text:
How does taking drugs speed up the development of drug resistant or viruses?
First, here is what I know:
Some infectious illnesses, such as HIV or Hepatitis B, can be treated with the help of some drugs. The problem is that the virus sometimes undergoes mutations which grant resistance to the drug.
First question : Is it so far right?
Secondly, what is not totally clear is why taking drug does speed up the development of the drug-resistant version of the virus. In my point of view, the drug resistant virus will develop anyway with or without taking drugs. I don't see what taking drugs changes. Is it like an intra-competition between the different mutated versions of the virus and in this case, taking drug will eliminate all the mutated versions that are not drug-resistant and, this way, favour the development of the drug-resistant versions?

Welcome to Bio.SE! your both assertions are quite correct. yes, mutations are random and it is the drug itself which favours evolution of drug-resistant strains by killing non-resistant ones.

Ok, thanks! If I understand well, there is a competition between all the forms, versions of the virus? If yes, why cannot they develop together? Is that because they need the same resources to develop?

I am no expert in evolution, so I can't give you very precise answers. The point is that without the drug, both resistant and nonresistant strains can live happily without competition (what would they compete for?) but when drug comes in, it kills nonresistant ones, leaving resistant ones able to dominate.

My central question is : why does taking drugs favour the development of drug-resistant strains? If there was no competition between strains, taking drugs would have no effect on the development of drug-resistant strains, and it's not the case. So, this is why I suggest a kind of competition between strains. Do you understand my reasoning?

I get your point. Someone more familiar with the topic (like @Remi.b) can explain this better to you.

No, they mutate at a similar rate; taking the drug does not affect mutation rate, but the idea of drugs is to inhibit the virus somehow. This happens in nature all the time (an organism develops - through a mutation - a product which can inhibit growth of a competitor. Taking the drug provides a selective advantage for the drug resistant 'organism' (or virus) to proliferate, as @another'Homosapien' has already stated.

In fact, I didn't talk about the mutation rate but about the growth rate of amutated drug-resistant strain which is higher when taking the drug, because of the elimination of a part of its "competitors". Is it right?

Actually, I believe I answered the exact question you asked, even on rereading it.


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What are some effective strategies for testing whether a trait is an adaptation?
Although signs of evolution are to be found everywhere across taxa, it sometimes seems difficult to discern whether a trait is a retained accident or an adaptation. It also seems like there is a temptation in people to come up with just-so stories to explain traits as adaptations. What is an effective strategy for coming up with tests to determine whether a trait is an adaptation or not?

See if the trait gives any significant advantages as compared to absences of trait. Also if the trait is present in almost all organisms and no variation is found, then see if it has any use. Like appendix is found in almost every human; although it can be surgically removed, normally it is present, but is useless in humans.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Calculating sample concentration factor (opposite of dilution)
I am starting up an algae project, and I am getting a bit confused about some details in calculating density. For example, I take a sample of 250 mL, and concentrate it down to 25 mL with a sand filtration apparatus (factor of 10). I am using a gridded sedgwick-rafter chamber to enumerate the density of algal cells on a cells/mL basis using this formula from Standard Methods 10200F: cells/mL = [(# organisms counted)* (1000 cu. mm.)/ (field area)(field depth)(# fields counted)].
Once I calculate cells/mL, should I DIVIDE that result by my concentration factor (10)? My instinct is to multiply, but wouldn't that be appropriate only if I diluted the sample?

Your original sample is more dilute than the sample you counted. The concentration is less and therefore you should divide your counted concentration by 10 to get the concentration in the original sample.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Why does fetal distress (hypoxia) cause bradycardia?
In a non stress test performed in the labor room, fetal bradycardia is a danger sign indicating fetal distress (hypoxia).
Why does fetal hypoxia cause bradycardia while hypoxia in adults cause tachycardia? What is the mechanism for both and why is it reverse?

Are you aware that in adults with hypovolemia, bradycardia is a sign of an impending cardiac arrest? Not saying ths is the answer, but asking if you're aware that the end point is similar.


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A better definition of ‘evolution’?
Occasionally on this site I’ve noticed the following definition of evolution being given:

Evolution is a change of allele frequency through time in a population

( For example, from here)
Recently the following (From here):

The statement "evolution is driven by mutations" is very misleading if not simply wrong. Just have a look at an intro course to evolutionary biology!
In short, evolution is a change of allele frequency over time.

But mutations are important to evolution, and I feel must be included in the definition.
Here’s why that concerns me:  One group of evolution deniers, and others like them, use comments like these above to try and show a weakness in evolution.
See:
http://creation.com/don-t-fall-for-the-bait-and-switch
With comments like:

“It is a bit of a trick played by using sloppy language. Evolutionists use adaptation, which is observed, to support evolution, which is an entirely different process. It is an example of bait and switch.”

Also:

“Next time someone says that evolution is an observed scientific fact make sure you get them to clearly define what they are talking about.
  They will almost certainly be referring to adaptation but want you to believe they have proved evolution.
  Don’t be fooled. Sloppy language leads to sloppy thinking.”

Ok, I hate to give them ‘air-time’ by posting that, but perhaps it will cause us to clarify ourselves better.  Answers like "a change of allele frequency through time" just end up feeding right into this kind of evolution-denial.
SO, here’s my question  Since there’s a lot people here smarter than me:  Can someone please offer up a stronger definition of evolution than just ‘a change in allele frequency over time’?
In researching answers I found this on Berkeley’s site:

“Biological evolution, simply put, is descent with modification. This definition encompasses small-scale evolution (changes in gene frequency in a population from one generation to the next) and large-scale evolution (the descent of different species from a common ancestor over many generations).”

I like that it goes beyond small-scale (which these others would just call adaptation).  But this doesn't mention natural selection, and mutations; which I feel are important distinctions given the kind of comments these deniers make. Is there a reason Berkeley's definition didn't include those distinctions?

EDIT:  Can someone explain the down-vote?  I followed everything outlined under How to ask a good question

You might try over at T.O. ... http://www.talkorigins.org/faqs/evolution-definition.html

I agree with the Berkeley statement and your assertation. "Change in allele frequency over time", by itself, is not sufficient.

But they're the ones using sloppy language.  Evolution IS adaptation which takes place over generations.  The mechanism by which the adaptation happens is mostly change in allele frequency, though other things like mutations, viruses inserting bits of genetic material, or wholesale co-opting of different life forms (e.g. mitochondria) play their parts too.  But we could observe the fact of evolution without knowing anything about the underlying genetic mechanisms.  As Darwin & Wallace actually did.

@jamesqf:  As I read it (and I have read a lot of their material), creationists fully believe in adaptation, speciation, and natural selection.  In their minds, these mechanisms are built into life’s design.  Animals where created with plenty of built-in variety, seen as adaptation via natural selection.  As rabbit spread the globe, some became desert rabbits, some arctic rabbits.  All done via a ‘change in (PRE-EXISTING) allele frequency over time’.  So when we use that phrase as our definition of evolution, it just confirms to them their own stance.

(cont).  The important ‘distinction’ I’m looking for: is one that includes the creation of new genetic information, which as I understand it to be, is via mutation.

It is pointless to say that "Creationists believe adaption" without knowing what they mean by it.  It is not at all clear that they are using the term to mean hereditary changes to the DNA. Also, not being tethered by the evidence, some Creationists might mean something very very different from other Creationists.

And the issue is, of course there is no evidence of all this "pre-existing" variation.  When a bacterial sample evolves resistance, it's due to a DNA change. There was no resistance allele hiding, it didn't exist until the mutation.  Creationists are just wrong about the facts here.

@RunzWitScissors: Well, the operative phrase there is "creationists fully believe".  It's a religious belief, and no amount of fact or logic is going to change that.  The most you can get them to do is weasel around the idea, with their "adaptation".

"Change in allele frequency" also encompasses mutations. The occurrence of a new mutation increases the frequency of that variant from 0 to whatever percent of the population the organism that carries it comprises. Similarly, the frequency of all the other variants at that locus decreases by the same percentage.

@RunzWitScissors the problem is the continued generation of new genetic material is not actually necessary for evolution, so there is absolutely no reason to add it in to the definition. If starting right now no mutations at all occurred ever, life would still continue to evolve for quite a long time.

@swbarnes:  True, but that doesn't see to deter them.  BTW, your bacterial resistance example quite frankly is one example of what they would call a bait-and-switch.  See here. and here.

"Evolutionists"... I'm not sure that I like that term. How about "members of the general public that understand reason". But more seriously, this should go on meta, not the main site. It seems to be more about if we, as a community, should be more careful when defining evolution.

The focus upon definition of term is a rhetorical strategy often employed to confuse the issue, especially by laity when discussing technical matters. Word meaning and use are easily a source of ambiguity, confusion, contradiction and such that the appeal to the dictionary definition is often an appeal to false authority. At the very least it is worth pointing out that aside from etymology and morphology, empirical disputes are not settled by consulting Merriam-Webster.
"Evolution" is a fairly general concept and it can be useful when discussing technicalities to specify "biological evolution".  For example, "water" might mean specifically "H2O" or generally "clear, odorless, tasteless liquid"  or possibly might be used without qualification in distinguishing "potable water" from ocean water, et cetera.
Consider that the definition of term is not so much the pertinent legacy of biological evolution (pace Darwin, Wallace et. alii). The kind of explanation biological evolution uses is it's hallmark. In particular, biological evolution removed teleology (the study of purpose)) from biology.
For example:
A teleological explanation of biology:
1) This plant is photosynthesizing in order to survive.
2) This plants species is surviving.
A biologically evolutionary explanation of species:
1) This plant is photosynthesizing
2) Plant species which photosynthesize have an increased likelihood of survival.
Note that survival is still at play, but the argument is no longer circular. This is not to say that cause has been cited, however, the logical structure of the argument no longer "begs the question"

This is the one I use for my intro to biology students.
"Biological evolution is a change in the number of times specific heritable characteristics(aka genes) occur within a population over time."
Keep in mind this is a description of the definition{law} of evolution not the theory of evolution. And is just a diffrent way of stating, "Evolution is a change of allele frequency through time in a population"
I use this becasue the possibility of evolution in machines, epigenetics, and xenobiology is discussed and students have a difficult time separating genes and nucleotide sequences, and not every student will know what allele frequency means.
defining evolution with natural selection would be pointless and circular, since natural selection is part of the theory that explains how and why evolution happens (but not the only mechanism by which it operates). We do not define gravity by the proposed mechanism but by the observed behavior of matter.
If mutation stopped tomorrow evolution would continue, It would not end until there was no life left to vary. So using mutation to define evolution would be false.
Deniers will deny no matter how you change the definition, there is no reason to bastardize the science to try to please them. You would be better spending your time discussing things like ring species or asking them to define "kind." Likewise speciation is the outcome and subset of evolution and completely covered in the existing definition. If they have a problem with speciation let them argue with it, speciation is only one form of evolution. If nothing else it will encourage them to learn something about what they argue.

