeeding women have extra nutritional needs, does that mean they have a higher BMR?
Why I thought the conclusion would be sensible: Since BMR is the energy needed to perform body functions (breathing, respiration, homeostasis, digestion, etc), pregnant woman or breastfeeding women, because of their extra 'activity' (due to the presence of the fetus) will have a higher BMR.

Basal metabolic rate for a particular organism is determined by the amount of calories that the organism needs for basal metabolic processes (i.e. basal energy demands). Since pregnant and breastfeeding women have increased caloric requirements (i.e. increased energy demands), then that means by definition their basal metabolic rate is increased.

A pregnant woman’s total energy expenditure during pregnancy is mainly because of a raised basal metabolic rate, or BMR. The energy necessity of basal metabolism is influenced by nutrition prior to pregnancy and the size of the fetus. According to a 1990 study, “Energy cost of physical activity throughout pregnancy and the first year postpartum in Dutch women with sedentary lifestyles” by Joop MA van Raaij, et al, “BMR is increasing throughout pregnancy mainly because of fetal demands.” BMR will decrease to preserve energy if maternal energy stores are too low when a woman becomes pregnant. Also, women having larger babies tend to have greater increases in their BMR and greater decreases in the rate of their energy stores than pregnant women having normal-weight or underweight babies.

could you add active links that users could click to go directly to these sources? it would greatly strengthen your answer. thanks for your contribution.


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Calculating gene separation -a genetics problem
I am really struggling with genetics. In particular, I have the following question

Now I am OK with calculating the separation of genes in centrimorgans when I have data like so:

But in the first question, I am not sure if this is even possible. I gone through many books to no avail.
The conclusions I have been able to draw so far are:

these mutations are carried on X due to similar proportions of males and females exhibiting the characteristics.
the order of genes seems to be white, miniature, forked due to white miniature and forked miniature occurring much more frequently than white forked. Also it seems that white and miniature genes are close than miniature and forked as the former is a more commonly exhibited phenotype.

All of this is alluding to me somehow being able to figure out the separation of the genes, but I do not know how. Or if this is at all possible in this problem..

Text on images are not very welcome. These texts are not searchable and cause problems for people with visual impairments.

Your second image appears completely black on my browser. @Remi.b is right, you should take the trouble to set out your question properly otherwise I shall vote to close.


text:
How long ago did protein synthesis from DNA start?
How long ago did DNA start to include sequences that code for protein?

where have you looked for information on this? online, google, wikipedia?

Protein isn't synthesised from DNA it's synthesized from RNA.

I've googled it first yes, I could not find it. And yes, I realize that protein get synthesized from RNA, but the protein is coded in the DNA. My question is, when did DNA code start to contain information on the proteins that are the result of gene expression. Sorry if my formulation caused confusion.

There are two questions being asked here.
1) When DNA was used to encode RNA via DNA dependent RNA polymerase
It is uncertain if the Last Universal Common Ancestor (LUCA) had this enzyme. There is some debate.
Also some  DNA polymerases of family A, B are structurally related to RNA polymerases https://www.ncbi.nlm.nih.gov/books/NBK6360/. So DNA may have come after RNA. The switch to DNA has been proposed to be a result from a reaction to the evolution of RNAse.
2) When RNA was used to encode protein via ribosome
LUCA has ribosome. So LUCA had proteins made from RNA
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2926754/
And LUCA has been estimated to have appear around 3.5-3.8 billion years ago. https://en.wikipedia.org/wiki/Last_universal_common_ancestor

Please define the abbreviation LUCA in your answer.

Last Universal Common Ancestor.

I worked that out, but I shouldn't have to. Define it in your answer so that everyone knows. The use of undefined acronyms is lazy and inconsiderate and decreases the value of an answer.

DNA and RNA... which actually stand for Deoxyribose Nucleic Acid and Ribose Nucleic Acid.

I am afraid that this will not wash. More people know what DNA and RNA are than know what it stands for. As you are not willing to clarify your answer, then I shall your do it for you, although I hardly think it worth it for such a poor question. Also the last common ancestor hasn't been around since 3.5-3.8 billion years ago — that would imply it is still around. It was thought to have lived then.

