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Do any terrestrial herbivores use auditory crypsis for predator avoidance?
Some terrestrial predators "stalk" their prey: they sneak up on it slowly, maintaining a low profile, while keeping as close to silent as possible.  This makes sense from an evolutionary perspective: silent predators catch more prey.
However, the prey near where I live are hopelessly noisy.  Deer will freeze if they suspect the presence of a predator, then bolt when they see one for sure.  Squirrels and other small mammals run around at top speed all the time - you can hear them dozens of feet away, rustling the dead leaves around.  Hedgehogs just wander, making a similar noise.  It seems like the only "stealth" option they have, as far as sound is concerned, is to remain still.
Are there any examples of terrestrial herbivores evolving to move more quietly in order to avoid predation? I'm not looking for a comprehensive list, but rather simply individual examples.

Why do you think it is really necessary for the herbivores to move silently? There are many strategies to stay alive.

Right - I don't know that it is necessary.  The thought hadn't really occurred to me until recently.  It struck me that I'd never seen one before, so I figured I'd ask if I was missing one.  "Freeze or bolt" seems like it's a pretty viable strategy, at least for the deer.

When you write "non-sentient" you're removing all mammals from your question (and some reptiles, like birds, as well).

Whoops, botched the meaning of that word.  Was going for "non-human".  Will fix title.

in a sort-of-related way - have you heard about the crickets in Hawaii that evolved to court in silence when predatory flies were using the courtship song as a locator signal

That's pretty cool!  It's like the long-timescale version of this question.

Great question, by the way!

Thanks!  Yeah I'd originally been curious about vertebrate behavior, but your answer sparks new trains of thought.  I'll leave it open for a few days to see if it garners more answers.

Sloths: the ultimate steal herbivore. They are capable of moving quickly, noisily, violently, and slashing with big dagger-like claws, but unless they've "been had", they remain quiet, near motionless, and are almost undetectable.

@MarkBailey, that's probably worth an answer of its own right.

One point from your question: as you say, deer freeze when they suspect a predator, and bolt when they see one; if they can see a predator, it can see them, and by that point becoming completely silent probably isn't much help.

Could the voters-to-close elaborate a bit? It doesn't sound to me like all possible answers to this would have to be opinion-based.

As the question is closed :-( I'll have to answer in a short comment: I think animals in open landscape don't have to gain much from being quiet. They will be seen anyway. Looking for animals MOVING quietly, one should think about forest animals instead. I think Elk (Am: Moose) can be a good example. They move quietly and considering their size surprisingly secret and quiet.

@RHA There is something to gain from stealth. Predatory animals "stalk prey" in these open environments. They remain unseen and this is a big advantage. Lions in the open Savannah are nigh-on invisible if they choose to be. Why would their prey avoid stealthy grazing? They could potentially remain unseen.

@arboviral I voted to close based on the breadth of the question. It requires analysis of many prey animals to build a case. No one answer could cover this question absolutely. I did attempt to provide an answer on this limiting my scope to the example animals & why each may or may not need to avoid stealth. But that is nowhere near enough to answer the question. I see the point of subjectivity though; to you most prey animals are not stealthy but the overwhelming majority of prey animals probably engage on some level in avoiding predation encounters by hiding, camouflage, or stealth.

@James I can certainly see a stronger case for 'too broad' (although as with any question containing the phrase "are there any examples of" you only need one example to be able to answer "yes"). I'm less convinced by 'opinion-based', which is the reason showing at the moment.

@James I agree with arboviral that 'opinion-based' is unconvincing. And that it takes only one example to answer the question. The question would be too broad if it were asking for all possible strategies to remain unheard, which is the direction the answers have taken it.  (freezing, stealth etc.). However the question specifically asks for examples of MOVING animals that try to be quiet. These are relatively rare (sharp observation from OP!), and I think there must an evolutionary reason for this. Pity that this interesting question is closed.

I've edited the question specifying that only a single exception would answer the question. It is no longer opinion based, and no longer broad. I've initiated a reopen vote.

Does soundproofing count?
Most predators locate prey using visual or olfactory cues; the only predators I can think of that use auditory cues are nocturnal ones - owls and bats. Bats, of course, use echolocation, so even completely silent prey are still detectable. It has been suggested that the soft, fur-like body coverings of some owlet moths (Noctuidae) and tiger moths (within the Arctiinae) help hide them from echolocating predators by passively absorbing sound, although subsequent studies have suggested that they may instead be mimicking the acoustic signature of unpalatable prey.

(public domain image: source)
I have a suspicion this isn't what you meant by 'land-dwelling herbivore', but insects are people too...
Edit: just discovered this paper from May that provides evidence supporting the hypothesis that the twisted tails of luna moths (Actias luna) disrupt tracking by echolocating bats.

Image owned by Shawn Hanrahan, licensed under CC BY-SA 2.5

Lucky for you, the question is not about vertebrates. Great answer! ;)

I think that there are too many examples of animals being deliberately quiet when grazing to count. I'll discuss specifically the exceptions you raise and how they are exceptional. Hopefully you'll see my point: A lot of grazers are quiet and cautious or failing that have other adaptive strategies for not being eaten.
Deer are incredibly quiet and cautious when grazing, and fast and agile once they decide it's not safe. Squirrels use trees as an defense - not many predators of theirs can even climb trees let alone keep up with a squirrel darting through them, (related question about bushy tails of squirrels being counter intuitive). And hedgehogs... well... how do you eat one without getting a mouthful of pain? On a bigger scale, here is a related video of a juvenile lion trying to attack a porcupine. Being unsubtle helps them.

Why do you close a question that you give an answer to. If a question is answerable, it shouldn't be closed...

@RHA I agree. I got the end of this answer, realized my answer doesn't and can't really answer the question fully. Why? The question requires a massively broad answer. Do note I don't think that this question is necessarily opinion based, it's just too broad.Feel free to down vote. I'm considering deleting it if the question remains available.

To be honest, I was just looking for one counter-example.  It seems like you've provided one - deer while grazing.  Thus, a comprehensive survey of animals is not necessary, merely a single example.


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Correlation of non-coding DNA with coding DNA
I sequenced the first exon of the MC1R gene of 15 labradors (genomic DNA) to look for the loss-of-function mutation (C.916C>T) and as expected, it was where it should have been (916th base pair). As i compared the SNPs with the phenotype of the dogs i found a second mutation that also correlated 100% with the phenotype of the dogs. The mutation is located 45 base pairs before the start codon of the first exon. As far as i'm concerned the region that lies right before the first exon should not be part of the coding DNA. If so, why could this mutation have been evolutionary conserved? Or am i simply mistaken in that the mutation before the first exon could also be part of the gene for MC1R (meaning there would be an intron before the first exon which i'm not sure if that's possible)?

Is that in a regulatory region of the gene or within a splicing region?

I only sequenced the first exon of the gene

That is contradictory. How can you sequence protein-coding parts only and find a mutation in a non-coding part?

I sequenced a little more than just the first exon of course because the results towards the ends of the sequencing product are usually not so clear

@AlexDeLarge exon need not be protein coding. UTRs are part of exons.

Which leads to my first question again: is this a regulatory region of the gene (probably not) or within a splicing region (more probably so)?

@Lukeception what did you sequence? RNA or genomic DNA?

Shame on me, of course you are right. ;) Still, @Lukeception should clarify in what part this second mutation is located.

@Lukeception If you do not provide additional information, this question cannot be answered. Please add all necessary details.

Which region did you exactly sequence? And the SNP is located in the intron behind exon 1?

So i sequenced a little more than the first exon. since it is the first exon, the mutation which is before the first exon should be in a noncoding region of the DNA, right? and yes, I sequenced genomic DNA.

@Lukeception Add these details to the question. Replying in comments would not be useful as nobody would scroll through the comments to understand the question. Moreover, comments are not indexed and therefore cannot be web-searched. Finally, your question should be complete in itself.

Am I missing something? Isn't this simply a second SNP very closely linked to the mutation of interest, so unlikely to segregate? Linkage disequilibrium.

If you have 2 different mutations (irrespectively of where they sit in regards to the final gene-product), and both correlate perfectly with a given phenotype, (and you have dismissed any other potential cause), you can not formally say, if the first mutation, or the second, or both mutations are required for your phenotype. (Though you can make educated guesses or rely on external information...)
Loss-of-function mutations do not have to be in the protein-coding region (but simply in one part of the genome, which is required for the expression of a gene towards a phenotype).
Polymorphisms can also be neutral - especially in artificially bred / selected animals, such as the wolf-like animals we now call labradors. You could easily envision a scenario where some neutral mutations was present in an individual, which would have a desirable / selectable mutation. If that neutral mutation is within a few 100bp of the selected mutation, it unlikely will have been uncoupled from the selected trait / mutation.

The region in the mRNA upstream of the start site is 5' UTR; 5' untranslated region.  Sometimes, UTRs have regulatory functions.  Or, the UTR mutation might just be along for the ride, and have no effect at all.  You generally can't look at a non coding SNP and tell if it's functional with no other information unless it messes with one of the first few bases of a known splice site.
EDIT:  I still don't understand.  Is the mutation in the first exon, before the start codon, or is it upstream of the first exon?  There is no splice site upstream of the first exon.

Just to clarify is the mutation is 45bp upstream of the protein start site, and outside the first exon. (the first exon needed not contain the protein start site. There are mRNA where the protein start site is in the second exon)
1 - Your mRNA does not start where you think it does. Mammals proteins have multiple isoforms. And perhaps your protein of interest has functional isoform with an alternative start site further upstream.
2- Labradors are inbred line. Most dog breeds are inbred. Perhaps the mutation outside the exon is just there for the ride.
3- The mutation has damaged the promoter. Your gene is fine. But since the promoter has been mutation, gene expression is now below levels needed to main normal phenotype.
4- The start of the first exon has been miss annotated.  The mutation is in the exon, specifically the 5UTR. And this mutation has effected ribosome binding in some manner

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How does one apply Bayesian inference to quantify a read the deeper you sequence?
For NGS sequencing technology, the "deeper" you sequence given fragments, the more certain you are of what is being sequenced. This sounds like a simple application of Bayes's Rule.
What is the normal approach in the field to quantify one's level of certainty in NGS sequencing with Bayesian methods? There is also a statistical question here in terms of how one aligns reads, etc.