I’m not sure if that definition is much better.  That definition fits perfectly well with their (creationists) model.  As that article specified, they fully believe in adaptation.  Those ‘heritable characteristics’ to them, were there to begin with and don’t ‘arise’ later.

that means they don't believe in mutation which a whole new problem, and can be dealt with by searching for a paper on mutation.  Try chasing their definition instead of  letting them use a strawman to get you to twist the definition of evolution to suit what they want.

since the focus seems to be a non-scientific argument this site may help you. http://www.talkorigins.org/

adaptation and evolution are not really distinct concepts, paleontologists might talk about tetrapods adaptation to life on land which has continued for hundreds of millions of years. Unsurprisingly it sounds like the creationists you talk to don't understand the terminology they are using.

They do seem to understand their terminology, but just point out that many forms of 'adaptation' don't involve the creation of new genetic information.  That's why I was calling for a better definition that just a change in frequency.

John: BTW, please explain further your comment that "If mutation stopped tomorrow evolution would continue".  You have me intrigued.

This is a much more correct definition, especially since it carefully distinguishes evolution as an observable fact from theories of the causes of evolution.

@RunzWitScissors evolution will continue until there is is absolutely no variation within a population which basically means until the population is extinct or entirely clones. evolution only requires variation in heritable characteristics and it can continue until that variation is exhausted. Normally mutation keeps adding new variation but it takes time for evolution to spread/eliminate mutations. Also it is rarely all or nothing, balances of multiple competing mutations exist (Evolutionarily Successful Strategies) so some variation will also tend to be preserved.

@RunzWitScissors in line with John's comment consider a population with two virus-resistance alleles. Virus A is common, so resistance allele A spreads in the population, leading to less virus A and more virus B, so now resistance allele B is selected for and spreads through the population, etc. Continual evolution even in the absence of mutation.

reference for Evolutionarily Stable Strategies (yes I know my error)http://www.nature.com/scitable/knowledge/library/game-theory-evolutionary-stable-strategies-and-the-25953132?utm_source=%CE%B1%CE%B8%CE%B7%CE%9D%CE%95%CE%91+subscribers&utm_campaign=0a22881ee9-01_a8inea_Newsletter12_17_2013&utm_medium=email&utm_term=0_903691d971-0a22881ee9-116007725&ct=t(01_a8inea_Newsletter12_17_2013)

@John & iayork - Certainly variation & adaptation via natural selection can continue without mutations.  Yet in light of the central theme of this post:  to a creationist, those things are simply a part of their creation-model.  The distinction between that and evolution is issue:  The change in existing genetic material to pull from (via mutations).  It's like arguing with someone: 'look, I can shuffle these cards, therefore cards evolved'.  Their response:  'I believe cards can be shuffled as well.  It's the sufficient addition of new well-working cards that are in question'.

@RunzWitScissors 1. shuffling is a randomizing process, NS is not. 2. then their problem is with mutation, speciation, the fossil record, and the implication of evolution. each of which can be dealt with individually. Including accessory process like mutation in the definition makes it  inaccurate. They are basically saying, "I believe you can walk around the block but I don't believe it is possible for a person to walk across the country." the process is the same they are claiming that it somehow stops running after a certain amount of time. this is a claim THEY must provide evidence for.

@John  Yes, I get that NS is not random. Card shuffling is an analogy for genetic variation in a population.  Shuffling existing cards is different than shuffling AND creating new cards.  And your 'around the block' 'across the country' analogy isn't accurate.  More like selecting various pre-existing vehicles to travel with, vs. selecting AND creating new vehicles to travel with.

@RunzWitScissors no both mechanisms are identical the only difference is the size of the population and the run time. New vehicles for the genes are created with each generation, species are just arbitrary but useful groupings inside the one single population that is all life. Once time is considered all populations blur into each other, all life is one giant ring species.

@RunzWitScissors creationists mistakenly believe species is constant and concrete and not just an artifact how human need to think.  when you show them what species actually are they retreat to their own undefined term "kinds" which the claim (without evidence) does not change.

I think that any definition that is useful for explaining evolution to laymen must contain the concept of natural selection. Here's my version:
Evolution is a gradual change in organisms over many generations caused by the combination of (1) random variation in genes among individuals and (2) the fact that those individuals that best survive and reproduce will transmit their genes to the next generation.${}^1$
That random variation arises (in part) from mutations is just a detail, in my mind. The fundamental mechanism, which is very hard to deny, is that even though variation in any individual's genes are completely random, the combination of this variation with survival of the fittest will produce a strong tendency to adapt to the environment. If someone has difficulty accepting / understanding this principle, it's easy to setup computer simulations that demonstrate the effect hands-on. In my experience this convinces pretty much everyone.
The "bait and switch" argument on the page you link to is fundamentally flawed because there is no difference between what they call "adaptation" and "evolution". Both are evolutionary processes, resulting from variation and natural selection. It's just that these creationists are willing to accept some consequences of evolution, but refuse to accept all of them. This is just a rhetorical device that lets them accuse scientists of "equivocation" (which sounds pretty sophisticated). Also, there are the usual falsehoods: "no intermediate forms", "mutations do not generate new information", and evolution is "just a hypothetical philosophy without observational scientific support".
But then again, creationist do not really care about the scientific arguments --- they only pretend to do so because they know science has credibility. They are driven by belief, and arguing with them is usually pointless.

${}^1$ I am aware that this is not the most general definition one could give, as it does not encompass genetic drift and other mechanisms described by modern evolutionary theory. But I think it's an appropriate one for explaining evolution, as in the discussion brought up by the OP.

I do like that answer.  Thank you.  BTW, please do share at least some of the bigger errors on that page.  An acquaintance gave me that link, and I'd love to point out some of them.

recombination is not necessary for evolution

If you really want to understand evolution consider explaining artificial selection first, it is basically the simplified version. these videos are very good approach laying everything out very clearly. https://www.youtube.com/watch?v=GhHOjC4oxh8.

@John,  I did not mention recombination?

@RunzWitScissors, I have added some comments on the creationist page. If you want to dig deeper, I would recommend Ken Miller's work, http://www.millerandlevine.com/km/evol/

This is a bad answer.  Modern evolutionary theory recognizes natural selection as one of the main drivers of evolution, but by no means is it the only one. Ignoring the past 75 years worth of understanding is a very bad start to a definition.

@Roland.  Good link, will check it out.  Regarding no difference between adaptation and evolution:  one is a subset of the other.  You can have adaptation without any change in existing genetic information.  Finch beak adaptation is one example.  Yes, creationists are willing to accept what you call 'some consequences':  just adaptation.  The entire point of their article is that too often 'adaptation' examples are given as examples of a process that can 'turn molecules into men'.  And the whole point of my post is to create a better definition of evolution than 'change in gene frequency'

@Roland.  Also, can you provide me some links refuting their case that mutations do not generate new information?  I'd love to pass those along.  (I have searched myself some but would like to find better ones).

@RunzWitScissors,  I think "information" is poorly defined in this context. But it's rather obvious that mutations can create new sequences, and so it provides a mechanism for exploring new genotypes.

@iayork,  I wasn't trying to summarize modern evolutionary theory. (And I don't think I'm the right person to do it.) I was shooting for an easy-to-understand definition that conveys the basic idea to the layman. And to be pedagogical, I think variation + natural selection should be the centerpiece.

If you're going to come up with a definition for a layman, maybe it shouldn't be actively misleading.  Your definition here is actively misleading.

@Roland My mistake your wording was a bit confusing.

Remember to define evolution you are looking for the basic observations that the theory was created to explain. That observations is that the variations in a population change over generations. points for mentioning equivocation,

@iayork  I don't think this is "actively misleading". I understand that "change in the heritable characteristics over generations" or some such is a more general definition that encompasses modern evolutionary theory, but that wasn't the issue here. I think it is necessary to focus on natural selection first if you want to teach evolution. If you wanted to teach physics, you would start with Newton's mechanics, not general relativity; Newton's is not the most up-to-date theory, but that doesn't mean that teaching it is misleading. Basics first. Refinement comes later.

If you don't actually understand what evolution is, you shouldn't be answering questions about it.

@Roland focusing on natural selection is counterproductive, a great way to explain evolution is to compare the mechanisms, natural selection, sexual selection, artificial selection, ect. To use your analogy we don't define thermodynamics as only Conservation of Energy.

@John,  well I agree with that. I very much like how Darwin introduces selection in the origin of species by starting with selective breeding, for example.  But those are all selection mechanisms, and I think they are included in the definition I suggested ("individuals that best survive").

except survival is secondary to passing on your genes, that is how things like kin selection and such function. may behaviors drastically reduce survival in return for helping spread genes, you could eliminate survival from the definition entirely. .


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How do coyotes remove cactus needles from their paws?
Here, in Arizona, coyotes roam and hunt in the desert.

While hiking with dogs, I often see spiny bits of Teddy bear cholla cactus on the ground.

