text:
Could random male-only-offspring mutation wipe out a species?
If we can engineer the extinction of a whole species of mosquitos with male-only-offspring genetic mutation, how come such scenario never happened naturally in the past to other species? Or has it?

What do you mean exactly by engineering a species with male-only-offspring genetic mutation?

I don't think you can make the population extinct this way.  Individuals whose genetics allow them to have female offspring would be hugely favored evolutionary.  You might drastically reduce the population, you might drastically reduce the incidence of mosquitoes biting humans, but I don't think you'll achieve extinction.

@swbarnes2 what mechanism would favour the unmodified individuals?Your comment is not answering this.

It has happened the R2D2 mutation in mice is famous for it, the mutation prevents or drastically reduces female offspring.  It can wipe out entire populations when it shows up, it doesn't wipe out the species becasue there are frankly too many mice, separated by too much distance, while breeding too fast for the gene to spread fast enough before the population crashes. If mice happened to live on only one island however they would be gone. These events are called selfish sweeps or selective sweeps that result from a transmission bias in a gene.
the opposite can also occur (female only) however this is slighly less likely to lead to instant extinction since a possible out exists. Lepidodactylus lugubris(a gecko) being a famous example and is a female only species that reproduced through parthenogenesis. These types of species are exceedingly rare and have problems however as they are very vulnerable to disease since they have low diversity. Species like this are driven extinct indirectly by the mutation that led to a female only species as their diversity sufferers drastically so disease or environmental change can wipe them out more easily.

The link appears to be broken.

@canadianer try it now.


text:
Is it comfirmed that Alzheimer's is a diabetes of the brain?
I read in this New Scientist report, that the mental decline during diabetes may be an early stage of Alzheimer's.  The hypothesis was based on a study with 20 rats.
Has there been any follow up research? Is Alzheimer's such a slow disease that this is will be remain hypothetical for a while?  Are there any other links between diabetes and Alzheimer's that can point in either way?
Or has research even confirmed (or refuted) another weaker hypothesis true, namely, the mental decline during diabetes and Alzheimer's have a common cause?
Many times newspapers say this or that is being research and we will know one day whether this is true or false; but the same newspapers hardly ever do follow up reporting.  So this is why I am asking this here.

You need to pay more attention to the statements. It is nowhere written (at least in peer-reviewed journals) that diabetes causes AD. They only say (if they did) that diabetes is a factor Correlation and causation are different. Also, dependence may not mean strictly causation. These terms may seem to have subtle differences but they mean different things.

@WYSIWYG I guess I should have used the wording "... that diabetes and Alzheimer's might have a common cause".

Far from being confirmed, the notion that diabetes is a significant factor in Alzheimers is held by at most a tiny, tiny minority of researchers.  New Scientist is notorious for wild-eyed hyping of fringe speculation; this is an example.

Some researchers consider Alzheimer's type 3 diabetes. There are lots of papers on the mechanisms involved.

source: Stack Exchange

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sort: votes


text:
Doubt in a multiple choice question involving cell organelles

Find the odd one out and state the category of the rest.

Chloroplast
Mitochondria
Nucleus
Grana

Now my answers are :

1st possibility : grana

Category : presence of DNA in others

2nd possibility : grana

Category : all others are cell organelles

Are their any more possibilities and are my answers reasonably correct?

hmmm, that is difficult to know what to answer - it's probably possible to find criteria where each can be considered an odd one out! what was the context? (e.g. was it a practice exam for a module/course on DNA?)

It was basically a worksheet on photosynthesis but i don't believe it is necessary to stick to the topic while answering, is it ?

well if your exam is on photosynthesis it is a good clue to think about the differences in that context, rather than e.g. which ones contain nucleic acids

But then there's no involvement of mitochondria in Photosynthesis right? @rg255

You're asking two questions at once here. Why not simplify it? I hope you don't mind, but I used this question as an example in meta to talk about how MCQs introduce several questions at once and would be better asked one part at a time.

I would say Nucleus is the odd one out. Chloroplast (which have Grana in them) and Mitochondria are involved in the process of creating/breaking down energy, whereas the Nucleus is, so to speak, the blue-prints of the cell.
To summarize:
Chloroplast is involved in Photosynthesis to create energy
Grana are in the Chloroplast, which is involved in Photosynthesis
Mitochondria are "the powerhouse of the cell" and help break down energy (ATP > ADP)
Nucleus is the cell's blue-prints
Therefore, it seems that the Nucleus is the least like the others.

I would also go with Nucleus

Are my answers correct ?

Technically, yes, your way of differentiating the Grana from the others is legitimate. However, I find that the Nucleus is more different from the others than the Grana is. Also, although Nucleus, Mitochondria and Chloroplast all have DNA, they are not all the same. Nucleus has DNA whereas Chloroplasts have ctDNA/cpDNA and Mitochondria has mtDNA. This is probably because there is a chance that both were organisms of their own, ages ago. http://learn.genetics.utah.edu/content/cells/organelles/

But your answer doesn't mention the category of the rest as i asked

You are looking for an answer of Grana that includes a third reason that Grana is the answer? Please try to be more clear. I believe what you want to know, (ei the similarity between the Chloroplast, Mitochondria and Grana) is that they are all used in the process or created and/or breaking down energy.

I think it should be grana..
Reasons-
1. It is not a cell organelle
2. It is not having double membrane
3. It does not have its own dna or ribosomes...

Your answers are correct, but there are more to consider:

Nucleus is odd because it's the only one not directly involved in cell metabolism and has nothing to do with endosymbionts. Most cells also only have one nucleus but multiple mitochondria and chloroplasts - and multiple grana per chloroplast.
Granum is odd because it's neither a eukaryotic cell organelle nor double-membrane-bound. As Felix_17 mentions, it also contains neither DNA nor ribosomes.

It's hard to argue for mitochondria or chloroplasts to be the odd one out because both share a lot of properties (endosymbionts, importance for cell metabolism, properties deriving from their bacterial origin), and their differences aren't shared with nuclei and grana.

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text:
Photosynthesis and its subtopics
Which of the following statements about photosynthesis is true?
a.  Photosynthesis is an energy consuming process
b.  The light-dependent reactions produce the energy-rich compounds that are used up in the light-independent reactions.
c.  The light independent reactions can only occur in night
d.  Photosynthesis and respiration cannot take place together in plants
I think both c and d are incorrect, but I'm unsure whether a or b is the correct option.
The reason why I think a is correct is that sunlight is used during photosynthesis and b because the hydrogen of $NADPH$ produced during light phase is used to combine with $CO_2$ by utilizing ATP (which again was produced in the light phase ) to make $C_6H_{12}O_6$ in the presence of enzyme Rubisco.

Which of the following is true about photosynthesis?
a.  Rate of photosynthesis is directly proportional to concentration of $CO_2$ in the air.
b.  Photosynthesis takes place only in the visible spectrum of the electromagnetic radiations.
c.  Rate of photosynthesis would be highest under the green light
d.  Structure of leaf has no effect on the rate of photosynthesis
Here I am also stuck between either a and b.
The reason why I think a is correct is that when $CO_2$ concentration increases the rate of photosynthesis also increases until the concentration reaches 0.1 % and it could be b because photosynthesis takes place in the presence of sunlight, not any other radiation.