This is a very broad question. There are possibly a thousand ways by which someone can apply bayesian inference to NGS data.

@WYSIWYG I'm happy to delete the question. Could you refer me to techniques used now?

You can have a  look at some of the RNAseq quanitification methods. There, one of the problem is to find out where exactly does a read come from (when there are many homologous regions). Bayesian methods are applied to infer the location of the read given its counts. From this the overall gene expression is estimated.

@WYSIWYG Sorry to be lazy, but the names of these methods?

I have a reasonable level of familiarity with Bayesian methods, but not so much with NGS. If you can explain the question better I might be able to add something here.

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Why is the formation of an enzyme-substrate complex endergonic (induced fit model)?
In the section about the induced fit model for enzyme substrate binding, my MCAT textbook claims that "The substrate has induced a change in the shape of the enzyme. This interaction requires energy, and therefore, this part of the reaction is endergonic."
As a chemist, I am a bit confused here because induced fit suggests that some kind of bonding must be happening between the enzyme and substrate (hydrogen, ionic, covalent, etc) that would induce a change in structure of both enzyme and substrate. Any kind of bond formation is STRICTLY enthalpically exothermic, so why is the formation of an enzyme-substrate complex endergonic?
Am I missing an entropic component here? Or is my assumption wrong, regarding how the induced fit chemistry operates?
I would assume that it would TAKE energy to then cleave/break all the bonds that induced structural change and release the catalyzed substrate...

Most reactions require an activation energy to cross an energy barrier (this you may already know) after which the reaction is downhill. Even though enzyme catalysed reactions have a relatively lower activation energy compared to that of an uncatalysed reaction, there is still a transition state that has a higher free energy compared to the products. This transition state corresponds to the enzyme-substrate complex.

            Image Source: https://en.wikibooks.org/wiki/Structural_Biochemistry/Enzyme/Activation_energy

Free energy has enthalpic and entropic components (ΔG=ΔH-TΔS). Even though formation of bonds may reduce the enthalpy, the locking of the substrate and enzyme in a conformation also decreases the entropy. This could lead to overall increase in free energy (See here. For more details you can refer to this book- The Enzymes: Mechanisms of Catalysis by Paul Sigman. ISBN: 0121227200).


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Why are so many recreational drugs serotonin 5-HT1A partial agonists?
I found out that many psychoactive drugs partially activate the 5HT1A receptor. Looking at Wikipedia, these include MDMA, LSD, CBD, Psliocybin/Psilocin, amphetamine and various other psychedelics, and they appear to all be serotonin 5-HT1A partial agonists.
Why is this receptor so popular for recreational drugs? Why are all these partial instead of full agonists? I looked at 5-HT1B and there weren't any recreational drugs that used this listed. I looked at other 5-HT receptors, and only 5-HT2A had other recreational drugs as agonists.
Why do so many recreational drugs affect these two 5-HT receptors?

I have taken the liberty to edit your question, mainly to remove any pointer to possible self-help content. This site explicitly bans self-help questions as we are not in a position to provide information on personal health issues whatsoever.

Interesting notion. However, the main effects of the indoleamine-class of psychoactive compounds, including psilocybin and LSD (Shulgin, 1997), are generally ascribed to 5-HT2A receptors and the glutamatergic system (Aghajanian & Marek, 1999). The stimulant effects of the phenetylamines (PEAs) such as amphetamine and related compounds (Shulgin, 1991) mainly target the dopamine (DA) and noradrenergic (NE) systems. I reckon that the 5HT1A effects are 'side effects', or secondary effects.
Antidepressants, such as the selective serotonin-reuptake inhibitors,  target the 5HT1A system and mainly do so by downregulating the pre-synaptic variant of the 5HT1A receptors, which have a regulatory role by decreasing 5HT release. Downregulating them takes about 2 weeks. After that time 5HT release is disinhibited and 5HT release is enhanced, which has antidepressant actions (source: Sci Am, 2013). Because many recreational drugs are not taken that long, my educated guess is that acute activation of 5HT1A by recreational drugs limits the drug's effect more than anything else.
Why are they partial agonists? Because they target other receptors better; the main effects of e.g., PEAs as described above shows you why. Many of those compounds mainly target the DA and NE system. Because they are aspecific ('dirty') drugs, they also target a variety of other receptor systems. Perhaps altering the main effect, perhaps not doing anything substantial to the trip.
Note that the PEA MDMA is kind of a one-of-a-kind psychoactive compound (Shulgin, 1991) that releases massive amounts of 5HT (Gartside et al., 1997).
On a side note, Wikipedia tends to list all available information on an item in a cluttered way that obscures the relevance of that information to the global picture.
References
- Aghajanian & Marek, Neuropsychopharmacology (1999); 21(2 Suppl): 16S-23S
- Gartside et al., Neuropharmacology (1997); 36(11-12): 1697-703
- Shulgin, Pihkal (1991), Transform Press
- Shulgin, Tihkal (1997), Transform Press

+1 I too have heard that antipsychotics that primarily target DAR can also affect 5HTR


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Cancer biology: Can tumors form from cells that are genetically identical to non-cancerous cells?
Can a tumor begin to form without any genetic mutations? I'm specifically interested in a tumor which could later lead to cancer.

Very good question!  I'm not aware of any cancer type where the genome is completely intact. There are cancer types caused by viruses such as human papillomavirus, but also here viral sequences get inserted into the host cell genome.

Someone has initiated a close vote on this question. This is not a broad question. It's a very specific question that will simply rely on the right expert coming along and saying "No. It appears this is a prerequisite for cancerous growth. See review X.", "This is semantically how we define a cancer according to citation A", or "Yes there is a rare case of cancers that work this way. See wikipedia link." Where is the breadth there?

This is a very interesting question, and one that has been at the heart of cancer research for a long time. I think it separates into three issues.
Are there non-genetic mechanisms that can induce uncontrolled cell proliferation?
Yes, at least in experimental settings. There are many viruses that induce proliferation in its host cell, and viral genes / proteins have been identified that can disable the host cell's cell cycle regulation machinery. A well-studied example is the SV40 Large-T gene (from Simian Virus 40); this gene can be expressed in cells to cause cell proliferation in a transient, reversible manner, and it does so by interacting with host proteins, without causing genetic changes. See for example this article.
Can such genetically normal cells progress to form tumors?
It depends on what you mean by "tumor". To my knowledge, tumors large enough to be a serious medical problem are always found to be genetically altered in one way or another. There are plenty of viruses that cause tumors in humans, for example Epstein-Barr and papilloma (HPV) virus, but in all cases viral sequences are found integrated into the host genome. This may be because development of large tumors requires many cell division, and any non-genetic change that drives proliferation is likely to be lost on the way.
On the other hand, HPV virus frequently causes warts, which technically are small benign tumors. As far as I know, no genetic modification of the host cell is required for this to happen; rather, the virus replicates from its own separate DNA while simultaneously driving keratinocyte cell proliferation to cause these growths. So this example shows that small "tumors" can be formed without any genetic cause. Perhaps there is a limit on how large tumors can grow without genetic changes.
Can genetically normal cells form cancer, meaning a malignant (invasive) tumors?
No, as far as I know, this has never been observed. Large, malignant tumors without genetic changes are unlikely for the reasons above. There are cases of metastatic cancer where the primary tumor is so small that it cannot be located, but in these cases the metastatic cells are again genetically altered. Experimentally, it is possible to produce invasive behavior in cell lines by expressing oncogenes like ras, but these genes are mutated to begin with. Also, normal cells have mechanisms that detect such alterations, causing senescence, and they must first be inactivated by mutations. Transformation to an invasive phenotype is not usually caused by viruses, probably because it would give no advantage to the virus (unlike cell proliferation).
For more information, Robert Weinberg's Cancer textbook does a good job of discussing these issues. This article also provides a historical perspective of tumor virology with some interesting pointers.

Given the incidence rate of cancer, it is likely that usually multiple somewhat independent events have to occur, so that cancer forms (see the famous interpretation of the underlying data/thinking by Hanahan et Weinberg 2000 )
Epigenetic changes seem to be a likely factor contributing to cancer ( summary of an experiment, where they are also causal/inducing )
People have been suspecting, with good rationale, that the intrinsic variability of (bio)chemical reactions, which often only involve a small number of copies of the involved molecules, could contribute to cancer ( e.g.: Ansel et al. 2008 ). (Note: directly addressing this hypothesis for cancer by experiments would be quite difficult / perhaps-impossible)
None of the above should be seen as opposing the relevance of genetic mutations

I would go with NO for the simple reason: For a cell to become malignant (cancerous), cells need to break several barriers. One is to be able to activate telomerase, an enzyme that restores telomeres and enables infinite cell divisions.
Another important part is to be able to ignore apoptosis. This is programmed cell death. Specific cell signals lead to systematic chemical changes and cell death. So for cancer cells, it is important to be able to ignore this signal.
These are only two basic things, there are more, for a cell to become cancerous.
Changes to this will necessarily lead to change in DNA. However, I don't have direct proof and I don't work in this area.

In curosity to the above answer: I agree that in the situation of cancer, there are changes in DNA and genetic mutations are found in all types of cancers. I also agree that to become cancerous, a cell has to break several barriers and at some point one of the barriers are mutations in DNA. But, how does it prove that a cell cannot start proliferating at a faster rate due to for example: just metabolic changes? How is it necessary that a genetic mutation has to be there to start maybe a cell proliferating more which could further lead to a situation of tumor and further cancer.

Because there are several safety mechanisms, like those I mentioned. Even if cell did multiply much faster, it will sooner or later die due to all the errors after telomeres are depleted. And similarly, even if cells suddenly started multiply, signal for apoptosis could easily stop this attempt at revolution.

or some metabolic changes leads to start in proliferation and activation of oncogenes...leading to start accumulating more genetic mutations and being able to fight with all the barriers which can stop the tumor growth. I still do not agree why a genetic mutation have to be  a start for a cell to sense for over-multiplication or to start becoming cancerous. It is probably the sum of all...(start could be anything..genetic, metabolic or epigenetic).Ultimately changes at all levels of regulations are disturbed in cancer cells.