Dogs often step on these and get stung by the needles. Trying to remove them from dog paws with hands usually results in hands getting pricked too. A pair of stones, sticks, or tweezers usually works. I imagine letting the dogs chew off the needles would result in having needles in their lips/mouth.
Q: What do coyotes do with stuck cactus needles? Do they remove them, if so how? Do coyotes and perhaps other desert animals have special adaptations for removing/avoiding cactus needles?

Their paws might be more callous and have more padding for the desert adaptation. Things can still get stuck in their paws but not cause serious issues and can fall off in time because of the adaptations. Wild animals can still be susceptible to splinter infections but it would be rare compared to humans or pets. I found some studies regarding to camels but not specifically for coyotes.


text:
What allows for no selection pressure against non-coding DNA?
Genomes of prokaryotes tend to have a higher proportion of coding DNA to non-coding DNA in their sequence than eukaryotes.
This means that either eukaryotes accumulated lots of non-coding DNA, much of which is regulatory, in the course of evolution — or that prokaryotes lost this proportion of non-coding DNA.
In order for transcription of a particular gene to occur, it seems that there must be some search performed on the DNA sequence to find the gene to be transcribed.
This search seems to be independent of the sequence length — if it weren't, that could act as a selection pressure, inducing loss of DNA that doesn't do anything. Therefore, it seems that the method by which this search is done must be O(1) — that is, it takes a constant amount of time to complete the search, regardless of the length of the sequence.
Such a method would be most welcome in computational sequence searches (in place of BLAST for example).
My question is, what, if anything, is currently known about the process of transcription that could explain this constant search time?
Or, if I am completely wrong in my assumptions, what are more reasonable assumptions?

can you add some references to the 'facts' you present in the question? (i.e. "genomes of prokaryotes tend to have a higher proportion of coding-DNA")

It doesn't take a constant amount of time, but the deletion of a single non-coding sequence is not going to noticeable change that time. more and more functions for introns are discovered everyday, so their may be far less junk than we think. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3325483/

I know this is a losing battle, but for the record: Very little eukaryotic non-coding DNA is regulatory.  Almost all of it is truly useless, and the simple reason for this is that there are many mechanisms that allow DNA in the genome to expand, and very few mechanisms that can safely remove non-functional DNA; it's therefore more adaptive to ignore the large amounts of harmless but useless DNA than to try to trim down the genome, which would provide very small benefits compared to the risk.

A) Here's the thing about evolution - just because something might have an adaptive benefit does not mean that trait will evolve ; this is contingent on the occurrence of the necessary mutations to produce a phenotype in the first place.
B) There are multiple copies of the transcriptional machinery (RNA pol, Transcription Factors) - numbering in the tens of thousands when you are talking of the core transcriptional machinery.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC84381/
The 3d structure of chromatin , as well as the large amounts of the core transcriptional machinery, prevent there from being too much adaptive benefit to losing large amounts of noncoding DNA.
C) Thirdly, there are suggestions that enhancer promoter contacts, which can greatly facilitate transcription, may be in some part at least determined by sequence motifs in the loops that bring together enhancers and promoters ; so there would be costs associated with losing ncDNA en masse. See www.nature.com/ng/journal/v48/n5/abs/ng.3539.html
D) Indeed, even when one looks at repeat elements derived from endogenous retroviruses, there are those that are of functional significance; Syncitin (which actually codes for a protein) is responsible for trophoblast fusion + placenta formation (See https://www.ncbi.nlm.nih.gov/pubmed/10693809 )  , and there are multiple repeats that themselves serve as enhancers of interferon response genes. See https://www.ncbi.nlm.nih.gov/pubmed/26941318


text:
Protein denaturation and edible toxins
As a protein denatured, it may lose its functions.
So theoretically if I heat some type of biological toxins like poisonous mushroom to 100 oC or higher temperature, will I able to eat it? (I know peoples still death after eat them even boiled to 100 oC, but why?)
Is there anyway to make them edible?
Update: i know some protein can survive in high temperature, for example: taq polymerase. Can i destroy it functions by boil it to higher temperature like 140-160 oC at higher atmosphere pressure and then return back to normal temperature?
Update2 : i found some information on the internet by searching keyword "toxin destroyed by heat" : http://aggie-horticulture.tamu.edu/food-technology/bacterial-food-poisoning/

The botulinum toxin is destroyed by boiling the food for 10 minutes.*
.
So it's depend on the type of protein, the heat and time.

So is there any way/formula to predict the temperature and time to destroy a protein? Or is there any absolute temperature and time to kill most type of protein ?

Why people still die after eat them even boiled to 100 oC, but why?

Well not all toxins are protein based. Some are just small molecules that fit into some vital protein in your body, causing  it to stop and death not long later. Some are cyclic peptides and are not denatured by heat. The peptide is simple, and has many carbon bonds to stablize its structure (it is a ring and has carbon bonds linking internally) https://en.wikipedia.org/wiki/%CE%91-amanitin

Or is there any absolute temperature and time to kill most type of protein ?

Autoclaving.. 134 °C (274 °F) for 18 minutes in a pressurized steam can destroy prions. And prions pretty tough. https://en.wikipedia.org/wiki/Prion

You could bit more elaborate the prion portion.

Still; wikipedia page that you've linked, tells "134 °C (274 °F) for 18 minutes in a pressurized steam autoclave has been found to be somewhat effective in deactivating the agent of disease". That does not mean killing prion.

then you have things like amatoxin which is a tiny little ring protein so it is highly resistant to heat. It survives normal cooking just fine.

Prions are not alive. A prion is protein with a specific folding pattern. And when it meets another protein of the appropriate kind, it can cause the normal protein to be refolded into the pattern it has. In this way a prion propagates. It is not a protein replicating but a folding pattern that is spreading. And the folding pattern of a prion is very stable, perhaps the most stable folding patterns known to man. Because prior to the understanding of what prions were, autoclaving at 121 C, for 17 min steam was considered sufficient to denature and sterilize everything.

It completely depends upon the chemical structure of the toxin.
For example; heavy-metal containing compounds such as copper sulfate (CuSO4), heating would not work at all because even on heating, the element copper (Cu) will remain Cu.
Same about radioactive poisoning.


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How do I improve expression using the GAL1 promoter in S. cerevisiae above the "leaky" level I'm currently seeing?
I am attempting to express GFP in S. cerevisiae using the GAL1 promoter.
I always grow an uninduced (in dextrose based SD medium) culture alongside my induced (in galactose based SD medium) culture. I see approximately the same very low level of fluoresence in both cultures, and also a band at 27kD on a PAGE gel. There is no overexpression of the GFP happening, the fluorescence is very weak by eye, and the cultures are not green in visible light, like E. coli cultures overexpressing GFP.
On the PAGE gel the amount of protein appears to be the same in both the uninduced and induced samples. I need to overexpress the protein, this leaky level of expression isn't acceptable. How do I go about fixing it? I am currently growing up a culture to do a plasmid prep to send for sequencing to make sure the promoter region of the plasmid is intact.

There are a couple of things that are strange here. First, you have low expression in the presence of galactose. The GAL1 promoter is really strong, so that strikes me as odd. Even if it was leaky, induced vs uninduced should be night and day. However, you should keep in mind you still may not be able to see it by eye. Second, it is weird that it would be leaky in the presence of glucose (or dextrose, in your case). The glucose should not only prevent the promoter from activating, but it should actually repress it.
A few potential fixes that come to mind:
1) Check your strain genotype. Some strains do not have gal4, the transcriptional activator of the GAL1 promoter, so if you don't have this, the system will not work in your strain. Likewise, you may not have an intact UAS, which would make the repression fail. Other issues may also arise which may make a strain unsuited for this system.
2) Sequence your promoter/gene. It is kind of a pain, but if you have a mutation in your Gal1 promoter, this could be the reason for all your problems. Also check the UAS, as this would create repression problems. Finally, check if the gene itself is inserted in the place you think it should be, if you got some recombination mishap this may be the problem. The appearance of an extra band at a low molecular weight makes me suspect this may be an issue.
3) On that note, try picking a different clone. Maybe you got unlucky and the colony you picked had a defect, and a different colony will be what you think it is.
4) If you haven't already, make fresh stocks of your galactose and glucose media. Maybe you got impurities or some other issue in your media, and therefore what you think you are giving the cells is not what you are giving the cells.
Anyway, that's all I got. Good luck!


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Is this a counter-example to Darwin's theory of evolution?
Somewhere I read following paragraphs giving one counter-example to Darwin's theory of evolution.
(By the way, I am a physicist and not a biologist, but I am interested in this field.)
Do these paragraphs point to the reality? What is the current status of "theory of evolution of species" ?

"Darwin cited the giraffe as an outstanding example of natural
  selection.  Supposedly, as a result of extended droughts, the supply
  of green leaves could be obtained only at the top of the trees, and
  therefore the shorter necked giraffe died off.  The giraffes which
  grew longer necks survived.  However, there is no evidence whatever in
  the fossil record or elsewhere that giraffes with short necks have
  ever existed.  And what would have happened to young giraffes with
  relatively short necks?
Darwin failed to realize that body characteristics in offsprings are
  determined and programmed by DNA factors of the Genes or the Genetic
  material of the parents, and not by the stretching of the neck or any
  other bodily exercise."

Where is that quotation from?

@James: I got an email from someone whom I do not recognize/know; this is similar to a spam email.

Ignore it. There is a lot of painfully wrong/uninformed statements in there. Berkeley is a good place to get an overview of the modern understanding of evolution.

As a matter of fact, there is fossil evidence of shorter-necked giraffe ancestors: http://www.livescience.com/52903-transitional-giraffe-fossils.html  Also remember that fossilization is a very rare happenstance (otherwise we'd be up to our necks in them), so not every intermediate form will have left fossil evidence.

Wow...Are some creationists spamming people to spread their believes now?!

That missing links are not found doesn't mean they are not there. Further, why on earth bother about spam?