Perhaps you didn't read this meta post.

@WYISWYG edited ... Now is it ok ?

Nope. Your title should convey the actual question.

@WYSIWYG i cant think of more .... can u suggest one please

First one: (b) because photosynthesis is overall energy producing process. Second one: (b) since graph between rate of photosynthesis & $CO_2$ concentration is not linear and becomes stagnant after threshold concentration.

Much improved, thank you - this is the sort of thing you need to be doing as standard, all to often we are having to drag this out of you, putting this effort in will give you reward: it will be more likely that someone can help you understand the problem, rather than just giving you facts to memorise. Remember to think about formatting and presentation too, take time to prepare your questions - it often feels like you've written them in a massive panic; just slow down and make sure you're doing it right from the start rather than waiting to be pushed by us :)

Thanks @rg255 but because i use mobile app so its tough to format

I would pull all questions of this type. I think they turn the site into a multiple-choice answering service and have no utility for anyone else. I'd urge people to ignore them.

@David knowledge is knowledge whether it comes in the form of a multiple choice question or a long answer question! Moreover why are you instructing the helpers to stop helping . Thats really rude of you. Everytime someone like you barges in a healthy conversation and/or question  answer sesssion on SE

@Abcd What you refer to as knowledge is memorized facts to answer a quiz. It has little to do with understanding biology, which is what this list should be about. I consider it unhealthy to such an extent that I posted a proposal on the Meta list explaining my viewpoint: http://meta.biology.stackexchange.com/questions/3369/change-homework-policy-to-disallow-multiple-choice-questions-mcqs. I have my own opinion as to who is being rude, but I would merely ask you to think of my remarks as a parallel to "Don't feed the trolls".

I agree with @David. I'm voting to close because this is the wrong type of format for the site. Perhaps splitting these questions up, and provide questions that ask specifics about photosynthesis would be better. I do appreciate the effort in explaining your thoughts which are reasonable and appear to have reading behind them. This should however be standard practice.

First question:
B. The net gain of ATP in Photosynthesis is 0, so it cannot be A. C & D are obviously not true.
Second question:
B. D is not true, C is not true (it is actually the opposite- Chloroplasts absorb all BUT green, so only green would be bad). Like another commentator said, the level of CO2 only aids the rate to a point, at which the rise is not great.
http://www.rsc.org/learn-chemistry/content/filerepository/CMP/00/001/068/Rate%20of%20photosynthesis%20limiting%20factors.pdf


text:
experimental procedure regarding AceCS1 overexpression
I'm new to biology and was just as to curious on how one can experimentally prove/disprove that AceCS1 overexpression in mammalian cells would yield enhanced rates of fatty acid synthesis through acetate.
Thanks.


text:
Why does BLAST reduce word size for short proteins?
I'm using BLAST to identify a short protein (BLASTp). If I check the short query then the word size reduces from 3 to 2. However the search will then be less reliable right? Because reducing the word size increases the chance of finding matches? So my instinct would be to raise the word size to almost the whole length of the query, because with a short query you want to search really specific to reduce output results, so apparently I'm missing something.
So I hope someone can explain me why reducing the word size from 3 to 2 is better for short proteins while using BLASTp

As a general rule, playing with the word size is a question of finding the right balance between specificity and sensitivity. I guess that's why they said that 'A good rule of thumb is that the query length must be at least twice the Word size. ' on a blast FAQ site. see here

No, the search won't be less reliable. It will only be more sensitive, more capable of finding matches. To understand this, you need to understand how the BLAST algorithm works, what the word size means.
When you use a word size of $N$, BLAST starts by looking for a match of length $N$ between your query and target sequences. If such a match is found, BLAST then attempts to extend the match as far as possible. So, for example, consider these two sequences:
> query
CRKKL
> target
CRAKL

As you can see, they are quite similar:
query           CRKKL
target          CRAKL
                ** **

Now, what happens if you try to find the target sequence with BLAST using the query sequence and a word size of 2 ($N=2$)? BLAST will take the first
$N$ characters of the query and try to match them against the target:
CR
CR
**

It will then try to extend:
CRK
CRA
**

It will find a gap and apply the gap penalty, but continue matching since the next characters match1, thereby increasing the overall score of the alignment:
CRKK
CRAK
** *

And so on and so forth. BLAST starts by matching the first $N$-sized word and then attempts to extend the alignment.
Now, what if we were using $N=3$?
CRK
CRA
**

Because the word size is now 3, we need at least three matching residues to match in order to attempt to extend the alignment. Since there is no 3-letter match, the target is missed.
So, decreasing the word size is better for finding small protein matches because it can use shorter matching sequences as an alignment seed.
As a general rule, playing with the word size is a question of finding the right balance between specificity and sensitivity. Decreasing the word size helps you find more matches (increases sensitivity) but it will also find more divergent sequences (decrease specificity). Increasing the word size will reduce the number of matches (decrease sensitivity) because you need a longer perfect match to start extending the alignment, but will increase specificity for the same reason.
If you raise the word size to something close to the size of the query, you will only find almost exact matches. That might be what you want to do and it is what algorithms like BLAT which are designed to find near exact matches (for example, mapping a sequence to the genome it came from) do. Usually, however, we want less than perfect matches since we are looking for homologous sequences and not the exact same query. In such cases, we will decrease the word size for smaller proteins to increase our chances of finding homologs.

1 This is a bit of a simplification. The rules for extending alignments are a more complex but it serves to illustrate the point.

If I understood correctly: If you want an almost exact match, the word size can be almost as high as the query length. However if you need to identify homologs (so assuming there isn't an exact match), you can better lower the word size to find more matches? @terdon

@RickBeeloo more or less, yes. Having a large word size means that you will need a large section of the target to be identical to the query in order to find that target. A smaller word size makes the search more sensitive.

But why does lowering the word size using a blastn reduces sensitivity and lowering the word size using protein blast does exactly the opposite? Thankyou for explaining everything by the way ,helps me al lot.  @terdon

@RickBeeloo the SE sites are for questions and answers and don't lend themselves to discussions. Ping me in chat if you want more details. That said, unless I'm mistaken, reducing the word size would also increase sensitivity for blastn.

Sorry I made a mistake you are right @terdon, increasing word size also increases sensitivity for nucleotide searches


text:
Why do some drugs require you to take them in an "upright position"?
A friend of mine was taking the supplement Metamucil and on the container it says to take in an "upright position." Why would this be necessary? Doesn't your digestive system push food/liquid downwards anyways?

Maybe you digest poorly when lying down, as compared to when upright. Is that not why "they" say to walk around a bit after eating a large meal and suffering from indigestion?

Metamucil is taken as a drink. You're more likely to aspirate versus swallow when drinking supine if you're ill with impaired swallowing reflexes.
It's also recommended that you take bisphophonates standing up so that gravity, and a glass of water, make sure the drug passes into the stomach. It can be highly corrosive if it gets stuck in the esophagus.


text:
Hamilton's Rule in practice
I came across this question in USABO 2013 open exam:

A mother antelope and its child are galloping along the plains, when they encounter a group of hungry lions. If the two antelopes try to escape the lions together, there is a 75% chance that both will be consumed and eaten, and a 25% chance that both will escape alive. If, however, the mother sacrifices herself to the lions, she may be able to buy her baby additional time to escape.
What is the minimum chance that the baby can have to escape from the lions following such a sacrifice such that the mother’s action will be evolutionarily favored?
You may assume that the baby antelope, once escaped, will be guaranteed to survive into a reproducing adult, and that the mother antelope is at the beginning of reproductive age.