@Crazy in principle you are right --- in a single cell, uncontrolled cell proliferation can be caused by non-genetic mechanisms (notably by viruses). I think the main reason why (large) tumors always show genetic changes is because the alterations that drive proliferation must remain intact over many generations of cells.

Endometriosis fits this definition.  In many ways endometriosis is like metastatic cancer.  Endometriosis is the movement of fragments of endometrial lining out of the uterus (prsumably via the fallopian tubes) to other sites in the body.  There these fragments implant and call in a vascular supply to feed them.  Endometriosis fragments usually cause trouble in the abdomen and pelvis but they can go anywhere, including skin, lung and the brain.  Metastasis is not an inappropriate name for this.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3942279/
https://www.ncbi.nlm.nih.gov/pubmed/21195968
These fragments grow and stick things together (like intestines), causing the same sort of problems that cancer can cause in these sites.  They bleed with the menstrual cycle.  Endometriosis in the lung can cause hemoptysis.  The masses of endometrial tissue and the blood and fluid they accumulate can become endometriomas: benign tumors which are accumulations of tissues and blood which can be mistaken for cancerous tumors on imaging.
The endometrial tissues causing this are not mutant.  They are just in the wrong place.  Endometriosis can, however, give rise to a true cancer.  Clear cell carcinoma is known to form in deposits of endometriosis.

This is a fascinating answer! However, in reading one of the reviews you link, they say "there is evidence that endometriosis
has genetic alterations similar to some cancer types" with reference to this paper: https://www.ncbi.nlm.nih.gov/pubmed/11093061 - though I am not sure of the field's recent consensus on this.

P.S. I do not recommend a downvote on this answer, because it will be very relevant to someone interested in this question - but the caveat that we are not certain about genetic alterations is pretty important.


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Ways to monitor enzyme kinetics with very fast time resolution?
I'm interested in any way to do time-resolved study of enzyme kinetics.  I am studying some physical variables that may affect kinetics, but I want to study how quickly they take effect, and how long the effect lasts.  The time scale of interest is milliseconds or less, so the typical spectrophotometric methods (which usually look at absorption change over fairly long times on the order of minutes) won't work.
Luciferase activity can be monitored by tracking the light emitted, and this has potentially very high time resolution as the time between reaction and light emission is on the order of microseconds.  However luciferase is a bit of an odd model, as it is not part of normal metabolism or signalling in most organisms.
Is there a way to track enzyme kinetics of any other enzymes with a similarly fast time resolution?
EDIT Just discovered one name for what I'm looking for: "transient kinetics".

Is the change you want to observe visible in the UV/Vis range and you're asking for a way to observe this with very high resolution?

@MadScientist: I'm looking for good model systems, not any specific enzyme.  The change of many enzymes is visible in UV/Vis, eg anything coupled to NAD/NADPH, unfortunately if doing a conventional progress curve type measurement the time resolution is more on the order of seconds or tens of seconds, not milliseconds.  So it either has to be a somehow sped up way of doing progress curve, or some other way.

Are you familiar with Stopped Flow? That sounds like what you're looking for.

Some ATPases can work with MANT-ATP or similar fluorescent ATP analogs that change their fluorescence properties upon protein binding as well as hydrolysis of their phosphate group. This has been used frequently (see here or here) to study enzyme kinetics on fast timescales.


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"Other" classification for epitopes in the Immune Epitope Database (IEDB)
I used the immune epitope database (IEDB) to search for epitopes. I found some epitopes derived from antigens called " other" by IEDB.  When I asked about it,  the answer was "We use the "other" category to group epitopes from the same species that only BLAST match to GenBank entries that are nonhomologous to the reference proteome".
Could someone explain this?

Welcome to BiologySE @Shad... you've got some abbreviations and technical language that may make it a bit hard for some individuals to follow... you may want to edit it a big (explain some more things) and visit the help center for additional pointers - thanks for your efforts and contribution http://biology.stackexchange.com/help/how-to-ask

I've done what @VanceLAlbaugh suggested for you as I have edit privileges. Good titles make questions more useful to other uses and increase your chances of getting an appropriate answer.

I presume that these epitopes represent peptides that have been eluted from MHC molecules and then sequenced by mass spec.  You can then compare these peptide sequences to a reference genome (more specifically to the proteins predicted to arise from the reference genome).  If the peptide matches perfectly to a predicted protein, then you assign it that identify.
But many peptides will not align to the predicted proteins, and so they can't be unambiguously assigned a gene of origin.
There are many reasons why MHC-derived peptides may not match the proteome.  Most obviously, the reference genomes are typically from a single individual, so if the sequenced peptide has a SNP, or other allelic variation, it won't line up.  As well, a significant number of peptides undergo some form of modification during antigen processing, such as deglycosylation changing Asn to Asp, proteasome-mediated cleavage and re-annealing, and so on.  These modified peptides also won't line up to the predicted proteome.


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Can restriction sites be used as PCR primers?
I have a DNA fragment that contains the gene of interest sandwiched by restriction enzyme sites. Then, can PCR amplify the entire fragment, recognizing the restriction enzyme sites?

Why not? PCR amplifies any sequence.

If you aren't digesting prior to amplification, sure.  Nothing in PCR cares about whether or not some other protein interacts with the site.  There are thousands of restriction enzymes in nature.  No one would ever be able to do PCR if you had to avoid every single potential restriction site.

Just a minor comment: some restriction enzymes like XbaI are sensitive to DNA methylation, so XbaI works on your PCR product but may not work on your gene.


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Why aren't there any transitional animals today?
You have probably heard this question before and in different formats. Usually, it is used as a "proof" to disprove the theory of evolution.

I understand that the apes we descended from are not the same apes we see today. However, I can't understand why there aren't any human-ape creatures anymore.
In the world of today, wouldn't an intermediate species (between apes and humans) "win" over both because it has the "feature" of the two.
A creature that can both climb trees and walk on two legs would be more suitable to live in forests than the current forest inhabitants. (apes and humans)

Every species on the planet is "transitional" - this is because there is no ultimate or final species. Species branch out from one another, sometimes species go extinct, leaving gaps between the extant branches.

Possible duplicate of Examples of extant animals in a submature morphologically unstable evolutionary state?

@C_Z_ I'm specifically interested in the human-ape thing.

"In the world of today, wouldn't an intermediate species (between apes and humans) "win" over both because it has the "feature" of the two." - ever heard the expression "Jack of all trades, master of none"? An intermediate might do ok in the adaptive landscape of either species flanked by it, but it won't be able to outcompete within them

@Mhmd I strongly recommend reading through the introductory course Understanding Evolution from the University of California, Berkeley. It will address a lot of the misconceptions you have.

Related (but closed): Where are the evolutionary “inbetweeners”?

Our closest relative are Chimps and Bonobos. Our lineages split from a common ancestor several million years ago. Since then every other species in the human lineage other than sapien went extinct (neanderthal genes not withstanding) and we have the fossil record to prove it. It isn't that surprising that the rest of what came to be the human lineage went extinct, just as most all of the ancestors of the chimpanzee lineage went extinct after the split. That there are chimps and bonobos just means they were well adapted to their niche ranges and survive today. Same with birds and dinosaurs.

But,if true,there should be billions of transitionals,like when you look at a good set of artist's paints....each colour changeing 1 tube at a time to the next colour.Where are they in the fossils?

Every species on the planet is "transitional" - this is because there is no ultimate or final species. Species branch out from one another, sometimes species go extinct, leaving gaps between the extant branches. But it also comes down to how you look at it; if you were comparing blue whales and humans, then chimpanzees (and many other species) would be "transitional", so some "transitional" species are extant, others are extinct. In fact, it is estimated that 1% of species that have ever existed are extant, the remaining 99% are extinct.
It's very hard to say why the "transitional" species of chimpanzees and humans went extinct. There's a lot of (sub-)species that would fall in that bracket, thus to answer that specifically would be too broad and speculative for this site.

Some concepts and key points

Speciation is a gradual process with species forming over time out of one in to two (or more).
Species is a hard concept to pin down because it applies binary/categorical classification to a very much continuous distribution
Evolution is a process of change, and in all likelihood it will be an unceasing process because at least one of the mechanisms will likely be affecting every species in some way. This means that every species is "transitional" because no species represents an end point.

This is just going to be a quick answer, as it's too long for a comment (I'll leave it to others to fill in the gaps if they wish). The image you present in your question is based on a false premise. Humans did not evolve from apes. Humans and apes evolved from a common ancestor, which was neither human nor ape. So, the arrow on the left of the image, saying There are millions of these, is incorrect. Our common ancestor is now extinct, as are all of the so-called "transitional species", another term which is incorrect because, as rg255 points out, all species on Earth are "transitional", because we are all evolving (at varying rates, to be sure). In between our last common ancestor (LCA) and modern Homo sapiens there were many species that existed for various amounts of time, then died out for various reasons, in some cases because of direct competition from more recently-evolved and better-adapted species.


text:
Needleman Algorithm for Optimal Alignment of two Amino Acid Sequences
I want to compute the optimal alignment of two amino acid sequences as per the following definition from a patent:

"The percentage of identity between two peptidic or nucleotidic
  sequences is a function of the number of amino acids or nucleotide
  residues that are identical in the two sequences when an alignment of
  these two sequences has been generated. Identical residues are defined
  as residues that are the same in the two sequences in a given position
  of the alignment. The percentage of sequence identity, as used herein,
  is calculated from the optimal alignment by taking the number of
  residues identical between two sequences dividing it by the total
  number of residues in the shortest sequence and multiplying by 100.
  The optimal alignment is the alignment in which the percentage of
  identity is the highest possible. Gaps may be introduced into one or
  both sequences in one or more positions of the alignment to obtain the
  optimal alignment. These gaps are then taken into account as
  non-identical residues for the calculation of the percentage of
  sequence identity."