"and not by the stretching of the neck or any other bodily exercise." was never put forward by Darwin, instead, it was Lamarck's theory of Acquired characteristics.

the three evolution videos from Stated Clearly are the best video explanations of evolution I have ever seen. I recommend watching them it will help you a lot. https://www.youtube.com/watch?v=0SCjhI86grU

Giraffe necks being long because of 'reaching' is false. The neck size is due sexual selection.
The writer of the paragraph fundamentally misunderstood Darwin, he never argued that the act of stretching of necks would make them longer in subsequent generations, that is Lamarkism, which is what Darwin argued against.
Darwin postulated that there exists some sort of information carrier which can be transmitted from parent to offspring. At the time there was no understanding of DNA or of any type of 'genetic material', all of early genetics actually was done statistically on abstract 'lines' of genes with no conception of DNA. Genetics as a field of study doesn't require a DNA model for genes.
Likewise, knowing what DNA is or isn't doesn't matter to the theory of evolution. Evolution is an intrinsic process of change in any system where there is heritable variation and selection. If you have self-assembling robots competing for a limited amount of scrap metal and which can make errors (and those errors are copied to future generations) they can be thought of as evolving.
Now given the restrictions on any system of heritability, variation and selection the result is evolution. Now the question is can evolution explain speciation that we see in the natural world.
I've studied genetics for just over 10 years and so far the answer has always been yes, it explains it amazingly well. There is no alternative theory or idea which can explain the observed variation in DNA between species, in cancer cells etc... as well as Darwinian evolution does.

In one of the posts here, some one wrote about the famous paper "Gould and Lewontin, the Spandrels of San Marco". Does that paper support Darwin's theory ? I have not read that paper; I came to know about it just few minutes ago. But looking all around, my view is that Darwin's theory is not accepted by ALL biologists. Is this my view correct ? Pardon me for my lack of biology knowledge.

That paper is about another, what I think is more of a semantic argument in genetics. Does evolution act at the level of the entire holistic organism or does it act at the nucleotide. Regardless, there is no doubt that both sides are discussing the action of Darwanian evolution.

Also to clarify, my professional experience is that all geneticist I have met accept and apply Darwin's theory. I would make the analogy that evolutionary theory is as much a consequence of our universe as is the relation of force to mass * acceleration.

A few comments. While it might be true that neck size is under sexual selection, it is not quite the point that the post is trying to make. Also, you would need a reference to backup the claim that mate choice is based on neck size in giraffes. You slightly misrepresent evolution as being the result of natural selection only while several processes affect evolution (such as genetic drift typically). I am not sure I understand the point of highlighting that early evolutionary biologist knew nothing about the structure of DNA (it is true but arguably off-topic for the post IMO).

A few comments (suite). The sentence  knowing what DNA is or isn't doesn't matter to the theory of evolution is quite misleading IMO. I am not sure either why you say "Now the question is can evolution explain speciation that we see in the natural world.". Also "Lamarckism", not "Lemarckism".

@remi.b I understand one can take a DNA-centric view of evolution and for all practical purposes that is correct. The point I'm trying to make is that evolution is a consequence of the properties of DNA based life, namely heredity, variation and competition. In that way one can know nothing about DNA but still understand the theory of evolution. Evolution is the process.

@Artem: And as a matter of simple fact, Darwin knew nothing about DNA (it wasn't discovered until a century later), or even Mendelian genetics.  His theory was based on observation.  Indeed, we could have evolution that's not based on DNA, as for instance self-reproducing machines.

@atom yes, the theory of evolution (whose modern version has, well, evolved enormously since Darwin's days) is absolutely accepted by the scientific community. There are some people (AFAIK exclusively in North America) who reject it but they are essentially considered crackpots by the broader community since they simply don't have any leg to stand on scientifically.

Darwin cited the giraffe as an outstanding example of natural selection. Supposedly, as a result of extended droughts, the supply of green leaves could be obtained only at the top of the trees, and therefore the shorter necked giraffe died off.

The term outstanding is funny in its usage here but otherwise this text is quite right so far.

However, there is no evidence whatever in the fossil record or elsewhere that giraffes with short necks have ever existed.

Actually there is. See this popular science article suggested by @James.

And what would have happened to young giraffes with relatively short necks?

The answer in the text above. It rightly says the shorter necked giraffe died off.

Darwin failed to realize that body characteristics in offsprings are determined and programmed by DNA factors of the Genes or the Genetic material of the parents [..]

This is an awfully phrased sentence making it very clear that the author has no idea about genetics.

not by the stretching of the neck or any other bodily exercise

Sure. The concept that individuals stretch their necks, necks become longer and this characteristic is passed on to the offspring is wrong indeed. This is known as Lamarckism. It is funny because the above text describe natural selection and it then says that it is wrong by making a straw man, misrepresenting natural selection as a Lamarckist process.

What is the current status of "theory of evolution of species" ?

You should have a look at the post Is evolution a fact?.
You should also have a look at an intro course to evolution. There are several online and free introductory ressource of information on evolutionary biology. Understanding Evolutionby UC Berkeley is probably one of the best. It is very short, very introductory and will already teach you a lot.

The theory of evolution of species is about as solid as the theory of general relativity.. may even better considering that there are no known situations in nature that invalidate it unlike say... when general relativity meets the very small and encounters the theory quantum of mechanics.
The  giraffid animal which had short neck... would not have been recognized as giraffe. it would have been the ancestral species to the giraffe. The closest living relative to a giraffe is the okapi. https://en.wikipedia.org/wiki/Giraffid


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Why do recessive lethal genetic diseases continue to exist?
I'm trying to understand, in a simplistic representation of a recessive genetic disease (e.g. Tay Sachs), why wouldn't it "disappear" over time (many generations). Please excuse the use of non-professional terminology below, I hope the point I'm trying to make will be clear.
Let's assume that, for simplicity, people marry at random and each couple has 4 children. Denote the probability of carrying the "bad" gene by p, then a couple of 2 non-carrying people will have 4 healthy children, a mixed couple will have, on average, 2 healthy and 2 carrying children, and a couple of 2 carrying people will have 1 healthy, 2 carrying, and one sick child (which we assume will not have children so we ignore it in further calculations).
Assuming large enough population and random couples and everyone gets married (for simplicity):
The probability of a couple of non-carrying: (1-p)^2
The probability of a mixed couple: 2 * p * (1-p)
The probability of a 2-carrying couple: p^2
The expected number of healthy children per couple: 4*(1-p)^2 + 2*2*p*(1-p) + p^2 = 4 - 8*p + 4*p^2 + 4*p - 4*p^2 + p^2= 4 - 4*p - p^2 = (2-p)^2
The expected number of carrying: 2*p*(1-p) + 2*p^2 = 2*p - 2*p^2 + 2*p^2 = 2p
Dividing to get the new probability for carrying the gene:
2p / (2-p)^2
Which for small enough p is clearly smaller than p (e.g. for p = 0.05 we get ~0.0263).
If I'm not mistaken this means that the number of those carrying the genes should become exponentially small (in the number of generations).
I realize this is a very simplistic model, marriages are not random, mutations occur etc. but I would expect the basic intuition to hold. What am I missing?

I haven't read the entirety of the question, but the salient point is that lethal genetic diseases are mostly very rare. Exponential decrease over time and 0 are not the same thing.

Technically you are correct but if my calculations hold, and we start with p=0.05, we'll be at p=10^-16 within 10 generations which is pretty much the same as 0

And yet we're not. There may be an error in the assumptions or the calculations. It would be a hard model to get to a good standard.

Firstly, sorry if this is not so much an answer as a comment, but it is too long to put in the comments section, although I'll try keep it concise...
I can see exactly what you're doing however my math differs at points, and would appreciate you looking over it.
"The expected number of healthy children per couple: 4*(1-p)^2 + 2*2*p*(1-p) + p^2 = 4 - 8*p + 4*p^2 + 4*p - 4*p^2 + p^2= 4 - 4*p - p^2 = (2-p)^2"
Is it not: ... =  4 - 8p + 4p^2 + 4p - 4p^2 + p^2 = 4 - 4p + p^2 = (p-2)^2
Furthermore: "The expected number of carrying: 2*p*(1-p) + 2*p^2 = 2*p - 2*p^2 + 2*p^2 = 2p" - why for the probability of carriers in mixed couples - "2*p*(1-p)" - why have you not multiplied through by two (as with expected healthy children), given that as you said "a mixed couple will have, on average, 2 healthy and 2 carrying children"?
Is it not: 2 *2p(1-p) + 2p^2 = 4p - 4p^2  + 2p^2 = 4p - 2p^2 = 2p(-p + 2)
In this respect I got different expectations. Lastly "Dividing to get the new probability for carrying the gene..." You have done (no. healthy) / (no. carriers). Is the probability for carrying the gene not (no. carriers)/(no. carriers + no. health) - that is the no. carriers as a fraction of the entire population to give a probability?
Using my expectations this would be: [2p(-p+2)] / [2p(-p+2) + (p-2)^2] = [2p(-p+2)] / [-2p^2 + 4p + p^2 - 4p +4] = [2p(-p+2)] / [-p^2 + 4] = [2p(-p+2)] / [(-p + 2)(p + 2)] = 2p / (p+2)
Therefore, with a new probability for carrying of 2p / (p+2), for our "hypothesis" of the diminishing probability of carrying to stand, we need the condition 2p / (p+2) < p to stand, solving for p:
2p < p(p+2) -> 2p < p^2 + 2p -> 0 < p^2 -> p > 0
Since, as a probability, p must be <= 1, and assuming (as we are) that carriers exist and so it must be > 0, p always satisfies this condition - ergo I would conclude that for any value of p - not just small, the probability of carrying will diminish in the next generation. Just as we "hypothesised". However a quick google of "plot y = 2x/(x+2)" would indicate to me that as p approaches 0 it's rate of "diminishing" actually decreases, and it does not get exponentially smaller as you indicated. But solving for y = 0 gives x = 0 so this model would suggest the gene is never actually fully eradicated?! Which of course confuses me, although on a macro scale it might make sense, as you can't have, for example, 0.1 children "carrying", and 99.9 "healthy", only 1 and 99 or 0 and 100.
Thanks for reading this far, any response would be really appreciated, especially given I might be miles off.
Philip.