I suppose one should use Hamilton's Rule ($r \cdot B > C$) to solve this issue. I'm not familiar with the working of this rule to put it into the question's context. To my understanding $r=0.5$ but this is pretty much how far I managed to go.

I'm voting to close this question because this style of homework question doesn't lend itself to the format of SE. It's unclear exactly what about the topic you don't know. This question may involve someone answering correctly, but only after long commentary about the topic. Other users might disagree and with a few edits this might be a very decent question.

http://meta.biology.stackexchange.com/questions/3393/this-is-the-title-of-the-meta-post-i-just-wrote @LittleDragon please use a more informative title.

I'm new to Bio SE, so sorry for the formatting. What can I do to improve my question?

I disagree with the close votes that say the question is "unclear" or "too broad". I agree it is a homework question but it is hard to suggest what kind of efforts the OP might do to make the question perfectly on-topic. I edited the post hoping to slightly improve it.

@James I agree that this question is a homework question, but what's the problem in answering it. It's quite visibile that  this question is a good one. Iwould not vote for closing the question.

It doesn't have to be that complicated.
The evolutionary value of the offspring to the mother is half that of herself (0.5). Then the relative value of both mother and offspring is 1 + 0.5 = 1.5. So the value of preserving both lives is about 3 times the value of preserving the offspring alone, given the simplistic assumptions from the question. Therefore, to choose to make this sacrifice, the probability of survival of the offspring alone must be at least 3 times the probability of both surviving otherwise. 3 times 25% = 75%.
Edit:

In terms of B and C as requested (though I think it's simpler to step away from this):
B is the benefit to the relative. This is not the probability of survival given the action of sacrifice, but the increased probability of survival. The baby already had a 25% chance of survival, but this action will increase that chance to some p, which we are looking for. B is the improvement in the situation:
B = p - 0.25
C is the cost to only the individual (the mother). This is not 1 (loss of survival), but the difference between the situation without making the sacrifice and the situation when she makes the sacrifice. She's only giving up a 25% chance of survival. So:

C = 0.25.
r is the relation between mother and offspring.

r = 0.5.
So the equation is:
0.5(p - 0.25) = 0.25
0.5 p - 0.125 = 0.25
0.5 p         = 0.375
p = 0.75
Someone feel free to format if you want...

That's be great if you could put that in the $rB>C$ equation! I will then discretely delete my answer as if I never wrote it :)

Hmm, this is an interesting way to view the question!

@Remi.b If I'm reading your math correctly, you made two mistakes. First, it seems that you are looking for the minimum probability of survival of the baby after the incident, independent of the mother's choice at this moment, given an assumption that immediate survival is guaranteed by the sacrifice. This is a much harder question, and not what was asked. I believe the correct answer to that harder question though, would have been 0.67, because in your scenario B=p(1-0.25) => p = C/(r*(1-0.25)) = 0.25/0.375. Does it make sense why B is p(1-0.25) in that scenario?

@Remi.b I suspect you also forgot the parent's contribution to fitness, which is assumed to be 1. This is added to the offspring's fitness, giving a total of 1.5 fitness if they escape the lions, and 0 fitness if they do not.

Of course, I can't help but point out the place where the math ceases to support the reality around us, thus begging a greater explanation: The mother has another choice, which, in higher mammals, is almost impossible to even consider. She could sacrifice the baby, probably as easily as simply outrunning him. All else being equal (and it's not - she has a better chance of survival alone than he does), this choice would have double the value - the obvious choice. So there's your take-away ponderable...

@MarkBailey The converse can be seen frequently in other species (eg rodents) which eat their children in times of severe stress. Perhaps it might be due to the difficulty in raising another child for K-specialists as opposed to the r-specialists.

There is another way to look at this question, which I suspect is even quicker (it is certainly more intuitive for me). Mathematically, it is identical to Mark's answer.
If the parent chooses to not sacrifice herself to save the child, they have a net fitness of 1.5 (1 parent + 0.5 child) if they escape, and 0 fitness if they do not. Therefore, their average fitness is 1.5*0.25 = 0.375.
If the parent sacrifices herself to save the child, they have a net fitness of 0.5 if the child escapes, and 0 if the child does not. Therefore, in order to have an average fitness >= 0.375, the probability of the child escaping must be >= 75%.


text:
Why would you mix polymerases in PCR?
I was reading a manual for kit that requires you to amplify DNA by PCR before analyzing it in the kit. The manual suggests mixing proofreading and non-proofreading polymerases:

For
  PCR
  products
  >2500
  bp
  in
  length,
  use
  a
  DNA
  polymerase
  blend
  containing
  Taq
  DNA
  polymerase
  supplemented
  with
  a
  proofreading
  DNA
  polymerase

How would this improve the amplification of long products? It suggests using only a proofreading polymerase for fragments below 2500 bases. Does the addition of a non-proofreading polymerase improve speed? I have TAQ and PFU Ultra, but both instructions say to use an extension time of 1 minute per kb.

The Taq polymerase is a rather fast enzyme (the synthesis rate is around 1 kb/min), but the backdraw is that it has no 3'- 5'exonuclease activity which would enable to proofread the newly synthesized DNA. This leads to the introduction of errors and the chance of getting these is higher the longer the DNA you want to synthesize is.
Polymerases which are able to proofread (which have the exonuclease activity) like Pfu have a much lower error rate, but are on the other hand also much slower, typically around 0,5 kb/min. Pfu is also more expensive than the Taq polymerase. See table 1 from reference 1 below:

To combine the advantages of both polymerases, you typically use a blend of Taq and Pfu. Then you get the high processivity of the Taq combined with the proofreading capacity of the Pfu and get good yields of DNA with a low amount of mutations. See also reference 2 for details on this system.
References:

Error Rate Comparison during Polymerase Chain Reaction by DNA
Polymerase
Effective amplification of long targets from cloned inserts and
human genomic DNA.

To add to the answer, the reason this works is because Taq will stall and fall off the DNA after a misincorporation. (Taq isn't particularly progressive.) If Taq just continued on after misincorporation, Pfu wouldn't have a chance to edit it. By falling off, Taq gives the slower Pfu time to bind to the DNA, edit out the misincorporation, and continue on. When there's no Pfu, Taq does eventually continue on past the misincorporation. But that process tends to be slower than that for Pfu binding and editing, so when Pfu is present the error correcting path is preferred.

So I've been having trouble with another project, which requires I use PCR to amplify a 4400 base gene, or an entire plasmid. I've been using PFU ultra alone, and the reaction takes 5 - 6 hours. How much Taq polymerase should I add to improve the reaction speed?


text:
Can a protein kinase phosphorylate both a threonine and tyrosine residue?
I know that some kinases can phosporylate both serine and threonine residues because of their structural similarities, but can such a kinase phosphorylate a tyrosine residue as well?
If not, then why?