The Needleman and Wunsch implementation at NCBI (https://blast.ncbi.nlm.nih.gov/Blast.cgi) mostly works but not exactly. Thanks to @David & @WYSIWIG from a related SE Thread that suggested this (Computing Percent Identity between DNA / Amino Acid Sequence)
I want to know if there is a way to fix the mismatch.
e.g. My test case is:
Seq1: ABDE
Seq2: AAAAAAAAAAABCDE

The NCBI implementation yields the following alignment which has only 3 identical residues:

But shouldn't an optimal alignment  with 4 identical residues be possible like so:
Seq1: ----------AB-DE
Seq2: AAAAAAAAAAABCDE

Thoughts? Any way to tweak the implementation to give the result I want? Alternatively any other algorithm that can be coerced into getting this alignment? BLAST or a variant?

Needleman-Wunsch does an end-to-end (global) alignment (BLAST uses Smith-Waterman). Needle from the EMBOSS toolkit performs Needleman-Wunsch alignment. It will report the highest scoring alignment. I am not sure which alignment it reports when there are two of them with equal scores (I don't think it is random).
I just tried your case: replaced B with W as the former does not denote any specific amino acid (it is ambiguous). It does give:
     1 ----------AW-DE      4
                 || ||
     1 AAAAAAAAAAAWCDE     15

Note that you can change this behaviour by altering the gap-open and gap-extend penalties. You can also change the end-gap penalties (gaps in the beginning or end of the alignment; not in the middle) in Needle.
In this case gap-open=10, gap-extend=0.5, end gap penalty=false and matrix=BLOSUM62
For performing a local alignment you can use Smith-Waterman. It just aligns the highest scoring region and does not do an end-to-end alignment. You can change gap-open and gap-extend penalties in Smith-Wateman and BLAST too, but these algorithms do not begin or end an alignment with a gap.
This is the output of Smith-Waterman with gap-open=1 and gap-extend=0.5 and BLOSUM62 as scoring matrix.
     1  AW-D  3
        || |
    11  AWCD 14

For more information see What is the difference between local and global sequence alignments?

Dang. What luck that I came across the wrong codes online at this link: http://www.fao.org/docrep/004/y2775e/y2775e0e.htm It says B denotes asparagine or aspartic acid. It is the top link at Google even. And the FAO seemed like an authoritative site. My bad!

@curious_cat Oh yes I didn't realize. Seems Needle accepts ambiguous codes like B and Z but many algorithms probably do not (though I am not too sure about this). Anyway, is your doubt clear?

Thanks. Yes, I think it is clear now. I am getting close to the patent optimal alignments by setting all penalties to zero. Maybe I will also provide a custom matrix now to make it a 1-0 alignment instead of the scoring function matrix that is natural propensity based like BLOSUM.

Your guess is made without knowing protein substitution probabilities.
Optimality of alignment in BLAST is a metrics of the scoring function. The scoring function depends on the word size (length of the seed that initiates an alignment), rewards and penalties for matches and mismatches - gap cost and substitution matrix. In general, BLAST uses BLOSUM and PAM-  these matrices are based on evolutionary data. More about scoring parameters you could read in the BLAST Help.
You could fine tune these parameters in "Algorithm parameters" in the very bottom of the analysis page. Knowing parameters you could decide does your wild guess alignment make sense or not.

That is a very bad test case.
The problem is that the sequences are too short and involve a long repetition. This means that the default gap penalties and the gap-length penalties are not applicable. They are designed to work with longer sequences, where the penalty of inserting a gap can be offset by an increase in matches. In any case you can get bad alignments at the ends of DNA sequences where the stretch of DNA that is aligned by introducing a gap is ‘off-screen’.
Even though the algorithm may be watertight, its implement in an alignment program makes certain assumptions where values for scores and penalties are involved. You have to know what these are and when they are applicable. There are even situations where you need to produce your own matrix to force alignment between pairs that you know from other information must align (active sites, regulatory motifs). This is quite valid because the program doesn't know about biology — you do.

An addition (on the same lines as providing your own matrix): PSI-BLAST does a calculation of a position specific scoring matrix using the homolog hits. With each iteration the hits are supposed to get better. This is a sort of machine learning; not really like putting your own matrix but it does take some biology into account.

As you say, this is a bit different. It's standard in MSA (multiple sequence alignment) — or at least Clustal does the same thing. But the key point is to think about the algorithm and the assumptions — difficult for a beginner obviously.


text:
Can the human body create glucose out of fat?
I read conflicting views about whether or not the human body can create glucose out of fat. Can it?

Odd chain fatty acids can, via propionyl CoA. There is a computational predicton that even acetyl-CoA can generate glucose. I don't think this is experimentally verified.

Only about 5–6% of triglyceride (fat) can be converted to glucose in humans.
This is because triglyceride is made up of one 3-carbon glycerol molecule and three 16- or 18-carbon fatty acids. The glycerol (3/51-to-57 = 5.2–5.9%) can be converted to glucose in the liver by gluconeogenesis (after conversion to dihydroxyacetone phosphate).
The fatty acid chains, however, are oxidized to acetyl-CoA, which cannot be converted to glucose in humans. Acetyl-CoA is a source of ATP when oxidized in the tricarboxylic acid cycle, but the carbon goes to carbon dioxide. (The molecule of oxaloacetate produced in the cycle only balances the one acetyl-CoA condenses with to enter the cycle, and so cannot be tapped off to gluconeogenesis.)
So triglyceride is a poor source of glucose in starvation, and that is not its primary function. Some Acetyl-CoA is converted to ketone bodies (acetoacetate and β-hydroxybutyrate) in starvation, which can replace part — but not all — of the brain’s requirement for glucose.
Plants and some bacteria can convert fatty acids to glucose because they possess the glyoxylate shunt enzymes that allow two molecules of Acetyl-CoA to be converted into malate and then oxaloacetate. This is generally lacking in mammals, although it has been reported in hibernating animals (thanks to @Roland for the last piece of info).

Good answer.  Some mammals do have the glyoxylate shunt though; hibernating animals use this to maintain blood glucose from fat reserves. See for example: http://www.ncbi.nlm.nih.gov/pubmed/2310778

@Roland — Very interesting — so the genes are present in the bear genome? (I found out by chance that the glyoxylate shunt genes were present in nematodes some years ago and got Kegg to correct their page, but was unaware of this.)

I'm not sure if the encoding genes in mammals have been identified, they may not be obvious homologs of the plant / bacteria / nematode genes. There are a only a few studies of this in mammals (bears, some hibernating rodents I think) and it's mainly by assays for the enzymatic activity or isotope tracing, if I remember correctly.

To be more detailed it is the irreversibly of the reaction carried by Pyruvate dehydrogenase that makes the conversion of the fatty acid chains to glucose impossible.
The fatty acids chains are converted to acetyl-CoA.
Acetyl-CoA to be converted into pyruvate need an enzyme that can do the Pyruvate Dehydrogenase's inverse reaction (in humans there is no such enzyme).
Than the pyruvete inside the mitochondria is converted into glucose(gluconeogenesis).


text:
Is QIAPI 1 a scam?
I find it strange that there isn't a wikipedia article on a drug that allegedly modulates human photosynthesis. I thought I might get a virus from some of the sites selling it, but others seemed decently official. I couldn't find any logs about it but there seems to be a lot of papers supporting the claims of its developers. The only testimonials I found were in spanish and I wasn't sure if they were real. Anyone heard about this stuff?

Regulating human photosynthesis? This is nonsense since humans don't do photosynthesis. Additionally it is unclear what you are asking about, so please add some references.

Based on what you are saying, yes. It is a scam.

Total Fraud
It's not true.  As things stand now, it is absolutely impossible for human beings to photosynthesise.  If you want a rather technical quote from D. C. Smith and E. A. Bernays:

A survey of modern associations in which protists or invertebrates are hosts shows that very few of the many species of photosynthetic microbes are adapted to an endosymbiotic existence. None occurs as intracellular symbionts in animals structurally more complex than cnidarians and platyhelminths. Photosynthetic symbionts are not usually capable of being the sole food source for hosts because they do not provide a balanced diet; most hosts therefore retain holozoic feeding. Interactions between hosts and intracellular symbionts are complex, and have to include mechanisms for inducing release of photosynthate from symbionts as well as controlling symbiont cell division. Possession of symbionts imposes a measurable cost on hosts. For the great majority of animals, the costs of adapting to herbivory or other forms of nutrition are probably less than that of hosting photosynthetic symbionts, especially when the need for exposure of a large surface area to light is borne in mind. Once hosts become multicellular, it is virtually impossible for any photosynthetic symbionts they possess to evolve into organelles because they are restricted to specific host cell types.

Otherwise, the simple link is: http://www.bbc.com/future/story/20120906-will-humans-ever-photosynthesise.
Short answer: no complex organism truly uses photosynthesis to produce its energy because of the major loss in efficiency of gaining energy from the sun on a multi-cellular level.  Too, the amount of energy that a human being needs for survival is so massive that we would have to have leafy protrusions all over ourselves to collect enough energy to make any difference whatsoever.

Two things: 1. Is this drug about photosynthetic symbionts? If not, your answer does not fit the question. 2. I am unsure if your short answer is correct. Plants use photosynthesis to create a carbon source for "producing" (rather making it available to them) energy in cellular respiration. Accordingly, photosynthesising humans would not need to convert all their energy from photosynthesis but rather supplement their carbohydrate uptake internally. Don't get me wrong, I also think this is a total fraud. Still, I am not convinced by this argument.

Sure, that's valid, @AlexDeLarge.  I'd just encourage you to read the article on BBC that I shared.


text:
Is this a firefly?

It glows without interruption. This photo was taken near Barcelona, Spain.

It looks like a firefly to me. The fact that it glows is a dead give away, the light producing organ on the abdomen looks right, and the pronotum ( the shield covering the head ) also matches. Many species of firefly have flightless members ( usually female ) that sit on the ground and signal the flying ones.

My doubt comes from the fact that it glows without stop. In some identification charts that I've looked, they all glow in intervals of at most 9 seconds.

Glowing non-stop does seem weird. That would use up a lot of luciferase, and require a significant input of energy. But I'm pretty sure it's still a type of firefly, I'm not aware of any other bioluminescent beetles.

Looks like a glowworm to me.

@Federico I know it's been 9 months since this question was answered, but please see my new answer (Feb 2017)  addressing the geographic unlikelihood that your specimen is L noctiluca.