Philip - Thanks a lot! you caught 2 errors (the first of 3 is just a typo replacing + and - and we arrive at the same result). So interestingly for every generation the new probability is 2/(p+2) the previous probability, and the factor indeed gets closer to 1 as p goes to 0. In practice trying to start with p=0.05 (one of every 20 people carrying) I get after 1,000,000 generations that still 2 of every 1,000,000 people are carrying, so even after a very very long time there genes will still be around. Awesome!

New probability is 2p/(p+2) rather than 2/(p+2), and running a quick simulation in Python I get probability falling from 0.2 to 0.000002 after 1,999,960 generations, but yes I agree with your conclusion that they will therefore be around for a long time- which begs the question how did they ever become widespread in the first place?...


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How much time does it take for the naive T Cell to get activated?
Suppose a naive T cell comes in contact with an APC. How much time does it take for the T Cell to get activated and within how much time does the T cell move away from the APC due to incompatibility in their receptor structure? What is the probability that there will be activation of a naive T cell by an APC (I mean to ask that how many T cells should come in contact with APC before a T cell gets activated, some number like say 1 out of every 1000 t cell gets activated by an APC at a particular time)? Any resource you can provide that gives a quantitative value of the interaction of T cell with APC, please do if possible.

Do you have any way to access Wiley Online articles? http://onlinelibrary.wiley.com/doi/10.1016/j.febslet.2010.10.010/abstract


text:
Meaning of proliferation rate of 3 day−1
The abstract of an article in Journal of Virology contains the following line:

We find that CD8+ cell proliferation begins 1 to 2 days after infection and occurs at an average rate of 3 day−1, reaching the maximum population size between days 5 and 6 after immunization.

What does this figure mean? Does it mean that per day the population after proliferation is 3 times the original population?

Proliferation means rapid cell division, giving rise to large number of cells.

I know that but what does 3 day−1 mean?

Its from math. 3/day is the same as 3 day^-1 (Three per day, in words)

@skymningen does it mean that each cell after proliferation becomes 3 cells per day?

X^(-Y)=1/(X^Y). Same way Meter/Second = m/s = ms^(-1)

hmm also to me it looks bit fuzzy. Did they mean "3 new cell appear per day on average"? or they mean "3 cell divide (and give rise to 6 cells) per day on avarage"? or something else?

I would guess that it means that each singular cell has an average rate of 3 proliferations per day. But I am better in maths than proliferation rates.

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


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Owl identification
This evening I spotted this beautiful owl that had become the centre of concern of my neighbourhood birds. There was a joint commotion of the House crows, Jungle bablers, Bulbuls and Maynas, which is still going on.
I wonder if this is a female Common Barn Owl.

Location: West Bengal, India.
P.S. I couldn't get better pictures.

That appears to be a barn owl, Tyto alba.

Based on the picture, this is a Barn Owl (Tyto alba). There are several subspecies of Barn Owl, 35 in fact. This bird is most likely the subspecies "stertens" also known as the Indian Barn Owl.

As to whether it is a female. It is dependent on the size and a few other features that cannot be determined in these photos.

Females significantly larger than males in body mass, total length, beak length, tarsus length, foot length and width, and wing loading, but not in wing chord or tail length ( Marti 1990a ). Female plumage typically darker than that of males but sexes overlap in this regard.

It's a barn owl. This is probably the most common owl in India and is found in most of peninsular India.


text:
Is "TATA signal" synonymous with "TATA box"?
In the text I'm translating I have a diagram of an expression vector. It has a lot of marks, and one says "TATA signal". I googled and found the expression "TATA box".
Are these expressions fully synonymous and interchangeable?
From Wikipedia:

Considered to be the core promoter sequence, it is the binding site of either general transcription factors or histones (the binding of a transcription factor blocks the binding of a histone and vice versa) and is involved in the process of transcription by RNA polymerase.

So basically "TATA box" serves as a signal to the transcription machinery that says "transcribe this"?

Is this TATA signal in the figure very close to the transcription start site?

@Chris - it is positioned just before the target gene (which we want to express) and just after the GAPDH promoter. I'm not sure where the transcription start site is on that diagram. Maybe the beginning of the target gene sequence is the transcription start site?

@Chris - but it's quite far from the origin of replication

The ori doesn't matter here - if it is located immediately upstream (around -25-35 if I remember correctly) then it should be the TATA box.

@Chris - if the ORI is located immediately upstream? Or if the TATA signal is located immediately upstream of the target gene?

I guess that you have a expression plasmid of some kind that you are looking at. There it doesn't matter, where the ori is. Only the position of the TATA box (or signal) relative to the TSS is important.

Probably this is the reason why they call it a TATA signal instead of a TATA box:

The TATA box was originally identified as a regulatory signal upstream
of many protein-coding genes transcribed by RNA polymerase II (Pol
II). However, some tRNA and 5S RNA genes and most RNA polymerase III
(Pol III)-transcribed genes with external promoters also possess TATA
boxes -25-30 bp upstream of the transcription start site (article)

This is a quite old article (1995) however inferring the text above signal is more/previously used to describe a TATA boxes near protein-coding genes whereas TATA boxes are more general, so also for non-protein coding genes.

"Box" is an archaic term from long ago. It's little used. "Signal" has now replaced it. "TATA box" and "TATA signal" are synonymous.

Why do you say it is archaic? I hear it frequently and it is still used widely in publications.

I think your are nog right that TATA box is "replaced" by TATA signal, give a quick search on pubMed and you will see that the most recent articles still use "TATA box". Do you have any references for your statement?


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Are there any examples in nature of two polypeptides joining into a single, continuous, third polypeptide?
Are there any examples in nature of two polypeptides join into a single, continuous, third polypeptide like this:

(Where all the indicated  amino and carboxyl groups are on the main polypeptide chain ( located on Cα of the respective amino acids )
And if this exists, is there any term for the phenomenon?

This could be a type of https://en.wikipedia.org/wiki/Post-translational_modification - see  the "Other proteins or peptides" section, although all of the examples given have covalent links to sidechains, not mainchains...

@gilleain Yes you guessed correctly, I meant amino and carboxyl of alpha carbon. Okay I'm updating the question.

I am not aware of anything precisely corresponding to your diagram, but the somewhat related behaviour of inteins may be of interest in this respect. They are defined in Wikipedia as:

An intein is a segment of a protein that is able to excise itself and join the remaining portions (the exteins) with a peptide bond in a process termed protein splicing.

So, unlike either ribosomal or non-ribosomal polypeptide (e.g. antibiotic) sythesis, they catalyse a peptide bond between peptides rather than an amino acid and a peptide. However these are already part of single polypeptide chain before the intein itself is spliced out.

[Modified from Intein_mech.png to fit page. — The mechanism of protein splicing involving inteins. In this scheme, the N-extein is shown in red, the intein in black, and the C-extein in blue. X represents either an oxygen or sulfur atom.]

I see! This concept is also similar with transposon that occur in DNA.

@AlwaysConfused — Yes, and self-splicing introns.

hmm the wikipedia page includes the term "intron" so I didn't mentioned it. So Transposition:DNA::splicing:RNA::intein-excision:Protein :P

@AlwaysConfused — self-splicing, not splisosome splicing. Much rarer.

@AlwaysConfused — I should qualify my last remark. Self-splicing is similar to the intein phenomenon in that the material being cut and joined (RNA or protein) is catalysing the process. Transpons use proteins they encode. But of course you are right in saying that they are examples of cutting and joining pieces of DNA (as, indeed, are other phenomena involving DNA, like recombination).

Does splicing of peptides in the proteasome count?  Proteasomes normally degrade proteins into small peptides, but the process is conceptually reversible -- peptide bonds can be generated as well as broken -- which leads to splicing of two smaller peptides into one longer one.  There is some evidence that this is a fairly common event:

Reports of proteasome-generated spliced epitopes exist, but they have been regarded as rare events. Here, however, we show that the proteasome-generated spliced peptide pool accounts for one-third of the entire HLA class I immunopeptidome in terms of diversity and one-fourth in terms of abundance.

--A large fraction of HLA class I ligands are proteasome-generated spliced peptides.


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Could the denaturation of protein during cooking could generate a prion, by any chance?
It may sound silly, but it appeared to me as a theoretical possibility; not a practical fear.
On a healthy and correctly folded protein if cooking process is applied (that includes heating and mixing with various other things), is there by any chance a possibility to develop a prion?

This is a good question, and I think there is definitely a possibility.  It depends on what you define as "prion" -- must it be infectious? or just pathogenic?  The 'plagues' we observe in Alzheimer's and Parkinson's seem not infectious, but are pathogenic nonetheless.  There is no reason why they cannot occur in food;  but protein is digested and decomposed into small peptides and amino acids, and even after that, cannot easily cross the blood-brain barrier.

Just my speculation here. Prions seem to need some sort of template to guide their folding as well as the cooperation of chaperone proteins. https://en.wikipedia.org/wiki/Prion  I would suspect that denaturing, and potential re-folding, of proteins during cooking would be rather random. So even if one, or very few, copies of a potential prion happened to be produced, the high temperatures, rapid pace of denaturation and the lack of chaperone proteins would not allow the formation of meaningful amount of potential prions to cause disease. Add to that the doubtful chance a prion would be produced in the first place, due to the lack of the usual physiological conditions and participants, feel free to eat cooked food!


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What is the metagenome like for other classes of animals?
Lately there's been a lot of discussion around the many non-human cells essential to a healthy human body — called the microbiome, or metagenome.  Much of this is in the gut microbiome.  See this question, for example.
The Human Microbiome Project at NIH emphasizes we are just beginning to measure the specifics of this for the human case.
I assume this is similarly true for all mammal species, and I don't know how much farther.  Fish have a fairly different body plan than mammals, including a fairly different gut. And coelenterates have an even more different body plan in many ways, again including the gut.
Does a typical fish depend on as large a microbiome as a human?  Is there much known about that?  What about jellyfish?