Ony a few protein kinases can phosphorylate all three amino acids — these are classified as dual-specific kinases (EC 2.7.12.1). Examples are APK1 from Arabidopsis or MEK kinases in mammals.
As with other enzymes, the residues at the substrate binding site determine which substrates can be accomodated there. Structures or Ser- Thr- and Tyr-kinases are available for inspection, should you wish to explore them.

Do you have a reference showing that the same catalytic domain in, for example, the MEK kinases phosphorylates both the Thr and Tyr simultaneously? I do know from working extensively with the MAPKs (Erk1/2 in particular) that the two residues can be under independent regulation. Part of that is obviously a function of different phosphatases, but I suspect there can be independent phosphorylation as well. Just not sure if it's by MEK1/2 or not.

Phosphorylation of MAP kinase by MEK at tyrosine 185 (pY185) and threonine 183 (pT183)...., ref: http://www.ncbi.nlm.nih.gov/books/NBK21529/

I have edited your original answer because, although essentially correct (+1), it had a mistakes in the EC number, and the Kegg link was specifically for MAPKs, whereas the Wiki page considers dual-specificity kinases, specifically. I also put in a link to the structures. As you had done the heavy lifting, I don't want to steal your thunder by posting an alternative answer. Do revert as you see fit.

Thanks for the edit! Can I give you half the credit?

@Ashafix yes, I'm aware of the "classical" understanding of the pathway, I'm talking about what really goes on in vivo.

Well, I guess more qualified people with some real hands on experience should comment on that.

@Ashafix OK, just wondering if you knew...


text:
Why do we take antibiotics if our immune system already produces them?
Why do we take antibiotics if our immune system already produces them? Is it because our body doesnt make enough or the specific complementary antibody to fit with the antigen?

Perhaps you could respond to the answers — or this comment — to clarify whether you were really confusing antibiotics and antibodies, or whether you were interested in "innate immunity".

Since people and animals routinely get sick, it is obvious that our immune system (which includes but isn't limited to antibodies) doesn't always protect against pathogens.  There are many reasons for this, far too many to summarize here, but one common reason is that it takes several days for the adaptive part of the immune system (which includes antibodies, among other things) to gear up and control an infection. Therefore, early treatment with antibiotics can help limit an infection before the immune system is fully engaged.
Pathogenic bacteria are often resistant to immunity in many ways as well; that's one of the adaptations that makes them pathogenic. That means that even later in an infection, antibiotics can supplement the immune response and help eliminate bacteria.  Note that many antibiotics require a functional immune system to be completely effective.

I assume from your question (and your pseudonym) that you are confused by terminology. Our adaptive immune system does not make antibiotics, it makes antibodies. Antibiotics are small molecules that interfere with bacterial metabolism. Antibodies are proteins that recognise foreign macromolecules. (You could regard both as “anti-bacterials” — perhaps this is what you were thinking of — but the immune system is not restricted to recognizing bacteria.)
We take antibiotics when we have an infection from bacteria that have evaded the immune system.

This isn't true. We do make antimicrobial peptides, which are essentially antibiotics.

@MattDMo The immune system makes antibiotics? I answered the question at the level it was asked. We are dealing with a first poster who is unfamiliar with scientific terms. We do not help him or anyone else by muddying our answers with esotericism.

Questions are simply a vehicle for producing answers. Remember, the point of Stack Exchange is not to answer an OP's specific question just for the OP, it is to produce a lasting repository of knowledge. If you're going to make an answer, make it an accurate, complete answer. Besides, antimicrobial peptides (AMPs) are not "esoteric" - they're a vital part of the innate immune system.

@mattdmo To be strictly fair, David is correct since the original definition of an antibiotic was that it was s substance made by bacteria and fungi. But the internet and non scientific use, progress, and synthetic antibacterial agents has invalidated the original definition.

So sulfonamides were not initially called antibiotics, but antibacterial agents because they were synthetic.

Methinks thou dost protest too much. But if I am wrong, retitle the question  something like immunity and antibiotics, rewrite it, and supply your answer. Because if you don't nobody will benefit from your contribution as they'll assume that it's a naive question that really should be pulled.

The op isn't involved in the discussion

@GrahamChiu  Op?

I give a short straightforward answer to an obvious misunderstanding and someone marks it down. OK.I'll make it less comprehensible by qualifying it, then will that person mark me up again. In my dreams! What's wrong with you guys?

We take antibiotics when our own immune system is insufficient to control infections. We do make antibiotics as localized defence systems

Defensins and cathelicidins belong to antimicrobial peptides (AMP), called also the natural antibiotics. They are found in Prokaryotes and Eukaryotes, also are synthesized in plants. These molecules were described in bacteria, invertebrates, vertebrates, also in mammals including humans.

But clearly these  can be overwhelmed by bacteria resistant to their action, or by overwhelming rates of reproduction of invading bacteria
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3487008/
Our mammalian physiology has further evolved the innate immune system, and the adaptive immune system to cope with invasions that bypass these simple non-adaptive molecular defenses.

Please provide a citation for your quote.


text:
Do people even notice when insects other than butterflies and beetles go extinct?
Lists of endangered animals only include beetles and butterflies if they bother to mention insects at all. Here is an example from where I live:
http://www.dec.ny.gov/animals/7494.html
All of the insects are beetles, dragonflies, moths, butterflies and there is a mayfly, but that is kind of similar to a butterfly when it comes to their "fanbases." Where are the ants, lice, silverfish and aphids? Is there a better list?

I am not aware of a better list, but you are right that (1) many insects have gone extinct recently, and (2) documentation of insect extinction is poor.  An article in Conservation Biology (2005) says

The biodiversity crisis is undeniably an insect biodiversity crisis. Yet insect conservation remains the awkward “kid sister” to vertebrate conservation. Nowhere is this clearer than in what we know, or rather do not know, about insect extinction, particularly for those extinctions that may have already occurred. ... What accounts for the tens of thousands of expected but undocumented insect extinctions? What does this discrepancy mean? How important is it to our understanding of extinction and the future of ecosystems? These should be questions at the heart of species conservation, yet they have hardly been addressed. No peer-reviewed articles have been published reviewing modern insect extinctions, and no estimates of global extinction rates have explicitly focused on insects.

--Modern Insect Extinctions, the Neglected Majority (my emphases)
The book Insect Conservation Biology (2012) may have more info, though it still seems to focus heavily on the more charismatic species like butterflies.