Thanks a lot! I appreciate your effort. I am definitely not an expert, but the map that you attach seems conclusive (the photographs are harder to distinguish).

I think @user137's answer is close, but I believe that Lampyris noctiluca is the wrong species.
This looks like Lampyris iberica (the Iberian Glow Worm). The Lampyris are a genus of european firefly beetles whose larvae and larviform females are among those organisms commonly called "glowworms".

© Prem Rose, 2016. http://www.inaturalist.org/photos/4351809

© Prem Rose, 2016. http://www.inaturalist.org/photos/4351808
These two species are very similar. According to De Cock et al. (2014),

Identification of Lampyris larvae stays difficult [due to a] lack of clear discriminating characteristics.

See here for more pictures of L. iberica (and here for more pictures of L. noctiluca for comparison).

However, according to work presented by De Cock et al. (2014), L. noctiluca is not found in Barcelona, but L. iberica IS found in Barcelona.

L. noctiluca shows an extreme Northern distribution, only
  present scattered over provinces in the North Atlantic region and Provinces in the Pyrenees, whereas L. iberica also occurs in
  central Northern provinces and the Southern extreme of Spain in Cádiz and the province of Málaga.

Both species present a conspicuous sexual dimorphism, with males being smaller and winged and females being larviforme, without wings and noticeably larger than the males.

I'm going to guess this is a Lampyris noctiluca, a species of firefly commonly found in Europe. The females are flightless, glow continuously for up to 2 hours, and are commonly referred to as glowworms, per anongoodnurse's comment.


text:
Japanese Crab Identification?

I saw a crab walking home from work the other night. We're by a river, but I was probably 500 feet away from the river when I saw this one. I apologize for the image quality, all I had was my terrible Ipad camera and no flash. I have provided the original image and one with brightness and contrast modified to make the crab easier to see. It's about 2.1 inches from leg to leg, I threw a 500 yen coin by the crab as a reference, but cropped it from the image.
I am located directly across from Haneda airport, which is on Tokyo bay. The river is close enough to the ocean that we get tides. I'd say the river level varies by as much as a meter, and there are many many crabs on the exposed riverbed at low tide. But again, this crab was far away, and would have needed to climb a three foot tall vertical wall at the river's edge.

The carapace shows the distinctive lines of Chiromantes dehaani (Kurobenkei-gani in Japanese). This species can be found quite far away from the ocean, commonly in brackish streams and rivers. The size fits your description, the width of the carapace is approximately 3-4 cm, giving the entire body roughly the same size as you observed. These crabs are also most active at night.
I have seen these crabs in sheltered areas slightly inland from the sea. Here is a photo of C. dehaani that I took in Tokyo:

While there is a slight possibility that this is Chiromantes haematocheir (Akategani in Japanese), your photo does not show the distinctive red claws and this species is less common in Tokyo Bay due to development and loss of its natural environment of mudflats. Therefore, I think it is save to identify this as C. dehanni.


text:
ExAC Browser: What does a "dubious variant annotation" mean?

I am studying a protein in the ExAC browser. However it is flagged with a "LoF flag". What exactly counts as a "dubious" variant in ExAC.
I couldn't find any further information neither at the variant's page nor in the FAQs.
Link to ExAC browser.
Link to variant site (This is a bad example, because there is a multi-allelic warning, but this is the variant shown in the picture)
Further links to variants with LC LoF flag:
14-45636336-C-T
14-45636346-C-CTA

Link please. I've never heard of it and shouldn't have to search.

This is interesting. Could you also show exactly what the variant page says?

I have asked for the definition of a dubious variant in the ExAC browser, or a source where I can find that definition. I can not imagine a clearer question. Pls don't mark my question as unclear on the sole ground that you don't know ExAC or can not answer the question.

It wasn't the unfamiliarity with the site and software, it was the fact that the original question had a result that didn't have enough information to reproduce the problem. If you could provide a link to your search that reported the dubious annotation (and maybe some additional context) I think initiating a reopen would be successful. Note that @David did not vote to close.

Not sure if this is related but theres been an effort recently to validate some of the predicted functional annotations. Its possible that the flag relates to inconsistencies between predicted function (LoF) and actual function in cell line systems. btw for reproducibility, this is the link to the page (press LoF button above export tables)

LC LoF stands for low quality loss of function. The variant is predicted to be a loss of function but has been filtered by LOFTEE. If you click on the transcripts drop down under annotation next to FANCM you'll see that at least one functional prediction is filtered. The FAQ gives more details in to how the filter criteria for LoF was set. Unfortunately, the question is on hold so I cannot post this as answer.

Briefly speaking you expect more or less uniform coverage for reads. So if you see a systematic difference in quality scores or coverage for minor and major alleles or for forward and reverse strand, it could be an SNV, but most likely it is a technical issue. That's a 'dubious variant'.
A lot of such biases are described in "Genotype and SNP calling from next-generation sequencing data":

Other types of filtering based on deviations from the HWE — generally
  low-quality scores, systematic differences in quality scores for major
  and minor alleles, aberrant LD patterns, extreme read depths, strand
  bias, and so on — can also help to improve the accuracy of genotype
  and SNP calling. The appropriate filters depend on the sequencing
  protocol and the upstream analyses. For example, a site with strand
  bias (where a disproportional number of plus and minus strands are
  observed) could be an indication of a problematic site that is more
  error prone and should be filtered out. However, if the sequencing has
  been performed on captured sequences, such as those used for exome
  capturing, then the bias might not be an indication of a problematic
  site but rather an artefact of the capture array.

Update
I've just received an answer from ExAC:

The "LC LoF” means that the variant was marked as a low confidence
  loss of function variant. If you click on the “Transcripts” dropdown
  on the variant page it will show the reason why the variant is of low
  confidence for that transcript. In this case it was flagged as
  “END_TRUNC”. An explanation of the LoF filters can be found here:
  https://github.com/konradjk/loftee

You are describing a dubious variant CALL. I think a dubious variant ANNOTATION refers to the classification as Loss of Function (LoF).
Maybe there is an inconsistency in ExAC, but I'm not sure. Are you?


text:
Identification of a mammal in cage
This unidentified animal was trapped in northern part of Kerala State India and images circulated through social media. Doea anyone know what species this is?

Normal animals can look really strange if they lose all their hair. It looks like this one might have lost its hair due to disease. I don't know enough about what animals are native the area to make any suggestions.

Looks like a lemur to me, due to the long tail and finger-like front digits.

@C_Z_ Agreed. If you compare this image to that of a healthy lemur, you can see identical paws, teeth, ears, tail and hind legs.

On a net search Lemurs are seen only in Madagascar. The tail appears to be longer than the body. Can it be a Toddy cat (Palm Civet) with loss of hair?

@RamManoharM it can be a palm civet. This seems like a picture of another semi-hairless palm civet in Kerala.

@WYSIWYG  I didn't even think about the bio geography of it/ This looks like a fat version of the OP picture, so I think you're right.

Could be a civet.

To me it looks like some kind of feline with mange.
It is unlikely to be a Lemur given the lack of thumbs on said animal. And this is India not Madagascar. Lemurs are only found on Madagascar.

This does not look like a lemur at all. This creature has whiskers... lemurs do not have whiskers.. More telling is the lack of tumbs. Lemurs have that... weird looking thumbs but thumbs. this animal does not. .https://www.google.com/search?q=lemur&biw=1252&bih=567&source=lnms&tbm=isch&sa=X&sqi=2&ved=0ahUKEwj0toOc7YjPAhUG4yYKHYFCDToQ_AUIBigB#tbm=isch&q=lemur+paws

Agreed, it's probably a cat, perhaps this https://www.google.com/search?q=Asian+Golden+Cat&sxsrf=ALeKk03eXvY-h6N7Ibq_GgdkzQej4BkQcA:1616468088878&source=lnms&tbm=isch&sa=X&ved=2ahUKEwi4kunxtMXvAhUQnxQKHfhkDuMQ_AUoAXoECA8QAw&biw=1267&bih=711#imgrc=4RDO6Zd8sVUI0M


text:
How well do Eppendorf cups seal?
I am considering to send some samples overseas in Eppendorf cups. They are the standard plastic cups of 1 to 2 mL capacity. Of course they may tip over during their journey and I'd like to know how well they seal or if there is any danger that anything leaks from inside the cup. The samples are fixed in alcohol if that is relevant.

Is this the proper StackExchange site to asks these questions?

Can you get some tubes with screw lids as these are used for freezing cells? They are tight.

@Stockfisch Why wouldn't questions about laboratory technique be welcome here? I'm not aware of a StackExchange designated for lab technique questions, though I often feel like one should exist. But that's a discussion for meta.

I have never had  problem with tubes leaking. However, if you are worried about them getting somehow popped open in transit, you might consider wrapping the lid in parafilm. Alternately, there are lid locks that you could use like these.
@Chris has a good point about screw-cap tubes, they could also work, and are probably a lot sturdier, in case of actual damage.

The screw cap vials would probably also benefit from parafilm. If you're extra paranoid, put each vial in a 50mL Falcon Tube to catch anything that leaks, then wrap the Falcon Tube in parafilm too.


text:
Does a plant have to have leaves to produce fruit?
Is it possible that a plant can still produce fruit, even though it may not have leaves? Are there any plant species that can produce fruit without leaves?

Welcome to BiologySE! Thanks for your question... you may want to consider editing or adding to it based on the help section "how to ask a good question" - you could definitely improve this question and earn more reputation points.  Check out the help site: http://biology.stackexchange.com/help/how-to-ask

@VanceLAlbaugh Hello and thank you, but I don't know anything else to add to this. The title already says enough right? (I'm not a biologist)

In short: yes, a plant have to have leaves to produce a fruit. Both from the evolutionary viewpoint as from the anatomical viewpoint.
All the fruit producing plants belong to a group we call Anthophyta (or Magnoliophyta), meaning in greek "plants with flowers". These fruit producing plants are all descendant from ancestors that have leaves, specifically what we call megaphyll ("big leaves").
Even Anthophyta that apparently stopped producing leaves, as cactuses, still have them. According to Mauseth (Botany: An Introduction to Plant Biology):

Although all flowering plants possess leaves, stems and roots, these parts have been modified so extensively in some species that they may not be recognizable without careful study. For example, cacti are often described as leafless, but they actually have small green leaves between 100 and 1000 micrometers long.