Thank you very much JayCkat, I found your answer to be clear and satisfactory. Sorry we did not meet your requirements David :/


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Is human "sperm warfare" a concept supported by biology?
I've recently read the "Sperm wars" book by Robert Baker. It deals with human sexuality and infidelity. The main premise of the book is that  human male has different kinds of sperm:

Regular sperm for fertilization
Toxic sperm that kill competitor sperm (similar in concept to white blood cells)
Slow, inactive sperm to block channels in female cervical filter

According to the author, when a female engages in infidelity or group sex, the sperm actually "goes to war" killing competition and preventing passage through cervical filter.
Are there are indeed different kinds of functional sperm in humans, and are their functions involved in sperm competition / warfare? In other words, does human sperm not only fertilize the egg, but also to block passage of competitor sperm and even kill it?

This guy seems to have reasonable credentials. Next step would be to search academic journals for this research and see whether peer reviewed.

The logical conclusion to this claim seems to be that a woman could not get pregnant (or would be much less likely to do so) while engaging in "infidelity" or group sex.  I'm pretty sure that this is contradicted by experimental evidence.

I wanted to respond to your question because while I don't know very much about this particular subject myself, I did have the pleasure of attending a talk by Robert Martin, author of How We Do It (https://www.amazon.com/How-We-Do-Evolution-Reproduction/dp/0465030157/ref=sr_1_2?ie=UTF8&qid=1492260860&sr=8-2&keywords=how+we+do+it).  In the talk and in his book he does address this topic (and the book Sperm Wars) and basically says that while it was a highly influential idea, the underlying science isn't reliable.  He argues that evidence suggests that humans have not evolved under multi-male types of mating systems. There is a lot of evidence to back this up, and revoke the idea of "killer sperms."  Check it out and see what you think!  If anything it is an interesting read.

Not in humans
Sperm competition is supported in humans (multiple sperm from multiple partners can be present in the same female)
Specialized sperm is not supported.
Specialized sperm is however confirmed in non-human non-vertebrate animals which was surprising, although what the different types of sperm do in these animals is not understood.


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What is the difference between "Bisphosphate" and "Diphosphate" in biochemistry?
I have often found bisphosphate compounds ( e.g. RuBP, RuBisCO, 2,3-BPGA etc.) and diphosphate compounds (e.g. ADP, GDP etc.) in biochemistry. They are commonly seen and are important compounds in both animals and plants but what is the basic difference between a bisphosphate and a diphosphate?

For example fructose 1,6 bisphosphate is used in step four of glycolysis but d location of the phosphate group has been mentioned already ,1 telling us carbon 1 and 6 telling us carbon 6(no offence) but i think its the same thing as bisphosphate.

[Source:Wikipedia]
As you can see in the above structure of ADP(Adenosine di-phosphate), the two phosphate groups in the compound are directly attached to one another. So it is named as di-phosphate. [Source] You can see this table for more examples.

[Source:Wikipedia]
In this structure of RuBP(Ribulose-1,5-bisphosphate), the two phosphate groups in the compound are not directly attached to one another, they are attached to first and fifth carbon, meaning they are attached to different atoms. Therefore, it is named as bis-phosphate. [Source](2nd comment)

I believe this is the correct distinction, but historically the two terms have been used interchangeably. As an example, a lot of biologists will still refer to 2,3-BPG as 2,3-DPG.


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What would happen if two different viruses penetrated one cell?
I want to know what would happen if two different kinds of viruses took over one cell.
Would nothing happen? Would the cell create both kinds of viruses? Would it make a fusion of the two viruses?

Are you thinking about viruses (which are "created" by cells)?