Lots of insects are considered threatened and endangered. The global IUCN Red List (International Union for Conservation of Nature), which is arguably the most important tool for evaluating species' threats globally, is listing 1382 insects as threatened (categories: Near threatened, vulnerable, endangered, criticaly endangered and extinct) and this includes a wide variety of taxa. A large number of taxa have also been evaluated as 'data deficient', which means that they might be threatened, but we do not have enought information to say. Overall, global assessments have only been done for a small proportion of all insects. However, there are also regional (country) IUCN red lists which include a much larger range of taxa.
The knowledge level differs widely between countries though, which means that some countries have hardly evaluated any insects at all while others have relatively good information. In Sweden (which I'm most familiar with), we have a comparatively good overview of insects, probably due to a long tradition of natural history. For instance, species counts on the Swedish Red List includes 196 Hymenoptera, 855 Coleoptera, 217 Diptera, 67 Hemiptera, 545 Lepidoptera, which represents 27%, 19%, 13%, 7% and 21% of all species found in these groups in Sweden. In Cerambycidae (Longhorn beetles), which I've worked with, about 45% of all species are currently red listed.
Generally, the knowledge level on species trends over time or occurrence patterns is limited in insects though, which can make the evaluations difficult. The red list includes 5 main criteria, and indirect data (e.g. amount of broad habitat classes) are often used as proxies for species abundances or potential number of subpopulations. The process of actually determining a species as extinct is difficult though (not only for insects), since rare insects are often found very seldomly. Some "naturally" rare species might be found as singletons with several years between each occurrence, and the cut-off for considering a species as extinct can then be hard to define (a long period of no occurrences could just be a sampling issue). The situation is made easier
if there is a clear trend from relatively high abundances trending towards extinction.


text:
How to restrict a BLAST search to include only a few protein sequences?
I am performing a BLAST search and I need to filter the output to a certain family of proteins.
Specifically, I need to get matches within the CYP152 family of the Cytochrome P450 proteins. I can parse the results to just P450 proteins fairly easily as the "hit def" field in the output will contain "Cytochrome P450" somewhere in there if it is in fact a P450 protein sequence, but the same is not true for CYP152.
Is there some way to do this? I am using ExPASy BLAST:
http://web.expasy.org/blast/
Thanks in advance

Do you have a list of protein names in the family?

Can't you just use taxonomy filter?, but I'm sure @terdon can help you out :)

@terdon I do not, that would make my life much easier. And Rick Beeloo the taxonomy filter is not that specific, at least as far as I have found.

You're basically doing it backwards. You should start by getting the sequences of the proteins in the family and then blast your query against them. Are you looking for hits against any species? Only some? Do you have access to a Linux or Unix (OSX will do) machine?

I run Ubuntu on my laptop. And okay, are there any good sources of information that you can recommend to me? I have been searching around and can find lots of info on the P450s but not much on the CYP152 subfamily. What I have is a sequence from one protein in the CYP152 subfamily (called OleT JE) and I am trying to compare it with all CYP152 proteins.

The gene identifiers that you get in BLAST output depends on the identifiers used during the BLAST database construction. So you may not find the exact identifier you are looking for.
For restricting the BLAST results to a smaller set of proteins/nucleic acid you can choose either of the two:

Make a database with the fasta sequences of the proteins/nucleic acids that you want. You have to install BLAST and run it from the commandline. Use makeblastdb to make the database. Now you align your queries against this database. Note that now your e-values would not be the same as what you would obtain from a search against the bigger database.
As you said in the question, you can parse the results later. You would have to know what identifiers were used in the blast database that you searched against. ExPASy-BLAST would most probably use the UniProt IDs (there is an ID convertor in the UniProt website to map UniProt IDs to other IDs). If you use NCBI-BLAST (nr database) then you would need to know the GenBank IDs.

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


text:
How is histamine useful against allergies?

Histamine is a chemical produced and stored within the body. It is a part of our immune response and is released during an allergic reaction.

Often histamine is responsible for hypersensitive response of the body towards certain specific compounds(allergens). It causes nasal congestion and pollen allergy. Also it acts as a powerful vasodilator, and causes inflammation. But is it really helpful against allergies?
I was wondering why antihistamines would be required to inhibit normal functioning of histamine, then realised that if histamine was not there, then perhaps we would not have allergies..

False premise? But if the question states anti histaminics instead of histamine, makes sense

Histamine is produced in allergic reactions. - True
Histamine is produced against allergic reactions - False
Okay. Lets get a few things right here first. An allergy is an inappropriate immune hypersensitive response. It is something, we are not supposed to have. A small harmless pollen grain, in normal people shouldn't initiate an allergic reaction.
IgE antibodies are produced against an allergen. These attach their Fc ends to the mast cell. When these antibodies are cross linked by the antigen, degranulation of the mast cell ensues which release various mediators one of which is histamine. So there is a lot of histamine produced in allergic reactions and common antihistaminics like cetirizine and terbinafine act by blocking histamine receptors thereby reducing its biological effects.
So, allergy is a bad thing. The whole IgE, cross linking, degranulation and histamine release wouldn't have happened in a normal person. Histamine isn't going to protect from allergies. It is the cause of allergic effects. Hence the antihistaminics work. You might know that if you have taken a cetirizine during a rash or severe sneezing.
So if allergy is a bad thing, what is the normal physiological role of IgE?
IgE has a role to play in the immune response against parasites where a similar mast cell degranulation process happens.
And if histamines are causing the allergic effects and allergy is bad, what is the normal role of histamine?
Histamine has several roles to play. One is that it is produces as a part of immune response by basophils and mast cells. It also is a neurotransmitter and also is important is gastric acid secretion physiology. The various functions of histamine have important pharmacological considerations while talking of antihistaminics.
Reference : Kuby, Immunology 6th Ed.


text:
Distribution of Exon and Intron Sizes
Goal
I am trying to get a distribution of Exons and intron sizes in Three-Spined Stickleback (Gasterosteus aculeatus).
Data downloaded
I downloaded some data from Ensembl. More precisely, I went there, selected "structure" in the "attributes" and selected
- Ensembl Gene ID
- Exon Chr Start (bp)
- Exon Chr End (bp)

There are two issues in these data:

Some exons end before they start
Some exons overlap

The first point is I assumed due to reversion, so I just reversed the start and end position when there was such inversion. The second point is more problematic as I don't know what such overlap could mean realistically.
Can you help finding the distribution of exon and intron sizes in three-spined stickleback?

What I did with the above data
Preparation
# read data

d = read.table(file.choose(), header=TRUE)
names(d)= c("ID", "start", "end")

# Reverse exons when needed

toReverse = which(d$start > d$end)
s = d$start[toReverse]
d$start[toReverse] = d$end[toReverse]
d$end[toReverse] = s

Exon Sizes -> Looks good
# Exon sizes

ExonSizes = d$end - d$start
hist(ExonSizes) # Cool, looks good!

Introns Sizes -> Looks bad
# Intron sizes
# This is a little slow. One might have better to switch to C++.
# The idea is to look at the distance between the end of an exon and the start of the next exon within each gene.

d$ID = paste(d$ID)
IntronSizes = c()
uniquegenes = unique(d$ID)
nbgenes = length(uniquegenes)
i=0
exon = 0
for (gene in uniquegenes)
{
    i=i+1
    cat(paste0(i," / ",nbgenes,"\n"))

    while (TRUE)
    {
        exon=exon+1
        if (d$ID[exon] == gene) {
   IntronSizes = append(IntronSizes, d[exon+1,]$start - d[exon,]$end)
        } else
        {
            break
        }
    }
}
hist(IntronSizes) # There are negative values. I don't know how to interpret them.

hist(log(abs(IntronSizes))) # That looks good but I doubt it makes much sense!