More important, spines are highly modified leaves (and that's the difference between spines and thorns). In a cactus, these highly modified leaves come from a structure called areole, that also produces another highly modified leaf: the flower.
Now to the anatomical part: flowers are specialised leaves:

http://www.ncbi.nlm.nih.gov/pubmed/11440721
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1677-04202005000400001
http://dx.doi.org/10.1016/S0960-9822(01)00024-0
http://www.ijdb.ehu.es/web/paper/052020pr

...and the list continues. According to Lodish, "Molecular Cell Biology" (http://www.ncbi.nlm.nih.gov/books/NBK21561/):

Genetic studies have shown that normal flower development requires three classes of floral organ – identity genes. In plants with mutations in all three classes, concentric whorls of leaf-like structures replace the floral organs, indicating that these structures are modified leaves. (emphasis mine)

And according to Durner, "Principles of Horticultural Physiology":

Flowers are modified leaves. Upon exposure to specific environmental signals such as daylength or temperature or at a specific point of plant development, shoot meristems start to form flowers rather than leaves. (emphasis mine)

And from a paper published in Nature, 2001 (http://www.nature.com/nature/journal/v409/n6819/full/409469a0.html):

Goethe was right when he proposed that flowers are modified leaves. It seems
  that four genes involved in plant development must be expressed together to
  turn leaves into floral organs. (emphasis mine)

Flowers have several parts, and one of them is the ovary, which will turn into the fruit after (but not necessarily) the fecundation. Thus, in conclusion, fruits are a modified part of a flower, and flowers are specialised leaves.
It's worth mentioning that all fruit plants have leaves, but of course not all plants with leaves have fruits.

It would be too far-fetched to call flowers as modified leaves. Some parts of the flower may be share same initial differentiation pathway as leaves but the entire flower is a highly developed organ.

So what happens if you cut off their leaves anyway?

"It would be too far-fetched to call flowers as modified leaves"... Well, I'm referencing Nature and a bunch of books. What else do you want?

No.
Cactuses
Who hasn't heard of these leafless plants?  But they undoubtedly do produce fruit - which is edible what's more.
So the answer?  No.  Some plants can and do produce fruit without leaves.

I think the cactus spines are technically modified leaves according to wikipedia. I would say the answer "No" should be "No*"!

Horsetails (Equisetum) don't have seeds, let alone fruits... They belong to Sphenopsida, a group of seedless plants. And cactus does have leaves.

Cactus spines are defined as modified leaves.  So I guess at this point it comes down to a question of defining leaves.

Equisetum belong to  "nonflowering plants" so how they could have true fruits?  Fruit develop from flower-ovary , whereas equisetum shows sporangia. Btw Equisetum have microphyllous leaves in whorl which forms the sheath.


text:
Why is sex pleasure giving activity but not childbirth?
Asking from an evolutionary viewpoint.
Sex is a pleasure giving activity so that it encourages reproduction and spreading of genes. But childbirth ,the most crucial part of the reproductive process, is equally opposite and many times hazardous to the health or even fatal to the mother.
why is that so? Not enough selection pressure (low death rate than succesful delivery rate)?

Maybe since abortion wasn't always an option back then?!

It's definitely not an adaptive trait to feel pain when giving birth - your nerves as electrical alarms don't care what is the cause of the pain you need. This has nothing to do with the fact that giving birth can be fatal to the mother. Apart from that, reproducing is the most important life function from the evolutionary perspective.

@probably yes but what i meant is why giving birth causes potential trauma and suffering to human body?

Nerves are electrical alarms for any type of damage. How would they recognize the pain comes from actually a useful thing?

What I'm trying to say is why birthing is not evolved to a level where it's no longer damaging and potentially fatal to the mother

Because it can't evolve like that. There is a trade-off between the size of the head (brain!) of the child and the risk for the mother. The flexible skull (fontanelles) is an adaptation to that.


text:
How is the acetone method different from QB buffer for extraction of plant protein?
I primarily work on animal tissue but I thought of running an SDS-PAGE for plant tissue just for fun. I searched for some protein extraction protocols online and I don't know which one to choose. One is the acetone trichloroacetic acid method where you use the precipitate (?) and chlorophyll stays in the supertanant while the other is a QB (full form?) extraction buffer which is similar to what we use in animal tissue (with a bit of DTT and PVP). Here, we use the supertanant after centrifugal ion and the chlorophyll stays in the loading sample(?). At least, this is what I gather. What are the functional differences and when to use which technique?
Since I'm planning to run a gel, which one would be the better technique?
Please correct me if wrong I'm new to this field
Protocols attached.

I can't find the mention of QB buffer in any of the linked protocols. BTW, acetone is used to remove lipids.

The extraction buffer itself is called the QB buffer I guess @WYSIWYG


text:
Amino Acid requirement + intake in relation to diet + meat type
I was arguing with a friend:
I said: The Yulin festivals cannot be condemned by western culture, as we also kill animals in equally cruel ways.
She said: It isn't just that the killing is cruel, but it doesn't help us, as humans do not derive the same essential amino acids from consuming these less traditional meats (e.g. dogs, cats, etc) like they would from consuming more traditional meats (e.g. cow, pig, goat, etc) She cites her father, a geneticist, as her source.

Question one:
Are my friend and her father correct? Does the consumption of a less traditional meat (e.g. cats, dogs, etc) provide fewer essential amino acids than the consumption of traditional meats (e.g. cows, pigs, chickens, etc)?
Question two:
My friend also made a comment about veganism and vegetarianism (I am a vegetarian), stating that for the same reason as her and her father's above comment, people who exclude meat from their diet need to use supplements. Is this correct, or would it also be possible to just vary diet to obtain these essential amino acids?

There is a big difference between amino acid production and essential amino acids.

Edited. Sorry about the lack of clarity.

I don't see how there could be significant differences in amino acid composition between Cattle or Pigs and Cats or Dogs. They are all mammals, and therefore relatively closely related. The major proteins should all have similar sequences. This paper might have better information, but it's paywalled. Besides, if you only judge meat by whether or not it has the perfect mix of amino acids for human consumption, then humans would have the best meat because they already contain everything a human needs in the right proportions.

There is a difference between animals in their requirements for amino acids. For example, cats need high amounts of taurine (and can't make it) and when fed diets lacking enough can go blind. This is why vegans trying to feed vegan diets to their pets can be very bad for the pet. Animal proteins have sufficient taurine for the cat.
However, the meat of a cat or dog is just as a complete source of protein for humans as any other meat. All essential amino acids are there in sufficient ratios. Suggesting otherwise by her father suggests some confusion between the dietary needs of cat vs. the nutritional value of the cat to another predator.
Your second question is easily answered by looking up essential amino acids.  Wiki is plenty sufficient to get the gist Wiki Link. In short, most plants don't contain the full complement of amino acids that humans require (and can't make on their own). So to get this full complement, it requires eating multiple plant products that together contain the required amino acids.
From Harvard School of Public Health

Protein is built from building blocks called amino acids. Our bodies make amino acids in two different ways: Either from scratch, or by modifying others. A few amino acids (known as the essential amino acids) must come from food.
Animal sources of protein tend to deliver all the amino acids we need.
  Other protein sources, such as fruits, vegetables, grains, nuts and seeds, lack one or more essential amino acids.
Vegetarians need to be aware of this. People who don’t eat meat, fish, poultry, eggs, or dairy products need to eat a variety of protein-containing foods each day in order to get all the amino acids needed to make new protein.

Good info, but are there sources? Thanks

Animal meat is generally animal meat. I could find nothing about essential amino acid composition between different kinds of animal meat. You can find lots of differences in fat content and some differences in mineral content based on the species, but that isn't your question.

One more thought about her father. Cats do have a genetic difference that doesn't allow them to make taurine from other amino acids. This may be what he was thinking of, as humans and most animals do have this pathway.  However, as mentioned above, this has no bearing for the consumer of the cat as food.


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Why does uncompetitive inhibition decrease the Michaelis constant?
I can't seem to find a good resource online that clearly outlines the difference between an uncompetitive, noncompetitive, and mixed inhibitor (I understand competitive inhibitor though).
More specifically, why does uncompetitive inhibition decrease the Michaelis constant?
From wikipedia:

This reduction in the effective concentration of the E-S complex increases the enzyme's apparent affinity for the substrate through Le Chatelier's principle (Km is lowered) and decreases the maximum enzyme activity (Vmax), as it takes longer for the substrate or product to leave the active site. Uncompetitive inhibition works best when substrate concentration is high. An uncompetitive inhibitor need not resemble the substrate of the reaction it is inhibiting.

The Lineweaver-Burk Plot:

By TimVickers - Own work, Public Domain, https://commons.wikimedia.org/w/index.php?curid=4549560

The uncompetetive inhibitor essentially "locks" the substrate in the enzyme thereby preventing the enzyme from catalyzing the substrate which would then decrease the amount of free enzyme. That should not, however, alter the value of $K_m$ because any copies of the enzyme that are still active ("not locked") maintain the same affinity for the substrate. I applied that same logic to noncompetitive inhibition (no change in $K_m$), hence the confusion.

First off, the difference between the types of inhibition:

competitive inhibition: The inhibitor only binds to the substrate-free form of the enzyme. (Not necessarily at the active site!)
uncompetitive inhibition: The inhibitor only binds to the substrate-bound form of the enzyme.
noncompetitive inhibition: The inhibitor binds equally well to both the substrate-bound and substrate-free forms of the enzyme. (Some people feel this is just a non-special special case of mixed inhibition.)
mixed inhibition: The inhibitor binds to both the substrate-free and substrate bound forms of the enzyme. (But not necessarily with the same affinity.)