There are multiple parts to an answer for this.
1) There is not only a microbiome in the gut. So microbiomes in general are very diverse. A fish microbiome on the scales will of course be very different to the one on a human skin.
2) Gut microbiomes are also quite different both in taxonomic and functional content, as they are in different ecological niches.
3) There are microbiome studies for nearly every type of organism I could imagine now. Fish, insects, snakes, you name it. They differ in diversity and composition of their microbiome, but also the used methods and databases do differ, so it is hard to compare them.
4) The further away from well studied microbiomes we get, the less specific will be our assignment of taxonomy and function, because we have not seen enough comparable microbes before. So more information will be hidden in the "dark matter" (in metagenomics: reads not assigned to a taxon and/or function).
Unfortunately I don't know of any jellyfish microbiomes so far. Their body (as far as I know ) seems to be much more "permeable" for sea water (-> their environment) and thus I would think that they generally would have aquatic bacteria in whatever corresponds to their gut. The sea microbiome is said to be very diverse and far too little studied, although there are cool projects like the Global Ocean Sampling Day to try and close this huge gap as best as possible.

Fish scales are an interesting example to think about.  It seems pretty likely that some of the microbiota on the scales are clearly essential to healthy function (once you understand what they are really doing), and others not at all important for good or ill. It could be a hard problem to figure out the difference between metagenome and plain old parasitism or mere proximity.

@ColinMcLarty I think you are misinterpreting the term metagenome. It does not exclude parasites or only include species essential to health. If it lives in your X (gut, mouth, urinary tract, skin ...) it's part of your X metagenome.

@CharlesE.Grant Ah.  In fact looking at https://en.wikipedia.org/wiki/Metagenomics I see it was not originally an organism that had a metagenome at all, but an environment--say a dirt sample, a stream, or a human gut.  That article suggests many people still use the term that way.  But NIH has their project on "the human metagenome."

@ColinMcLarty, Its the same usage. It's just considering an entire organism (humans) as the environment.


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How do bile salts affect lipase activity?
BACKGROUND: It is well known that bile salts are needed for emulsification of fats. It is then said that this increases the surface area for activity of pancreatic lipase, implying that bile salts make pancreatic lipase more effective. But it is also said that pancreatic lipase do need a colipase to overcome the inhibitory effect from bile salts.

QUESTION: So what does bile salts actually do? Do they increase or decrease lipase activity? How does colipase overcome it?

MY ATTEMPT: After some research , I found that bile salts above critical micelle concentration have inhibitory effect, but could not still comprehend how does the colipase makes lipase more efficient. Also if greater concentration is inhibitory then why does our body just secrete it in sufficient amounts? Isn't it be more efficient than to make a whole protein(colipase)?

Let us first clear out some basic concepts regarding lipase, colipase and bile salts. The pancreatic lipase has an optimum pH range of about pH 8.0 (Worthington). This can be understood easily by Le Chatelier's principle: as the reaction moves forward, there is reduction of pH (due to formation of fatty acids). So, a basic pH would help the reaction in moving forward. See this diagram (Worthington):

It can also be understood on the basis of lipase's optimum pH, which lies between pH 8-9. See the graph (orange line) (Chegg):

This optimum pH is brought about by bile salts. Bile salts are slightly alkaline, with pH range of about 7-8 (Britannica). This helps lipase in catalysing its reaction. Bile salts also help lipase by increasing the surface area of fat droplets. Bile molecules have a hydrophobic and hydrophilic part. The hydrophobic part is attracted towards fat while the hydrophilic part is attracted towards water. This helps stabilize fat droplets by emulsification i.e. breaking the fat droplet(s) into smaller parts. This also increases the surface area of fat droplets.
Now, the matter gets complicated when we talk about concentration. Since bile molecules contain hydrophilic and hydrophobic ends, they tend to form micelles with increasing concentration (just like soap). As long as its concentration is below critical micelle concentration, it will carry on emulsification and increase lipase activity. But when its concentration becomes more than the critical micelle concentration, it will form micelles and not carry on emulsion. This significantly reduces lipase activity by not only decreasing surface area, but also reducing pH to slightly acidic (Erlanson et al, 1973). This is where colipase helps. Colipase binds to the C-terminal, non-catalytic domain of lipase and stabilizes its active conformation and increases the hydrophobicity binding site (Verger et al, 1999). Colipase strongly binds to the ester bond of the triglyceride molecule, by which its hydrolysis by lipase becomes easy (Mansbach, 2011). Thus, colipase helps in overcoming the inhibitory effect or bile salts on lipase.

Thanks. Why don't our body secrete bile salts in less than CMC. Won't that be more energy efficient than making a protein( in this case colipase)?

It might be due to lack of regulation. All mechanisms I know about (CCK, secretin, enterohepatic circulation) only act as positive feedback loops. Also, gallbladder performs the job of concentrating bile, which doesn't seem to have any strong regulative mechanism either.

The optimal pH of lipase probably has more to do with general acid/base catalysis than Le Chatelier.

@canadianer I just used Le Chatelier to give an idea of effect of pH on lipase. I'll check that point out too. Thanks for suggesting :)

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


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Changing genetic code of E. coli to accept synthetic amino acids?
I read in my Biology textbook that an experiment has been done in which one of   E. coli's stop codon has been altered to accept a synthetic amino acid. I do not get how it can be done. Taking the fact into account that every permutation of the 4 natural nitrogenous bases codes for a particular amino acid means that if the stop codon, let's say UGA, is altered to UUA it will code for Leucine. How does this leave a possibility for the production of a codon which codes for a synthetic amino acid? I will appreciate your kind explanation. Thank you a lot.

They would use the codon UGA to code for a synthetic amino acid.

This has been done by engineering a synthetic tRNA that can recognize the stop codon. The synthetic tRNA possesses a non-natural amino acid that is processed normally by the Ribosome and incorporated into the growing polypeptide chain.

This answer was accepted; however, it is still advisable that you add references :)


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Why are the walls of the bronchioles folded?

The bronchiole shown in the section above has folded epithelium, why is this so?

I think most of the answers here are wrong. The smooth muscle around the bronchiole can expand and contract, so the epithelium has to have a morphology that allows this. I'm not too familiar with bronchiole histology so I'll keep this as just a comment rather than a full answer, but I wouldn't be surprised if fixation/processing also led to an atypical "constriction" of the bronchioles beyond their normal state in a healthy animal/human.

Those foldings are called as mucosal folds, formed by the contraction of smooth muscles , are also present in trachea, and in many other organs such as gallbladder etc.
Physiologically: This folding causes an increase in area for better action of mucus which protects the body from entry of dirt, pathogens and loosing the moisture.
Anaomically: as @Bryan pointed out that the folding permits the  contraction and relaxation of smooth muscles around the bronchioles.
Source 1
Source 2

This is the best answer so far, but it would be much improved if you can find some references to support what you say to make it clear that this is the correct answer.


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Is it better to maximize sleep, or align to ~1.5 hr cycles
What is better for the body, to sleep 6 hours (4 deep sleep cycles) or to sleep 7 hours, but interrupting the last sleep cycle. I know I feel a lot better with 6, but am curious as to its medical consequences. Does the brain have a chance to repair/clean itself properly with this lesser amount?

Personally speaking, I feel very tired if I have only 6 hours of sleep, but am totally ok with 7. Is this sleep cycle theory correct?

Neither
Sleep cycles do not have a set length.
sleep for 7 hours every night and you won't interrupt a sleep cycle. 6 hours may be fine for a person but it is unlikely.
You feel tired when you interrupt a sleep cycle becasue many of the sleep inducing hormones are still present in your system.
http://apsychoserver.psych.arizona.edu/jjbareprints/psyc501a/readings/Carskadon%20Dement%202011.pdf
If you are sleeping different lengths every night (or say sleeping longer on the weekend) that will also make you feel tired. Normally your body adjusts the length of your sleep cycle to how long it predicts you will sleep for, if that is constantly changing however it cannot do this and you often wake up in the middle of a cycle making you feel tired. Sleep the same length of time for ~14 days and you will see your sleep cycle stabilize.
http://journals.sagepub.com/doi/abs/10.1177/1534650103259743
https://www.researchgate.net/profile/Martin_Moore-ede/publication/15765130_Human_Sleep_Its_Duration_and_Organization_Depend_on_its_Circadian_Phase/links/557881b308aeb6d8c01f1715.pdf
http://healthysleep.med.harvard.edu/healthy/science/what/sleep-patterns-rem-nrem

The thing about sleep is that there is no "one size fits all". Think about it, if we are all biochemical different, then why would we all need the same amount of sleep? Why would all of our sleep cycles last the same amount of time?
I was once a severely insomniatic person. I would worry about not getting that perfect eight hours of sleep that everyone talks about being so important, and despite trying my hardest to get eight hours of sleep it would never happen. I would either get no sleep at all, or I'd sleep in and get over twelve hours of sleep.
One day I was talking with my professor who specialized in sleep, and he suggested that I aim for four or five hours of sleep and to see how I start to feel. He also said to pick a specific time that I want to wake up everyday. Oddly enough, it fixed my problems. I can now go an entire day without thinking about how tired and fatigued I am.
So to answer your question, it does not matter. Wake up when you need to wake up, and go to bed when you are feeling tired. If you find that you feel good throughout the day having only slept 6 hours, then only sleep six hours. If you feel tired throughout the day, then you might need more sleep.
Your body will "tell" you if you need more or less sleep. But you need to listen to it.
*Edit
What I'm saying plays in to what Raja's comment is getting at, "is sleep cycle theory correct"?


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Non-splenic pools of erythrocytes?
In splenectomized animals, where could red blood cells be released from, to explain an increased hematocrit after exercise or muscular contractions?