When it looks like an exon ends before it begins, thats because its on the minus strand. Strand information should also be in your gtf file, so you can check for this just in case. As for overlapping, sometimes an exon has multiple splice sites. Also, genes can overlap. Both cases would cause exons to overlap. Nothing weird going on there, you can include them without worry

At the command line:
wget ftp://ftp.ensembl.org/pub/release-84/gtf/gasterosteus_aculeatus/Gasterosteus_aculeatus.BROADS1.84.gtf.gz
gunzip Gasterosteus_aculeatus.BROADS1.84.gtf.gz

Then in R:
library(GenomicFeatures)
txdb = makeTxDbFromGFF("Gasterosteus_aculeatus.BROADS1.84.gtf")
hist(log10(width(unique(exons(txdb))))) # exons
hist(log10(width(unique(unlist(intronsByTranscript(txdb)))))) # introns

Note that some of the annotated exons (and the introns between them) are incredibly unlikely to be correct. For example, there are 1 base long exons and introns. I don't think anyone actually believes those are correct, but the distribution is probably otherwise approximately correct.
Edit: For what it's worth, there are no negative sized exons in the GTF file. My guess is that the overlapping exons are from different transcripts (or genes on opposite strands).
Edit2: If you want to get your introns from a "union gene model", then use something like reduce(exonsBy(txdb, by='gene')) and then lapply gaps() to that. The results will be correct and the process will probably take less time than what you've been trying.

Perfect +1 Thanks a lot! For future users, please note that GenomicFeatures is a bioconductor package and that with MAC OSX wget must be replaced by curl

May I ask you to further explain your second edit? What is a "union gene model"? Do you mean that I might want to get a distribution of per-gene average exon length?

The explanation of a union gene model ends up being a bit long for a comment. Have a look at the right part of subfigure A here: http://www.nature.com/nbt/journal/v31/n1/images/nbt.2450-F1.jpg The "exon-union model" is the same thing as a "union gene model". In this case, you're still getting the distribution of all introns in the genome, you're just redefining "intron" to not be something biologically correct (though this redefinition can be useful for some purposes).

Oh sure I got it. I did not thing of that. I will need to go with a union gene model for my purpose. I'll try to get that as soon as I'll understand what kind of objects I am dealing with!


text:
Can a human being live without any carbohydrates?
Nowadays low-carb is in fashion, but what I recently wondered is whether a human can live without any carbohydrates at all?
Of course this would be hard to do in reality, as most food will contain proteins as well as carbohydrates, but let's assume it would be possible to circumvent any carbohydrates.

No, humans cannot live without carbohydrates. Low-carb diets seem to work well in some people for short-term weight loss, but they can be rather damaging long-term. While a diet consisting of meat and meat may sound good to some people, you would not be very healthy for very long on it.

see this previous question and answer... amino acids are all ketogenic or glucogenic and can be broken down into all Krebs Cycle intermediates... http://biology.stackexchange.com/a/41255/16299

Have a look at: https://en.wikipedia.org/wiki/No-carbohydrate_diet It should answer most of your question and give you some good references.

The Atkins diet is based on that. Without carb intake, however, the citric acid cycle (CAC) eventually basically stops and proteins will be utilized to be converted to carb intermediates to feed the CAC. Progressive and strict use of the Atkins diet will eventually kill you as the CAC is essential to life.
The idea behind Atkins is that fats will be used to feed the CAC, and that will happen until the carbohydrates that keep the cycle running are depleted. At that point one will develop ketosis and the CAC stops, and with it the production of ATP. Note that fatty acids can be fed into the CAC, but are not sufficient to keep it running; fats burn on a fire of carbs.


text:
Is it necessary to remove a bullet from the body?
So here is the proof: William Lawis Pace lived with bullet in his head for many years & even hit 100.
However, both in real life and movies, we often see doctors struggling to remove bullets from the human body.
My Question: Is it necessary to take bullets out of a human?

I would think that this is somewhat dependent on what part of the body it has lodged in.

Of course it is. William Lawis Pace is clearly the exception (and suffered due to the wound). He was incredibly lucky to survive for so long. Also, I think the question is oversimplifying the gun-shot treatment (practical advice and academic references here). The aim is not to simply remove the bullet.

@James - it's not the bullet left in the body per se that causes the suffering; it is the damage the bullet does. If inert, it may not do further harm. In repairing the damage it has done (lacerating blood vessles, perforating bowel, etc.), the surgeon finds and removes the bullet, partly to make sure that's the end of the destructive trajectory, and partly because who wants a foreign body in their body? Please trust me when I say it's not extremely rare to have portions of bullets and shrapnel remain in the body after surgery. It depends on a number of factors, including risk of removal.

I'm voting to close this question as off-topic because the OP already has proof that removing a bullet is not necessary to life.

It depends on the size and the location. After both world wars plenty of people had odd bits of shrapnel wandering about inside them for years, because it would be too difficult or dangerous to get it out.
We had a dog who carried a few shotgun pellets inside her, shallowly enough for one to feel one of them under her skin. No point in subjecting the dog to the stress of an operation.
But with a bullet bullet, the size means that it would be almost certainly worth trying to get it out. Again, depending a bit on location and how much trouble it's causing. Abdominal cavity = one answer, muscle = another.


text:
Ecological specialization and relative abundance
I am reading Evolution in Changing Environments by R. Levin but have a hard time.
Claim
At page 25, Levin says as a conclusion

The more efficient a caste at meeting the contingency for which it is specialized, the lower its abundance. This is seen in Figure 2.5b

Here is figure 2.5b It is actually a reprodcution I did in R but ressemble closely the original

W1 is the fitness in environment 1 and W2 is the fitness in environment 2. The figures comes with the following legend:

The optimal population consists of two castes in the proportions of the line segments by the Adaptive Function (dotted line). Thus castes C1 and C2 are more or less equally common, but a population of C1 and the more specialized C3 will be mostly C1.

The terms "Adaptive Function" is not really defined in the book but it basically mean the overall fitness given the fitness components W1 and W2. The terms "castes" and "contingencies" aren't accurately defined either. In his model, the population experiences only these two environments, where $p$ is the probability to be found in one specific environment. As I understand little from this book, it is hard to know what kind of a prior information I could/should give you.
Question
Can you help me to understand the above statement and why it makes sense?


text:
I saw these patterns on a hill. Which insect makes such a pattern?

Description of the location

It is in India
The place is 300-400 m above sea level.
There is no water body nearby.

Which insect makes these patterns?

Welcome to Biology.SE. Can you please add the broader scale location (continent, country/region)?

@Remi.b Continent:Asia,Country:India

Specifically where in India? And which hill?

It could be an antlion. Antlions are a group of about 2000 species that can be found all around the world (including India). Antlions mainly live in the kind of dry areas you describe and that we see in your picture. I don't think one could be more accurate and tell the genus without a picture of the individual but I might be wrong.
Here is an adult antlion:

and here is a larva antlion

The small pits you see are made by larvae. The larvae make these small trap pits to capture ants (and some other small insects). The larvae is buried in the soil at the center of the pit and simply waits for prey to fall into the pit. Below is a picture of such a pit:

Parents had similar sand pits in their garden. It always occurred in groups, always in dry sand areas. It was similar to the one you have posted but different from the OP's images - at the center of the pit there's no "hole" or "well" that exist on every single hole in OP's pictures. At one time when I noticed that holes in the garden, I first thought about antlions, too, but after carefully digging a few pits out I have not found any residents. Maybe in our garden the insects have aleady moved out and the "well" has collapsed.. I don't know. Just an observation. I still think it's antlion.