Secondly, you need to separate out the concept of binding affinity of the substrate from the concept of $K_m$. The binding affinity of the enzyme towards the substrate is just what you think it is: the equilibrium constant between the bound and unbound forms of the enzyme, in the absence of catalysis and inhibitor.
The $K_m$, on the other hand, is an overall parameter of the rate equation, and doesn't necessarily have a direct relation to substrate binding. The confusion between the two arises from the fact that in simple enzymatic systems, under the simplified conditions we normally study them in, $K_m$ is a pretty decent approximation of the substrate binding affinity. Thus you'll have introductory textbooks saying that "$K_m$ is a measure of substrate affinity". -- a gross oversimplification. They're certainly related, but they're not exactly identical - especially when you get to more complex reaction schemes. Confusing the two leads to problems.
The enzyme inhibition cases are an example of this. Enzyme inhibitors (even competitive ones ones) don't change the intrinsic binding affinity of the free enzyme to substrate. Instead, they draw off some of the enzyme from the productive pathway. Because they change the concentration of particular enzyme species, they change the observed rate equation. How they change the rate equation depends on which enzyme species they change the concentration of.
For a full accounting, you really should look at the derivations of the rate equations, and how the extra equilibria of the inhibitor binding changes things. (e.g. here or here) But for something of an intuitive explanation:
pure noncompetitive inhibition reduces the concentrations of substrate-bound and substrate-free forms equally. (The concentration of product-bound forms being negligible in the standard initial rate equations.) This is basically the same as reducing the total amount of enzyme, i.e. reducing $V_{max}$ or apparent $k_{cat}$.
competitive At saturating substrate concentration, the amount of free enzyme (and thus the effect of inhibition) is negligible. The rate at saturating substrate (i.e. $k_{cat}$) is thus the same. Therefore, it's the apparent $K_m$ that changes. (NOTE! The actual affinity to the substrate isn't changed by the inhibitor. Instead, the inhibitor specifically reduces the amount of free enzyme available, in a way that can be compensated for by higher substrate concentrations. This just so happens to change the rate equation in the same way changing the $K_m$ does.)
uncompetitive At negligible substrate concentrations, the amount of substrate bound enzyme (and the effect of inhibition) is negligible. Thus the rate should be the same with and without the inhibitor. If you recall, the enzymatic reaction rate at negligible substrate is parameterized by $k_{cat}/K_m$. For uncompetitive inhibition, this needs to stay the same. Thus both $k_{cat}$ and $K_m$ need to change in the rate equation, to the same proportion.
mixed - A mixture of the above effects, depending on the relative affinities to the substrate bound/unbound forms of the enzyme.


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Why did we evolve to control our breath?
I had this question in my mind and tried to think of why we would evolve to be able to control our breath. I remembered the Aquatic Ape Hypothesis, which makes a lot of sense and would explain it, though it is not a confirmed scientific theory (but that is another topic).
I also found this question, but it has not been answered properly. A Google search hasn't given me much either.
So my question is, what is the current scientific thinking on this topic (if there is one)?
edit I know that the Aquatic Ape Hypothesis is not a scientific theory. I did not ask anything about it, I only brought it up because it came up a lot when I was looking for an answer to my question. I do not want "maybe this is why it evolved", I was more interested in some creditable scientific paper or something similar.

The aquatic ape theory is a complete conspiracy. Even the link you provided debunks it. I would ask simply "What advantages does holding your breath provide?" and I imagine answers would be along the lines of "stops breathing through smoke or smog, quieter than breathing, allows water crossings of rivers and lakes" (probably others I have missed). I'm not sure whether you're asking for these things, or an tree of life node at which we can pinpoint breath holding with different functions appearing and disappearing.

Speaking is part of the things we do thanks to controlling our breath. Note also that other mammals are also able to vocalize and therefore there are good reasons to think that this is unrelated to recent hominid evolution. In any case, the aquatic ape theory is not a theory but a hypothesis (see here for semantic) that is for the moment supported by very little to no evidence.

@James 'conspiracy' is a bit strong, isn't it? It's popular with some non-scientists but has never been accepted as a credible or useful hypothesis by the scientific mainstream due to fundamental flaws. (For anyone interested in the idea and some of its flaws, the Wikipedia page on it is actually quite good: https://en.wikipedia.org/wiki/Aquatic_ape_hypothesis).

It should also read "hypothesis" and not "theory". A theory in science is a standing theoretical building with the possibility to prove it.

@matthias-schreiber Don't worry, I realised you weren't proposing the AAH and I think you were absolutely right to mention it given the context. If you hadn't someone else would have!

I some time ago read that it has to do with both bipedal movement (allowing the decoupling of step and breath anatomically), endurance running which seemed to be important in our ancestors, and the evolution of language (in which the production of phonemes, in fact, is not possible without controlling breath). I cannot find the source, though, so I will not make this into an answer.

I'd take a look at mammalian dive reflex... humans have a much weaker response than aquatic mammals, so it is quite possible that this is also seen in other apes as well. And that may be a good reason to need to evolve breath control, to do what no longer comes reflexively. It could also be a fact of our consciousness over the biological processes that are occurring inside of us and we have an idea of cause an effect that other animals may not. If I hold my breath I can get the juicy oysters underwater...   master it and you eat better and survive to reproduce and well natural selection.

It is also very difficult to form an evolutionary argument surrounding a behavior, especially if the environmental pressure than led to it occurred hundreds of millennia ago. And if you want credible scientific articles, then learn to use resources like PubMed, Academic Search Complete, not Google. Even Google Scholar can be a bit iffy.

A lot of mammals can control their breathing, dogs for instance can also hold their breath. Basically anything that can vocalize can control its breathing.

From the abstract of MacLarnon & Hewitt, "The evolution of human speech: the role of enhanced breathing control", Am J Phys Anthropol. 1999 Jul;109(3):341-63:

Evidence presented herein shows that modern humans and Neanderthals have an expanded thoracic vertebral canal compared with australopithecines and Homo ergaster, who had canals of the same relative size as extant nonhuman primates. Based on previously published analyses, these results demonstrate that there was an increase in thoracic innervation during human evolution. Possible explanations for this increase include postural control for bipedalism, increased difficulty of parturition, respiration for endurance running, an aquatic phase, and choking avoidance. These can all be ruled out, either because of their evolutionary timing, or because they are insufficiently demanding neurologically. The remaining possible functional cause is increased control of breathing for speech.

It would be nice to see some explanation for any downvote -- I'll try to improve the answer if possible.


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Can you naturally change your DNA that's passed to your offsprings?
Is it possible to change the genes that you'll pass on to your offsprings by natural activity and behavior.
For example if you do body building for quite a long time build strong muscles then would your offsprings have stronger muscle builds than average?
Or is random mutation is the only way DNA would change naturally?

No, this does not happen. This is the view of Lamarck on evolution which is wrong. The only natural way of changing DNA is by mutation.

@Chris Could OP be getting confused by epigenetics?

@user137 Possible. Then this question needs clarification.

Clarify your question please.

As far as I know, yes, but not in the sense you are asking. Sperms with Y chromosomes are only so slightly lighter than those with X chromosomes, so if you are male and weakened so much that for your sperms it makes a difference (but still are fit enough to engage in sexual activity), you will have more male offspring. But no, no, no chance that your offspring has stronger hair if you visit the hairdresser more often.

This is in between an extended comment and an answer.
What do you mean by "Natural"?
The question makes no sense as the term "natural" isn't properly defined. (I am voting to close as unclear).
For example, if you go to an area where there is "naturally" a high radioactivity, this will increase your mutation rate. Is this a natural way to change your mutation rate (even though you need a specific device to compare the level of radioactivity)?
As another example, some diets may potentially increase once mutation rate, but again you need a fair amount of research to figure out what diet does what.
Yet another example, a plant that is stressed tend to increase its mutation rate. This, I suppose sounds quite "natural".
In any of the above examples, the mutation are random in the sense that they do not have a foreseen impact on the phenotype of the offsprings.

if you do body building for quite a long time build strong muscles then would your offsprings have stronger muscle builds than average?

This sounds very Lamarckian. We've known for more than 150 years this is not how evolution works. If you are unaware of these concepts, you should have a look at Understanding Evolution (UC Berkeley) (or other introductory source of information) to get a notion of what evolution is about.
In the comments, one person talked about epigenetics. I think there is no point talking about epigenetics for the moment as it may do nothing but disturb the OP if indeed (s)he does not have some introductory basis to evolutionary biology.

Would a diet high in Cobalt-60 and nitrite salts maximize your mutation rate?

Yes, typically!

It's called the Manhattan Project Diet.


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Deletion of codons at the start of a sequence in preparation for heterogeneous expression. Why?
I am reading a patent where they isolate a gene from cDNA constructed from RNA extracted from plant matter.
The subsequent step (in preparation for heterogeneous expression in E Coli.) puzzles me:

The codon optimization I can understand but this part confuses me "...remove the first 23 codons from the DNA sequence and replace [the start?] by the ATGGCT sequence."
Why would one remove a set of codons at the start of a sequence? How did they decide how many to remove Is there an obvious reason I am missing?  Also what is special about the ATGGCT sequence.
Any ideas why they would do this?
The start of the new sequence (1650 bp) looks like this:
atggctaccg ataatgacag ctctgaaaac cgtcgtatgg gtaattacaa gccgtccatc       60

tggaactacg acttcctgca gtccctggct acccgccaca atatcatgga agagcgccac      120

whereas the original sequence (1710 bp) was this:
atggattctt ccaccgccac cgccatgaga gctccattca ttgatcatac tgatcatgtg       60

aatctcagaa ctgataacga ttcctcagag aatcgaagga tggggaatta taaacccagt      120

Another point I am confused about is that 1710 - 23 x 3 + 6 is 1647. But the new seq. is 1650 bp. What gives?

Obvious reasons would be: a signal peptide, nope, doesn't look like one, annoying restriction sites, nah, not the case either

Proteolytic cleavage and N-end rule

@Ashafix Can you elaborate more on that? How is the N-end rule applicable in this case? If I translate both those sequences the first Amino Acid is Met. So no stabilizing residue seems to have been added.