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Why do some grasshoppers have a black exoskeleton?
What species of grasshoppers have black exoskeletons? Is there a scientific difference in species between field crickets and grasshoppers?

where have you looked for this answer so far? have you done any work?

Could you clarify the question? Right now it's very vague. Are you asking: "what species of grasshoppers are black?" If so, you should provide your location, size of the insect you're interested in, and preferably a picture of the grasshopper. Without these, your question is far too broad and likely will be closed.

Further, we typically ask that you perform (and demonstrate) some type of effort to answer your question on your own. For more details, please see How to ask a good question on the help page

So is your question about identifying species or wondering why evolution has caused some grasshoppers (or field crickets) to be black in color?

Field crickets are rather distinct from grasshoppers. Although both groups are in the Order Orthoptera, grasshoppers are insects of the suborder Caelifera and field crickets are in the family Gryllidae of the suborder Ensifera.
For a discussion on insect coloraiton, see here.
If you'd like a specific species ID, please provide more information as requested in the comments.
Generally, field crickets are black, red or brown in color.

However, some species of grasshoppers are likewise black:

For example: Romalea species such as R. microptera and dark nymphs and morphs of R. guttata

Finally, here is a simple checklist of some typical differences between grasshoppers and crickets.


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Do bile salts enter into enterocytes?
Wikipedia says :

The contents of these micelles (but not the bile salts) enter the enterocytes (epithelial cells lining the small intestine) .....

So, where do the bile salts go? Additionally, what prevents them from being absorbed by the plasma membrane?

The fatty acids within micelles are taken up by enterocytes in the upper/middle part of the small intestine (duodenum/jejunum) through selective transporters in their plasma membrane, which do not accept bile acids. The SLC27A4 protein is thought to be the principal transporter for fatty acids in enterocytes, although there has been some controversy about this.
As a result of this selective uptake of fatty acids in this part of the intestine, the bile acids are left behind in the micelles, as they are emptied of fatty acids. They travel down the small intestine until they reach the ileum, where enterocytes express a bile acid transporter, SLC10A2, which performs active uptake of the bile acids. The bile acids are then secreted on the opposite (basolateral) side of these enterocytes; enter the portal vein; and travel back to the liver, where they are reused. This is known as the enterohepatic circulation. A review of these mechanisms is found here.
So the uptake of fatty acids and bile acids differs by location in the intestine. First the emulsified fatty acids are extracted, then the bile acids are recovered in the ileum. There is also some passive transport (diffusion) of bile acids into enterocytes throughout the intestine, but this is considered a minor mechanism.


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How much tissue is required to do RNA-seq analysis on a single organism?
How much tissue would be required to do RNA-seq analysis on a single organism?
More specifically, if a person wanted an RNA-seq analysis of expression for a single organ, how much tissue would they need to donate?

Depends on a lot of parameters? Can you add some more details?

Our DNA core wants 1.5 ug of RNA.  I find that I can obtain that amount from a standard Trizol prep from about 1 mg of Arabidopsis floral tissue.  I usually double or triple what I harvest to account for random variation in yield.

Any sources to add? +1 for this contribution and welcome 2 Bio

ThermoFisher has literally everything in tabular format. As a side note I'd also peg an A260/A280 > 1.8 as equally important as yield for best results.

http://healthcare.utah.edu/huntsmancancerinstitute/research/shared-resources/center-managed/high-throughput-genomics-site/services/illumina-sequencing/rna-sequencing.php

The Illumina TruSeq RNA Sample Prep Kit v2 with oligo(dT) selection
  recommends an input of 100 to 1000 ng of total RNA in a volume of 30
  ul for library construction.
The Epicentre TotalScript RNA-Seq Kit (Epicentre cat# TSRNA1296) is
  designed for an input of 1-5 ng of total RNA in a volume of 12 ul to a
  RNA sequencing library.

Whether you will get a complete picture of a whole organ from such a small slice is an entirely different question.  The brain has different regions, with different gene expression.


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Calculating ultrametric distance matrix
I am fairly new to phylogenetic analysis, so I'm guessing this is a basic question. If I have a bunch of aligned sequences, and I ultimately only care about pairwise distance (e.g. for calculating phylogenetic diversity) then is there any way to make sure these distances reflect an ultrametric tree without having to first calculate the tree itself? From what I can tell, to create an ultrametric distance matrix I have to first calculate an ultrametric tree and then use this tree to get distances. But this seems a bit backwards to me, since I can create a pairwise distance matrix without needing to create a tree, but I can't tell if there is a way to ensure that this matrix assumes some sort of underlying molecular clock so as to make sure the distances reflect an ultrametric tree.
I assume I'm just fundamentally failing to grasp something. Any help would be much appreciated.

You might also ask your question here: http://cs.stackexchange.com/

In my understanding you cannot skip the tree construction, since there is no guarantee that the pairwise distances are compatible with a tree, even for non-ultrametric trees. That is, to create a pairwise distance matrix that reflects patristic distances between tree leaves you need to create a tree first. Even without the ultrametricity condition.
The complicating factor here is that distance matrices compatible with trees must also respect distances to unobserved internal nodes...
This blog post about how to make a tree ultrametric might be relevant.


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Detecting nuclear DNA in suspension of mitochondria
Is there a way to detect nuclear DNA in a suspension of mitochondria extracted from leukocytes? I need to make sure there is no nuclear DNA in the suspension before extracting mtDNA from the mitochondria.

Centrifuge the suspension in Cesium Chloride solution at a particular g value which causes the mitochondria to settle to the bottom of the centrifuge tube but leaves nuclear DNA forming a layer near the top of the centrifuge tube. This is since the nuclear DNA is less dense than the mitochondria. Using a needle syringe, extract a small part of the centrifuged suspension from the very bottom of the centrifuge tube. This extract is most likely to contain no nuclear DNA. Hope this helps :).


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Haploid eukaryotes?
I was wondering whether there are any eukaryotes which never have a diploid phase. I can't think of any. Fungi have diploid stages, and I know any sexually reproducing organisms will have at least transient diploid stages (I am not referring to such transient stages- I mean extended diploid stages so I am counting as a 'haploid' organism one that only ever has two sets of chromosomes for a very short time while it undergoes meiosis.)

what about bees, males are haploid from the gamete stage.

Update: There are plenty of eukaryotes that occur in haploid stage as the dominant life cycle stage. See metagenesis in cnidarian animals and "alternation of generation" in algae, protists and fungi.
......

I am not referring to such transient stages.- I mean extended diploid stages so I am counting as a 'haploid' organism one that only ever has two sets of chromosomes for a very short time while it undergoes meiosis.

Yes there exist a vast lot; and such life cycle pattern is called haplontic life cycle (also called haploid lifecycle)

Outline of haploid life-cycle
Most of the Green algae like Chlamydomonas,  Volvox, Spirogyra etc. are prominent example.
Among fungi; Mucor, Schizosaccharomyces are some prominent example.
Among Protozoans; an example of haploid life-cycle  is seen in Wood-roach(Cryptocercus)'s some gut - microfauna such as Trichonympha

(Table from Google Books, Protozoology by Karl Gottlieb Grell)

Among slime-molds, Dictyostelium shows haploid lifecycle.

Dictyostelium life cycle diagram

  from Biology- A dynamic Science, by Russell et al (Google Books)

Book-Reference:

Advanced BIOLOGY, principles and applications, C.J. Clegg and D. G. Mackean, First Edition (1994), John Murray publications.
College Botany, Vol-2, By Gangulee and Kar, New Central Book Agency, Kolkata.

Some apicomplexans such as Plasmodium spp. are haploid during their asexual stages. The organism spends more time (at least in the human host) in the asexual stage than sexual. source

Plasmodium spp. are haploid in both human and mosquito hosts except for a brief stage in the mosquito midgut where two haploid malaria gametes present in the mosquito's blood meal fuse to form a diploid zygote. This zygote immediately undergoes meiosis to generate four haploid cells that continue in the haploid form, reproducing through mitosis, until several thousand are present in a small sac, the oocyst, attached to the gut wall.

“Sexual” Population Structure and Genetics of the Malaria Agent P. falciparum

Welcome to Biology.SE! This looks like a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

To offer a more multicellular look on life: there are many Hymenoptera species that are haploids their whole life. Many Hymenoptera are haplodiploidy meaning that one sex's life cycle starts out as diploid zygotes and the other sex's life cycle starts out as haploids. Many male bees, ants, wasps, and etc start their life as an unfertilized haploid eggs and remain haploid until their death. Of course, these haploid males cannot be made without a diploid female so this example may technically break your rule.


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The Evolution of Fruits
I was cooking rice this morning and was fascinated by the color and it's sweetness and began to ask...

How did fruits evolve?
Did they come from a single cell?
Which cell?
How did that cell branch off from  the cell that became animals? Is there any evidence for this kind of thinking or just a lotta theories? How did we get rice, mangoes, beans, orange, coconuts, peanuts, apples, bananas, if there is no "Designer", where did ALL these come from and how did they evolve?

This question is too broad. Please narrow it down to (preferrably) single question to get better answers.

Too broad with shades of a creationism agenda.

@AlexDeLarge You are right, sorry. In the popular culture it is never considered a fruit but botanically speaking it is a fruit. I'm removing my comment.

@GbolahanFaluade. Welcome to Biology.SE. What have you found so far? Have you tried to google fruit evolution?

Turn the "Designer" question around: Why would a sensible designer have wasted time on all these randomly-different seed dispersal methods, instead of using just one good one?

I'm flagging to close this as it's opinion-based, although it's also far too broad.