Wow.  I had no idea that adult antlions turn into dragonflies!

It's not a dragonfly. Dragonflies can't fold their wings, while an antlion can fold its wings in a manner similar to a damselfly or a caddisfly.

Actually, it's neither a dragonfly nor a damselfly, which are both Odonata. Antlions are Neuroptera, an order more related to Coleoptera.

authors: Bob Jarvis - Слава Україні


text:
How are the dominance and additive effects reflected in the mean and variance of the offsprings of two individuals with known phenotype?
If I estimated the genetic additive σ2A, genetic dominance σ2D and environmental effect σ2E of a trait in a population, what will be the predicted value of the offsprings of two individuals with known phenotypes?
My understanding: given that the two individuals are not close siblings, and that the mean of the two parents is μparents, the offspring will have a mean of:
μoffspring = μparents + μparents x σ2D
and the variance will be the environmental variance,  σ2E
How the additive effect  σ2A plays a role in a single mating ? (assuming thousands of offsprings (like in some plants) )?

I was starting to make complicated calculations but actually to answer this question one does not need much quantitative genetics. The expected should just be the average between the parent phenotypes $\mu_{offspring} = \frac{1}{2}\left(\mu_{mother} + \mu_{father}\right)$, isn't it? Note btw that the covariance between any parent and the offspring will be $\frac{r \sigma^2_A}{\sigma^2_P}$ and the correlation between the mid-parent and the offspring should be $\frac{1}{\sqrt{2}}\frac{\sigma^2_A}{\sigma^2_P}$, where $\sigma^2_P = \sigma^2_A+\sigma^2_D+\sigma^2_E$

Is the question for an advanced class in quantitative genetics on just an introductory class in evolutionary biology or genetics? If the question is only about the expected offspring phenotype, then I think it is as easy as $\mu_{offspring} = \frac{1}{2}\left(\mu_{mother} + \mu_{father}\right)$.

I see, but how the dominance effect changes the mean? and what will be the variance of the offspring population - is it just the environmental related variance?

The offspring population will have a variance that will be much greater than just the environmental variance. If the trait of interest in not fitness, then the expected variance in the offspring population will be the same if you assume infinite population size and no mutation.

However, you are not asking this question in your post. That gets me confused as to what the question is. Can please highlight (in bold or something) the one single question of your post?

I see you edited the question. Thanks. What do you mean "plays a role" in your highlighted question? Also, I don't quite see the parallel between the question in the title and the one highlighted in the post. I don't want to be pedantic, I am just trying to make sure I really understand what you're asking.

I would like to simulate a population in which I know the real heritability, dominance effects and environment effect, estimated from sibling ANOVA, parent-offspring regression and comparing different environments.  Although I can understand the role of these effects on a large population, I am not sure how to apply this to the predicted parameters of each individual offspring of two individual parents. What will be the right formula to estimate the phenotype of  each offspring in the simulation?

I don't understand. What do you mean by  in which I know the real heritability. Do you mean you want to force heritability to remain constant? However, in the same time you say, you want to estimate it as if you don't want heritability to be constant. By simulate, I suppose you refer to numerical simulation of course, not analytical simulation/modelling.

Let say I have large phenotypic data, spanning many parents, children and environments. I estimated the broad sense Heritability from siblings ANOVA, the narrow sense heritability from parent-offs.  regression (~σ2A). and the environment effect from comparing individuals across environments. So now, given a random parent values, The predicted children mean will be the parent mean + some X value, associated with the dominance effect, and variance coming from the enviro. effect.  how to calculate this "X" factor ? This what puzzles me. - what will be the mean and var. of the population?

oohh...I think I got your question. when you say "children mean" and "parent mean", you imply "mean of the children population" and "mean of the parent population" (assuming discrete generations). I wrote an answer. let me know if it is what you expected.

What is the expected phenotypic trait of an offspring given the phenotypic trait of its parents?

The expected trait of the offspring is equal to the mean of the parents traits.
For this I assumed we don't have more information about the genetic of the trait (typically, without knowing the directionality of dominance and number).

What is the expected phenotypic trait of the offspring population given the phenotypic trait of the parent population?

As a consequence of the above, the expected mean phenotypic trait of the offspring population is equal to the mean of the parent population (in absence of selection).

What is the expected variance in the offspring population?

No drift, no selection
In absence of drift and selection (and environmental changes), the variance of the offspring population equals the variance of the parent population.
Directional selection only
In presence of directional selection, please have a look at How does Natural Selection shape Genetic Variation? and ask follow-up question if needed.
Drift only
In presence of drift only, the heterozygosity is reduced by a factor $\frac{1}{2N}$, where $N$ is the population size. The loss of genetic variance is then dependent on (1) the frequency, (2) the dominance and (3) the effect size of alleles at loci causing this genetic variance. There is therefore no simple answer. The only generalization that can be done is that (1) the expected variance of the offspring population is lower than the variance of the parent population and (2) the smaller the population size, the higher is the expected loss of genetic variance
General Note
My feeling about quantitative genetics (but I am not really an expert in that field) is that it is often frustrating to see that generalization is often impossible and general solution to recursive equations often don't exist implying that predictions to more than one generation must be calculated through iteration.
I suspect that an expert in quantitative genetics would be able to say much more than me in this post.
The book Introduction to Quantitative Genetics (by Falconer and Mackay) is probably still the best book to increase your knowledge in quantitative genetics.


text:
Explain a transpiration graph

The solution is A, but I think both A and C are correct. For choice C, stomata that protected by hairs will have a greater amount of water vapour around them, hence lower water potential gradient. Hence, this results in the reduction in the rate of transpiration, as well as choice A.

Though I don't come across graphs like these too often, I guess the answer should be A because...
From the graph, it is clear that Leaf 1 has more mass than Leaf 2 after 5 hours. This means there is a lower rate of transpiration in Leaf 1, which can definitely be explained by a thicker cuticle (since the thicker the cuticle, less is the water lost). Hence choice A is correct.
Now, look at choice C. Like you said, in leaves where stomata are protected by hairs, there will be lower rate of transpiration. Then, obviously Leaf 2 should have a higher mass than Leaf 1, right? But this is not the case (as per the graph). Hence, choice C is incorrect.


text:
To what extent is the genetic code more than just a code?
It is worth specifying the exact meaning of "code" in this question. A code is a map from one space to another space with which it has no algorithmic connection. Thus representing 321 as 0x141 is not an instance of a code, because there is an algorithm; but representing 321 as the letter Ł is a code (Unicode, in this case) because there is no intrinsic connection between the number and the symbol. The only way of knowing which number matches which symbol is to look it up in a book.
Popular presentations of the way cells work speak of the DNA/RNA code as a code. There is no algorithmic transcription of RNA to proteins. The transcription from codons to amino acids is a code which human beings interpret by looking it up in a table. Cellular machinery interprets it by the fact that GUN→Val transfer RNA is present in the cell but a GUN→Glu transfer RNA is not. During protein synthesis, each transfer RNA molecule, having acquired a molecule of its designated amino acid, pairs with the codon it is designed to pair with. The code table is thus defined by the set of tRNAs that happen to be floating around in the cell.
(There may well have been some over-simplifications in the above picture).
On the other hand, the DNA code is not a code in the sense that the DNA molecule (and still more RNA) is not a passive repository of code sequences but a reactive entity, and those reactions depend on the nucleotide sequence in a way different from the tRNA-mediated encoding. Coding regions; non-coding regions; long strings of single nucleotides; initiation sites; 3-D structure of the molecule – all these depend on the nucleotide sequences in a way separate from their role as codons.
This is why this is a "to what extent?" question.
A thought experiment
To the extent that the genetic code is a code, an experiment of this kind ought to be possible, and perhaps even not far from practicability. To the extent that the code isn't a code, it wouldn't work.