The easiest answer would be to ask the authors of the patent.
Several other possibilities (see comments) were excluded, such as:

restriction sites which interfere with cloning
signal peptide
proteolytic cleavage

Although it's just a theory, removing part of the N-terminus might improve protein stability and half-life time because the first 30-40 amino acids lack an ordered structure (as judged by submitting the structure to Phyre). Those structures are known to aggregate and influence protein stability.
References:
The use of systematic N- and C-terminal deletions to promote production and structural studies of recombinant proteins.
Sequence composition of disordered regions fine-tunes protein half-life
Production of prone-to-aggregate proteins


text:
Names for the degrees for symptoms from drought (or other damage) done to trees
Looking out my window, I see trees suffering from drought. I once knew the name for the degrees visible, but I have forgotten and can't find it on the net.
Attempt at describing "level of dryness"

Level 1
The tree is completely without leaves (at a season where it should have at least some leaves).
Level 2
The tree has at least some bushels of leaves on the main branches, interspersed with dry areas without any leaves.
Level 3
The tree has leaves all around the main branches (those which are attached to the stem), but not on any secondary branches.
Level 4
The tree has leaves on the main branches and secondary branches.

Explicit question
What are the names for those levels, or other levels, in case I missed some?


text:
How can I perform a 1:1 sequence-structure alignment for a pdb template dimer and homologous dimer sequence?
I have:
1. A PDB dimer protein structure template of a real solved protein.
2. An unsolved, but highly homologous dimer protein (>90% sequence identity.)
How can I use MODELLER to make a theoretical model of my dimer of unknown structure, using the homologous dimer template?
I know I need a PIR alignment file, probably with a 1:1 sequence-structure alignment.  However, I do not know how to make this file.
Please advise?


text:
O-Group names of Salmonella serotypes?
What liposaccharides are represented by the O-group designations of Salmonalla serovars in the Kauffman-White classification scheme?  I mean to ask, how do the numbers in a Sal serovar (1, 9, & 12 for Enteriditis, for example) describe the oligosaccharide(s) present on the cell membrane?  Continuing said example, does 1, 9, 12  indicate three different types of liposaccharides, or one type of oligosaccahride containing three distinct features?


text:
Could a large constrictor kill a small animal?
According to this article there was a python whose body circumference was 85cm.  This means its diameter was 27cm.
Would it be possible for this snake to constrict animals that are about the same size as its diameter?  It is hard to imagine it having enough flexibility to constrict a swamp rat, for example, whose size is less than 27cm.  Could it kill such animals by another method, say with its jaws or by crushing them by rolling over them?  Or are such small animals simply off its target list?

Constrictors doesn't have uniform body circumference from head to tail. They coil around the prey accordingly. In your example, if the prey is very small, it just swallows. If its little big, it coils a little bit (check some videos like this) say two turn coil. This will only cover top half feet of constrictor's length which is of lesser diameter than the body.
So basically, they crush the prey and perform a kill. Its not a necessity for any constrictor to use its entire body to coil around a prey. They adjust their coil level to control the prey.


text:
Why is the Pentose Phosphate Pathway so active in erythrocytes?
Is it because glyceraldehyde -3-phosphate (a molecule which when enter glycolysis help produce ATP through substrate level phosphorylation) can be prepared without losing an ATP through this process?

I've replaced the abbreviation in your title. Avoid all but the most familiar abbreviations (such as DNA) unless you define them (and this cannot be done in titles).

I've modified your title again. The use of "predominate" could have been taken to imply it processed more glucose than glycolysis. However in resting erythrocytes the figure seems to be 10% PPP. Still a lot compared with many other cells, but less than glycolysis.

Thanks for the correction though I actually meant 'Why is the Pentose Phosphate Pathway so active in erythrocytes?' so its ok.

Can you please cite a reference which says that erythrocytes use PPP relatively more than other cells? I was actually not aware of this; I don't think this some common textbook fact that I missed.

No. Your supposition is incorrect — the phosphate in glyceraldehyde 3-phosphate has to come from somewhere, and it comes from glucose 6-phosphate. The reason a second ATP is required before you get to the triose phosphate stage in glycolysis is that you are generating two molecules of triose phosphate. In the pentose phosphate pathway (energy-producing non-oxidative branch) you are not generating two molecules of triose-P from one hexose-P, you are generating two hexose-P and one trisose-P from three hexose-P, as shown in my Diagrams 2 and 3 below. (The other three carbon atoms are lost as CO2.)
A good way of approaching this question is to ask “What can be produced by the pentose phosphate pathway that cannot be produced by glycolysis?”.
Glycolysis may be summarized in this context as:

Glucose + NAD+ ➝ Pyruvate + NADH + 2ATP

But to allow glycolysis to continue the NADH is reoxidized to NAD+:

Pyruvate + NADH ➝ Lactate + NAD+

So the sole product of glycolysis for the erythrocyte is ATP (primarily for active cation transport to maintain cell shape) lactate passes into the blood for recycling.

The Pentose Phosphate Pathway (the oxidative stage) is shown in Diagram 1, above, and may be summarized in the way done for glycolysis as:

Glucose + ATP + 2NADP+ ➝ Ribulose 5-P + CO2 + 2NADPH

Ribulose 5-P has two possible fates, but only one differs from glycolysis, so the two distinguishing products of the pathway are ribose and NADPH.
Ribose is important for nucleic acid synthesis, particularly in dividing cells, explaining the increased activity of the pentose phosphate pathway in those cells. This cannot be the reason for the high activity of the pathway in erythrocytes as they have no nuclei and do not divide. In fact the ribulose 5-P is fed back into glycolysis for generation of ATP as shown in diagrams 2 and 3.
NADPH, then, is the answer in this case. It is the reducing agent used in the cytoplasm for synthetic processes (unlike NADH used particularly for ATP generation in the mitochondria), and so the pentose phosphate pathway is found in cells such as adipose, mammary gland and liver, that synthesize fatty acids, and cells that synthesize steroids. However that is not there is no fatty acid or steroid synthesis in the erythrocyte.
NADPH is important in erythrocytes as it is the specific source of reducing power required to keep the molecule glutathione in a reduced state. This has an important protective role in reducing cellular molecules that have become oxidized by molecular oxygen, a problem that is more acute in erythrocytes than in perhaps any other cells as they are the carriers of molecular oxygen. The cell membrane is particularly prone to oxidative damage. You can read about this online in this chapter in Berg et al.

I came across this line 'This stress is most acute in red blood cells because, lacking mitochondria, they have no alternative means of generating reducing power.'.
Does it mean that normal cells with mitochondria are better equipped for combating oxidative stress? Is it due to NADH and FADH2 formed in the mitochondrial matrix during Beta oxidation and Krebs cycle? Can NADH and FADH2 act as reducing agents for glutathione just as NADPH?

I quoted the line from that chapter you linked.
However my question still remains the same Can NADH and FADH2 act as reducing agents since they say that in absence of Mitochondria RBCs have no alternative means of generating reducing power?

I'll reply in two comments because of length restriction. I don’t find the line you quote at all convincing or helpful in any way. First, if what was required were NADH, that could be generated in glycolysis as far as pyruvate, with the pyruvate going into the blood and returning to the liver. (Pyruvate can pass in and out of cells.) Second, I imagine protection against reactive oxidative species in the mitochondrion is required because the mitochondrion is the site of the electorn transport chain at which oxygen acts. Thus protection in the mitochondrion is only designed to be used there.

The mammalian glutathione reductase only uses NADPH. It does not use NADH or FADH2. This is entirely consistent with the differential use of these two reducing nucleotide coenzymes in mitochondrion and cytoplasm.

I have now updated my answer, including my own illustrations, to make it slightly more comprehensive and, I hope, of more general use. It is meant to be an introductory general answer to the question, but if anyone thinks there are defects or points that should be added, please comment.

An anonymous user keeps submitting edits which in my opinion diminish rather than improve the answer. His explanation is the cryptic "decryption". If he explains himself in a comment I will be happy to discuss any points he raises. Otherwise I shall continue to reject his proposals.


text:
Predator prey interaction
I went through a line in my textbook which read:

"But for predators, prey species could achieve very high population densities and cause ecosystem instability."

I was not able to understand the meaning 'but for predators'. Can anyone please help me to interpret it's meaning?link to page where this line is mentioned
Edit: In terms of biology, I was unable to understand the meaning of the sentence,  and I wanted to make sure that I don't misunderstand things... And this is why I posted the question.. I feel that the answer given is correct and in case, you find better explanation, please do post.

Can you provide a longer quote and what book it is from? To me, this isn't really answerable at the moment.

@fileunderwater - This is the text I was able to find. Third paragraph under the table.

@GForce yes... This is where I read from... Ncert 12th biology.. Organism and population.. To be precise

I'm voting to close this question as off-topic because it's about English language.

@user24693 You should add this info to the actual question (title, author, and preferably a longer quote.

@fileunderwater  ok... Next time when I post a question,  I will make it sure that I write all the details.. Thank you

@rg255 But I thought questioning it on a biology site would be a better option... As I was intrested in knowing the answer by biology perspective

I disagree with GForce's explanation; the meaning is not that growth of prey populations causes instability in predator species.
The sentence is merely saying that without predation, prey population growth is more likely to be at a level which leads to ecosystem instability. The term "but for predation" means "if it wasn't for the effects of predation". In other words:

"Ecosystem instability can occur when population growth of some species goes unchecked by predation."

See here for more explanation, where this example comes from in which it says that running a red light caused a crash:

"but for running the red light, the collision would not have occurred"

Biologically this makes sense in the sentence you show; without predators a species is limited by its supply of resources, and it can use these resources at an unsustainable level, whereas if you add predators to the mix there is additional extrinsic effects on population size, not determined by ecosystem properties such as space or nutrients.

I agree with this explanation and a practical example of this is the cascading effect of the wolf species canis lupus. Their reintroduction to the Yellowstone national park in the late 90s saw the proliferation of many life forms and also the change in the geological nature of the area, this effect was simply a result of the wolves changing the pathways of the moose species which were initially along the stream banks.

It's essentially saying that high densities of prey species can cause ecosystem instability not only for themselves but also for the predators which prey upon them.
In other words, high densities of prey species not only cause ecosystem instability by competing with each other, but this instability can move up the food chain and affect predators at higher trophic levels. One example would be a high density prey species having a population crash and having a corresponding adverse effect on predators which feed upon them. Without prey to feed on, predator populations would crash as well.