Fruit did not evolve from a single cell( except in the sense that plants did)  it evolved from seeds and their casing in angiosperms. Fruit is a means to disperse seeds. This will get you started on the different methods of seed dispersion.
https://www.britannica.com/science/seed-plant-reproductive-part
By enclosing their seeds in material animals want to eat, plants get animals to transport their seeds long distances and deposit them in a warm pile of fertilizer. Sugar is the easiest macronutrient for plants to produce so that is the what they pack their fruit with. animals tend to eat new growth which often contains seeds so it is easy to see how animals with seeds tough enough to survive digestion (which many seeds do) would quickly spread. Any adaptation that made animals more likely to eat these parts and spread their seeds would likewise spread.
I suggest familiarizing yourself with basic plant phylogeny first, since if you had you would know only one group of plants produce fruit, and so would not have asked half your questions. So please go do a few minutes of research and come back with a more coherent question.
If you want a complete retelling of the entirety of plant evolution you can do that yourself, show a little initiative and start here.
http://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-14-23
https://www.accessscience.com/content/plant-phylogeny/524400
Also rice is not a fruit. It is the plant's seeds you are eating, it did not evolve to taste good, you evolved to think it tastes good becasue it is nutritious, in much the same way meat tastes good. You are essentially murdering their offspring.
I also suggest learning what a theory is.


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Why are there not effective pharmaceutical treatments to prevent weight gain?
Hunger is caused by signals from the brain, so is there a way to suppress the signal of hunger in the same way we suppress the signal of pain with painkillers?
If people felt less hungry, they would eat less and find it easier to lose weight, so why aren't there pharmaceutical hunger suppressants yet?

I think the problem here is with the assertation that "If people felt less hungry, they would eat less..."  Seems to me that most overweight people eat (and choose what to eat) for a variety of reasons.  Actual hunger is low on the list.

The two main factors are:

Hunger is more complex to treat than pain (more pathways, more potential targets), and I would argue against your suggestion that we are good at treating pain: despite the term "painkiller" we aren't great at blocking pain except for with local anesthetics that block all nervous activity (lidocaine for example). For systemic pain relief, there are lots of long-term efficacy issues with either opiates or NSAIDs, and that isn't even taking into account:
Side effects. Amphetamines are great for suppressing appetite. They also mess with the cardiovascular system, are habit-forming, and cause psychological issues. "Fen-phen" is a famous example of an anti-obesity drug that had major side effects leading to massive lawsuits. A more recent supplement, Ephedra, had many of the same problems and was banned by the US FDA for those reasons.

There are some drugs that are used to treat obesity, but many of these have come into regulatory issues with side effects and are only used in special cases like in diabetics or as an absolute last resort.

+1 DNP comes to mind. Pharmaceuticals are much more dangerous than diet and exercise which, in many (most?) cases, is a cure.


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What happens if nerve impulses go the wrong way?
So in nerve impulses, I get that the refractory period is important because it stops the action potentials going the wrong way along the axon. I have two questions:

What would the impact be of the action potential going the wrong way along the axon?
Are there any diseases that maybe cause the refractory period to be shortened so that the action potential goes the wrong way?

Thanks for any help!

I'll try to write up a full answer unless someone beats me to it... in the meantime, no it isn't really possible for the refractory period to be short enough for the action potential to travel in both directions. You can sort of think about it like the refractory "zone" is "chasing" the action potential down the axon. Making the refractory period shorter in time just shortens in space this refractory "zone".

(of course, if you induce an action potential artificially by using an electrical shock midway down the axon, it will travel in both directions; this has some important experimental implications but wouldn't occur otherwise in most neurons of a vertebrate nervous system)

There are some exceptions in insects and some special neurons elsewhere that have a looser definition of axons and dendrites, where signals can propagate in more than one direction, but this is part of the normal function of those circuits.

The propagation of the action potential is MUCH slower than the refractory period. The propagation speed is determined by the cable equation http://www.cnbc.cmu.edu/~bard/passive2/node9.html which is a formalism developed by Hodgkin & Huxley in the 1930s to measure signal transmission through a biological cable (e.g. an axon). The speed of the propagation is measured by a constant. The voltage does decay and thus spread in all directions, but the propagation only matters towards the direction of signal transmission. Ionic action in the soma would destroy the usefulness of transmission not down the axon. With that being said, neurites in arthropod nervous systems for instance http://stg.rutgers.edu/ can receive input and deliver output leading to very complicated patterns of waves inwards and outwards. Despite this, the stomatogastric ganglion can produce very robust and stable rhythmic neural patterns.

"The propagation of the action potential is MUCH slower than the refractory period" - is this a typo? It is very much not correct.


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Tissues in plants and animals

What is the equivalent connective tissue in plants?

Connective tissue in animals are mostly made up of collagen.

What about in plants?

Connective tissue in animals are mostly made up of collagen

Tissue is not like a simple chemical mixture ; rather tissue means a group or assemblage of cells, obeying certain defining-characteristics.
Animal connective tissues contain collagen mostly in the extracellular matrix. There are also other cell-constituents like phospholipid(membranes), DNA, RNA, etc.  Blood is a liquid connective tissue which do not contain collagen in its matrix (plasma)

What is the equivalent connective tissue in plants?

Connective tissue is defined as all the tissues originated from the mesoderm layer of the animal embryo.

Now plants have a different mode of development than animals (plausibly due to evolution in separate route). So no part of a plant-body is homologous with a part of animal-body. It is impossible to bring a compare.

However; plants too; have their extracellular matrix; which is more popular as plant's cell wall (that contain cellulose, hemicellulose, etc.) as well there are intercellular spaces.

Still, if you forcefully want to bring a comparison; then the ground-tissue system of plant maybe called as a rough analogy with connective tissues in animals ( Similarly epidermal tissue of plant maybe a rough analogy with epithelial tissue of animals)


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psbA-trnH intergeneteic spacer inversion
What kind of software tool would you recommend as best suited to detect psbA-trnH inverisons?
I have 1x coverage Sanger .fasta files and >2000 sequences, with 1 sequence per species.
Most tools I have found are only suitable for next generation seuqncing data or inversions that are larger than 50 bp.
Here is an example:

(dotted line)

Please [edit] your question and highlight the precise inversion you are looking for. I know you've shown us the relevant region but what is the "non-inversed" sequence and what is the inversed one? I don't see anything obvious in your alignment.

The inversion is where the dotted line is, for example. Non-inversed is TTCTAG and inversed is CTAGAA.
I don't know what I am looking for, that is what the question is about. I need to find the inversion. The pictures are just examples of what it could look like.

Yes, that much I understood :) However, since you've posted an image and not an actual alignment (not text that I can copy and investigate), we need more detail. I can't see what the inversion is and what the reference is. You also show two separate alignments with completely different regions marked. Your second seems to be referring to 5nt while your first to more than 20.

Yes exactly, I have 10000 sequences across all plant families and I don't know which length or which positons the inversions have, or if they exist at all. That's why I need help to find them. Maybe there is a tool that I am not aware of. Posting an alignment is not possible, because the standard alignment tools do not align this region, it gets spaced out, because it looks very diverse, however it's not. Alignments seen above are corrected by hand.


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Terminology for quantitative response of T cells to antigen complexes
In the article, there is a statement which is:

Although DCs are
  remarkably efficient in evoking T cell responses with few antigen–
  MHC complexes (1–100 per DC) (1–3), they must first
  encounter a T cell with appropriate antigen specificity (one in
  105 to 106).

What does the part  "Although DCs are remarkably efficient in evoking T cell responses with few antigen– MHC complexes (1–100 per DC) (1–3)" mean?
What is the significance of the value "1–100 per DC"?
What does evoking T cell responses with few antigen–MHC complexes mean?

I've replaced your title by something meaningful (in the light of @PeterCollngridge answer). I appreciate it's difficult to formulate a good title if you don't understand the meaning, but titles are important in allowing people to select questions of interest and for indexing.

It means that a dendritic cell only needs between 1 and 100 antigen–MHC complexes on its surface in order to activate a T cell.

A dendritic cell uses an extrinsic pathway to take whole foreign peptides and cut them into segments of 14-20+ residues that are loaded onto MHC-II molecules. The MHC-II interaction with the T cell receptor is what tells the T cell to activate along with some costimulatory signals from the DC.
The dendritic cell doesn't know how to cut the peptides, though. So when it engulfs a bacterial protein for example, and cuts it up, and presents these extracellularly to T cells, no single peptide loaded on MHC-II are exactly the same. There could be thousands of potential antigens.
T cells on the other hand are specific: Every single T cell receptor on a single T cell clone is specific for the same antigen. It's encoded in their genome during VDJ recombination! So the DC is only efficient in that they probably only need 100 or less unique peptide presentations to find a T cell specific for one of those antigens, which is quoted to be 1:100,000 to 1:1,000,000.


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What is the name of cell structures that have an adaptation to increase their surface area?
Epithelial cells that line the small intestine have an adaptation to increase their surface area - what is the name of these structures? And why would the small intestine require a large surface area?

What research have you done before asking it here?

@another'Homosapien' I already found microvillus before coming on here, just to confirm.

They are called microvilli, that forms the brush-border of villi

The small intestine requires a high surface area in order to increase the rate of absorption of digested food.

The greater surface area also provides for more secretion of the "brush border" enzymes responsible for the finishing touches of digestion.


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Are Sharks able to detect electromagnetic waves using their Electroreception ability?
I will include some publications and links that may help. I could not concluded an answer with my limited knowledge on the subject.
Shark Passive electroreception sensitive to low frequency (below 50 Hz).
Peer-reviewed Publications (Elasmobranch Research Laboratory).

Short answer yes sharks have an organ called the Ampullae of Lorenzini that allows them to sense electric fields given off by other animals. If you want to learn more check out this link http://www.sharksinfo.com/electroreception.html


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What is the difference between ferritin and hemoglobin?
I have been reading that ferritin is the store of iron but hemoglobin is actually the amount of this in blood.
Does hemoglobin get sourced from ferritin? Is it possible for a person to be low on ferritin but normal on hemoglobin? Will he feel any symptoms of anaemia, if so?

Does hemoglobin get sourced from ferritin?

Yes, of course it is. Ferritin is the superior Group.

Is it possible for a person to be low on ferritin but normal on
  hemoglobin?

Yes, since these things don't have something in common.

Will he feel any symptoms of anaemia, if so?
  Why should he?? No, he won't get any crazy feelings from this.

Please do add some references