One infected cell may produce hundreds of new viruses. By the time the disease occurs, many thousands of cells may be infected and producing new viruses. These new viruses are released from the cell, often in bunches, and are almost identical. Sometimes the host cell makes mistakes in copying the virus nucleic acid, causing some genetic variation. However, the outsides of these new viruses tend to be pretty much all the same, and they will usually infect only some more of the same kind of cells that produce them ¯ either in the same host animal or, if they can get out, other animals. Viruses produced in the respiratory tract are usually shed in droplets from the mouth and nose; viruses produced in the digestive tract are usually shed in feces but sometimes also in vomitus.
One person or animal is usually infected with only one kind of virus at a time, so the bunches of virus they produce and shed are all the same. Then, if this virus infects another person, even if two of the same kind of virus bump into a single susceptible cell, the infection will still be all of one type. However (much less likely), if viruses from two different infections get mixed up in the air or in sewage and get into a single person, it is possible that two different viruses will attach to receptors on the same cell and infect that cell together. If the two viruses are closely related, their nucleic acids may "recombine" while they are being copied. When this happens, part of the genetic information from one virus is linked to the genetic information from another virus, and the new virus that is produced is a "hybrid."
If you read about influenza that is traveling about in populations you will see that the outside of the influenza virus has an H type and an N type. For example, you might read that this year's main influenza virus is type H3N2.A reason to get a new flu vaccination each year is that the vaccine has to be made to immunize us against this type. Somewhere out in the world, a double infection as described above may happen between two different types of influenza viruses and some of the new virus may be type H5N4. Once this new type is established, a new vaccine is needed, or people won't be protected. Development and production of vaccines are expensive, and distributing them and getting people to use them is difficult. So, here is at least one situation where your question about two viruses infecting one cell may have serious public health results. Of course, influenza viruses that develop in birds, and sometimes other animals, may also be transmitted to people. Not many other kinds of viruses can jump host species like this, but it is possible that Ebola was transmitted to people from apes, perhaps from eating "bush meat." Viruses and other infectious agents that are transmitted from animals to people are said to be "zoonotic"; once this happens, the virus can usually be transmitted from person to person after that. Obviously, this too is an important public health concern.
http://www.madsci.org/posts/archives/2007-12/1198562498.Vi.r.html

Well, it depends on the virus.
Assuming the virus were different strains of the same species, the viruses can swap their genetic material. Producing both parent strains and hybrid strains. Good example is the influenza virus.
If the virus are very different, and are not lytic in nature (ie they don't kill the host cell), the two viruses the can co-exist. And the poor host cell ends up producing viral particles of both virus.
It is possible that the two ended fighting each other. But I have not read anything like that before. Instead I have read, what happens in HIV, where infection with one strains of HIV prevent reinfection with a second strain.


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White water bird with black 'hat'

The white bird in this picture, swimming between the ducks, was seen in Beijing, China, in januari 2017. It was cold: the water seen in the picture is liquid, but not far from this, the water was frozen. We also saw it standing on the ice.
It has an orange beak with what seems to be a small black spot at its end. It also has black as the top of its head. We did not find a similar bird when searching ducks, goose or even swans. What species is this?

Interesting species. I wonder if it is a variant of mallard.

@Sanjukta Ghosh. It is not a species. It is a race/variation/form/etc of the species Mallard (Anas platyrhynchos).

This duck has several features that could put it in a number of variants of domestic duck. It could be a hybird with a magpie duck or ancona duck? Magpie ducks have black caps, similar to the duck in the photo, but also have black backs. Anconas have some black on the face.

@JC11 What breed is the pure white mallard? It is quite frequent.

Possibly a Magpie Duck, but not certain because of the paucity of black elsewhere on the body.

@theforestecologist and JC11 I just want to remark that all the breed that you cite still belong to the species "mallard". Like dalmatian is a bree of the species "dog". I think that at this stage is pointless to assign a specific breed being most likely a mix of different ones (as suggested).

@Sanjukta Ghosh Domestic Mallards can come in a variety of colours including white. I think it we were to pinpoint the origin of the duck in question, it is likely a mix of magpie duck and domestic mallard, but that mix may not be half and half, it could be much more complex. "have fun", The Magpie is not a breed of mallard specifically, it could be an ancestor of an Indian runner which could be a Muscovy. In domestic breeds, the origin species can be many mixtures and complex. I think the best answer for this question is that this is a domestic duck and give possibilities of which type.

It is a domestic form of mallard. They are bigger, often white or mostly white. Try to google image domestic mallard and you will see the phenotypic variety that domestication has created.
Note the irregular and not symmetrical shape of the "hat" and read the description below from the biggest research center on birds of the world.
Extracted from:
http://www.birds.cornell.edu/crows/domducks.htm

(...)lots of white is often involved, including all-white breeds like the popular Pekin Duck (...) Usually these white spots are not symmetrical across both sides, and that asymmetry should tip you off to think domestic influence.

Please support your claim with citations. A claim not supported with references do not make a good answer, even if you are quite certain of it.

@Sanjukta Ghosh. Google image domestic mallard it's more than enough  to prove that is a domestic mallard. There is no wild duck with a pattern of colors remotely similar to the one in the picture.

Google images search is not an authentic reference because it extracts images from different kinds of sources (which include flickr and personal blogs) that may not have the correct information. But the webpage of Cornell Lab of Ornithology you linked is a good reference.


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Can genetics be an answer to our human flaws?
Ok I have been thinking genetics is that part of biology wich has the ability to change the genes of an organism as such it changes their abilities as well if so why cant we use this technique to change the problems that we face for example:
The cells of plants contain chlorophylle as such they can create their own food thanks to sunlight+water+CO2 what if we take the gene responsible for this and transfer it to a human being like this he will not have any need to eat(but he still can if he wants for more energy like meat-eater plants) however a downside would be green skin but I think is worth another one would be the lizards wich have the ability to regenerate limbs and other body parts that were lost this can help those who suffer from absence of body parts. Wouldn't this be amazing like a human with different abilities to adapt and survive these that I mentioned are simply core of our problems these days there can still be more to it.  SO why isn't this technique used for a solution to our problems?

Making green humans wouldn't work, as a human doesn't have nearly enough surface area to collect the energy they need to survive - even if they lay on a sunny nude beach all day :-)  It takes roughly an acre (about 4000 m^2) to support a human.

It would be much easier to make a glow-in-the-dark human with some GFP as it has been done with cats already.

Related http://biology.stackexchange.com/q/17676/3340

Here are three elements you want to consider

we are not able to make genetic manipulation of all the cells in a grown-up individual. There exist a whole bunch of treatment making use of genetic engineering in adult humans but they are typically quite costly.
The phenotypic traits that you mention are extremely complex. There is no simple gene that will allow a lizard to regenerate a lost limb. You will have to learn more about cell specialization in order to understand why lizards have a power of regeneration that we don't. Similarly, you can't just transfer a few genes and expect a human to be able to photosynthetize. Photosynthesis is a very complex process which require the ability to perform a whole bunch of reaction, which require organelles we don't have for the reactions to take place, which requires the ability to gather and concentrate lots of $CO_2$, etc... It is really really not that easy. You should learn more about the specific traits you are mentioning to get a notion for why it is not that easy.
Genetic manipulation on human is vastly illegal for ethical reasons. But these ethical reasons are to be discussed on philosophy.SE.


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Why can nervous inflammation radiate symmetrically in the limbs?
I have had carpal tunnel syndrome in my hands this week, when the nerve in the pith of your palm, through thumb and index, is pinched, and swells, inside the wrist ligament tunnel.
In a few days, the inflammation declared itself in the other wrist. It's usually the case with CTS, it's rare that a person will have problems in only one had.

As soon as one hand is injured, the other tends to seize up and stop functioning as badly as the first one, within a week or so.

Why and how does a nervous injury such as CTS radiate symmetrically through the nervous system, differently from a sprain or a contusion?
What other factors in neuroscience demonstrate nervous symmetry, related to the CTS symmetry problem?

Padua et al. (1998) did find that 87% of followed patients developed bilateral CTS (i.e., carpal tunnel syndrome in both hands).

Most patients that develop unilateral symptoms, eventually have the symptoms spread to the contralateral (opposite) arm.

Bagatur & Zorer (2011) found that 59% of patients they followed reported bilateral symptoms initially, while 73% of remaining patients had symptoms eventually develop in the contralateral arm (even after receiving surgery on the first!)

So why? From what I could gather, we don't really know. From Bagatur & Zorer (2011):

we assume that bilaterality may be time-dependent... [but] a definite conclusion could not be drawn.

However, research regarding "double crush syndrome" suggests that perhaps issues closer to the cervical spinal cord may play some role:

Pierre-Jerome & Bekkelund (2003) found that cervical intervertebral foramina were narrower in observed patients and affected nerve roots.

Although their research provided evidence for ipsilateral double crush symptoms, their study provides credence to the fact that more cervically-oriented issues (often which should show up bilaterally) could lead to CTS symptoms.

Not the greatest of answers, but a thorough search really didin;t turn up anything more recent or helpful. I'll update if I find additional info.

Citations

Bagatur, A. E., & Zorer, G. (2001). The carpal tunnel syndrome is a bilateral disorder. Bone & Joint Journal, 83(5), 655-658.
Padua, L., Padua, R., Nazzaro, M., & Tonali, P. (1998). Incidence of bilateral symptoms in carpal tunnel syndrome. The Journal of Hand Surgery: British & European Volume, 23(5), 603-606.
Pierre-Jerome, C., Bekkelund, S. I., Pierre-Jerome, C., & Bekkelund, S. I. (2003). Magnetic resonance assessment of the double-crush phenomenon in patients with carpal tunnel syndrome: a bilateral quantitative study. Scandinavian journal of plastic and reconstructive surgery and hand surgery, 37(1), 46-53.


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What does static electricity generated by plastic combs do to our hair?
It is said that wooden combs should be preferred to comb hair as compared to plastic combs. Reason is that plastic combs generate static electricity.
Question: What does static electricity do to our hair that it is said that we should use wooden combs to prevent that electricity generation?
Is it bad for hair? Does it get generated always when we comb hair?

The motion of the comb against your hair remove electrons from the hair and deposits them on the comb. The positively charged hair and negatively charge comb now attract each other due to their opposite charges. You can read about this is any introductory Physics text, the topic is "static electricity". I doubt any harm is done to your hair, the issue is that it may be difficult to get your hair lying perfectly flat because of this attraction. This effect is more pronounced in low humidity.
If you want to see an exaggerated example of this, rub an inflated rubber balloon several times, quickly in the same direction, against your hair. Then bring it back near your hair while observing in a mirror.
Edit: I hesitated adding this because folks on this particular SE are sticklers for references. My source for the following is a workshop I attended at Chico State University circa 1990. This workshop was taught by a couple PhD Physics professors to enrich Physics teachers in electircity and magnetism.
When you dry clothes in a drier, static electricity is generated resulting in "static cling". But the cling that persists after a load is done is only part of the story. Constantly, at least once clothes are sufficiently dry, electrons are being stripped from one type of material by another. These electrons snap back from where they accumulate to where they were removed. This results in microscopic "sparking" that causes an ever-so-sight amount of wear on the cloth. So, the professors went on, the use of fabric softening anti-cling tissues minimizes this and prolongs the life of clothes. My take is that this is subtle and is more likely to be evidenced by the quality of appearance of the surface of a garment after many washings than it prematurely falling apart. I don't know for sure how significant this is, especially if you replenish your wardrobe regularly.
So, this may also apply to hair. But, unlike a particular garment, hair is constantly replenishing itself. (Well, not on my head.) So I seriously doubt this static discharge damages hair to any measurable extent. Perhaps if you were to run a comb through your hair for a couple hours every day you might see an effect. Bottom line for me, I use anti-static tissues, fragrance free; typically I get 20 years of use from my washable items and consider the tissues cheep insurance.  But I use plastic combs on what remains of my hair without any worry.


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Sterilize/disinfect sugar for lab use
How do I sterilize/disinfect ordinary table sugar for lab use?
I'm using the sugar in an agar and I want it to be as clean as possible. Are there any effective, conventional ways of doing this?

Autoclaving media with carbohydrates (or sugar solutions on its own) is not a good idea for two reasons:

The Maillard reaction: This occurs when you heat mixtures of amino acids and sugars. The amino group of an amino acid reacts with a carbonyl group of a sugar, fusing the two molecules together. This is a common reaction in the kitchen which is for example responsible for making the bread crust brown. It also changes flavors.
Caramellization: This is the heat induced breakdown of sugars - also leading to brown products, but much more undefined than the Maillard reaction. What products arise depends on pH, temperature and other reactands.

Both reactions may lead to products which can be inhibitory to microbe growth and should be avoided. There is also a paper which analyzed the effect of autoclaving on sugars which might be interesting to read in this context (see reference below).
So prepare a higher concentrated stock solution of your sugars, which can then be added under sterile conditions to your autoclaved and cooled down media or the agar solution (still warm enough to pour).
Sterilize this solution by filtrating it through a 0.2µM filter - depending on the volume either through syringe filters or through bottle top filters.
Make sure to maintain sterile conditions.
References:

Sugar degradation during autoclaving: Effects of duration and
solution volume on breakdown of glucose


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How do T cells deal with the obstructions in their path of migration?
When T cells move in the blood, are their any obstructions(other cells) while they migrate? If there are then how do the T cells overcome such obstructions in their path? Do they move past them or does their movement lead to displacement of the obstructions?

You might want to look this up https://en.wikipedia.org/wiki/Leukocyte_extravasation

@Polisetty thats a wonderful article you have shared. I did not know this had a term. Thanks a lot!