Elucidate the structure of GAU-to-Glu tRNA and GAA-to-Asp tRNA, neither of which exist in nature.
Synthesise RNA that codes for them and insert it into a suitable cell, making it a machine for synthesizing these two tRNAs. Manufacture a large quantity of these tRNAs.
Taking the DNA of a target cell (not necessarily the same species as before), replace the genes coding for GAU-to-Asp and GAA-to-Glu tRNA with genes coding for GAU-to-Glu tRNA and GAA-to-Asp tRNA. Such a cell would not live, since it would mistranscribe most of its proteins.
Before reinserting the DNA, make a copy of it, replacing every occurrence of GAT with GAA and every occurrence of GAA with GAT.
Just before reinserting the DNA, flood the cell with the new tRNAs manufactured in step 2. This changes the code.
Reinsert the DNA.

The cell should now be viable. Everywhere that GAT used to code for Asp in the original cell, GAA is now found; but since the only tRNA available to the synthesis process is GAA-to-Asp, this means that Asp is still inserted exactly where it should be inserted. The change in DNA sequence is exactly compensated for by the change in available tRNAs - that is, the change in the code.
Purpose of the thought experiment
On the one hand, postulate success. The modified cell, using a different genetic code from anything else on the planet, has the advantage of being immune to all viruses. Or will being immune to viruses turn out not to be an advantage after all? The modified cell will also be very much inbred, since it cannot exchange genetic material with anything else. Advantage, or disadvantage?
On the other hand, consider the possibility of failure. Failure would appear to be because GAT and GAA (or GAU and GAA) are subtly different in their chemical properties quite apart from their role as codons. DNA and RNA might adopt different conformations, ones sufficiently different to change the nature and kinetics of their reactions as macromolecules as opposed to information repositories.
Which brings us exactly to the title of this question. If the genetic code is a pure code, then the experiment will work - just as I could make a variant Intel x86 chip in which the code for Add does subtraction and the code for Subtract does addition, and compensate for it by modifying all my programs accordingly. To the extent that the code is more than a code, the experiment will work less well.
But to what extent?

The post was talking about messenger RNA and mRNA but could only make sense if transfer RNA and tRNA was meant, so I've edited the dozen plus instances.

See also: https://biology.stackexchange.com/questions/21918/are-the-dna-codon-mappings-arbitrary

You call it a thought experiment but something like this has actually been done. Not entirely similar as they don't switch 2, but still they replace a codon.
An overview: https://en.wikipedia.org/wiki/Expanded_genetic_code
Big thing: in the two articles leading up to this one they replaced all 314 UAG stop codons in E.coli K12 and used the now unused UAG codon for some fancy stuff: https://www.ncbi.nlm.nih.gov/pubmed/25607366

+1 for alternate uses of stop codons. This is a great example

Hasn’t your question already been answered by those organisms (and organelles) that have a different genetic code from the standard genetic code (originally known as ‘universal’)? Essentially they have performed the experiment for you by developing machinery to decode mRNA differently (transfer RNAs with appropriately different anticodon/amino-acid accepting ability — that’s what determine how the code is interpreted).
And I think DNA is a red herring here. The genetic code is a code to decipher information in regions of mRNA that specify proteins. It does not — and was never intended to — apply to anything else. Thus, it does not apply to the 5' and 3' untranslated regions of mRNAs, where there may be other combinations of nucleotides that are interpreted differently (e.g. ribosome-binding sequences in prokaryotes, polyA-addition signals in eukaryotes). Use of a modified (T for U) genetic code is only used with DNA to make predictions about regions that specify the protein-encoding parts of mRNAs (i.e. whether they can, and if so, what the amino acid sequence of the protein will be).
[Apologies if you were aware of all this molecular biological background and I have misunderstood your argument.]

On one hand, designing an experiment which would kill (and resurrect) a cell is not possible: once a cell malfunctions, it's likely damaged beyond repair.  However, other than that I don't think this experiment kind of cannot actually be done. You would just have to simultaneously expose different cultures (grown in the same conditions) to different inserted DNA or RNA. This would include exposures you would predict cause both cell death and survival or growth and "control" exposures you know would kill or spare cells. This is done routinely with bacteria, yeast, and mammalian cancer cells.
Depending on your interpretation of a "true code" this would be testable. Clearly a DNA ATG maps to AUG in a particularly well defined way. mRNA AUG is also decoded to Met but the mechanism here is important: the tRNA is a "decoding" class of molecules, these have a complementary recognition site for an mRNA codon, e.g, UAC, and a binding site for an amino acid such as Met on the other end. These decoding molecules are otherwise identical in structures and interchangeable, indeed there are some bacterial species that use "non-canonical" decoding tRNAs different to other species and "genetic re-coding" where additional amino acids or frameshifts are encoded by our STOP codons.
I don't know if tRNA here fits your analogy as an algorithm or compiler but evolution has produced a vast range of exceptions we could test the genetic "code" on. Basically we work with a table that we're familiar with and some bacteria use a different one with additional amino acids like selenocysteine. Recent experiments have even added DNA/RNA bases not occurring in nature and "non-canonical" amino acids not used in naturally occurring cells, others are attempting synthetic biology to engineer their own cells as you've proposed.
However, it's worth noting gene expression isn't a simple one-to-one mapping. The amount and variant of gene expression is also important, many regulatory sequences affect expression of DNA, splicing of mRNA, or ribosomal binding. Once a protein is produced it is often cleaved, phosphorylated, or glycosylated and can form complexes with identical or different proteins. Whether the "exon" DNA encodes a "raw" protein sequence is intriguing and as much as I would hypothesise that DNA to protein is a true code, in the context of a complex biological system other factors beyond the raw sequence affect gene function.


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Do all +ssRNA viruses have similar structures and life cycles?
Take HCV for example. HCV doesn't package any enzymes in it's virions. When it infects a cell, it first translates its RNA genome. It's RdRp is synthesized with other non-structural proteins. Then its RdRp began replicating the RNA genome. Newly synthesized RNA are served as either translation templates or genomes of new virions. Finally new virions are assembled and released.
So do all +ssRNA viruses have the same pattern? There's no enzyme in the virions, and all the enzymes are synthesized after entry into the cells. They have the same life cycles: entry→translation(non-structural)→replication→translation(structural)→assembly→release.


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Since RNA viruses and retroviruses all have high mutation rates, why do only a few viruses have the virtue of variability?
We have been taught that it's difficult to make vaccines to influenza, HIV and HCV because they lack the proofreading mechanism, hence have high mutation rates. But most RNA viruses and retroviruses are still antigenically stable, such as measles, rabies, polio, yellow fever, HBV etc. So why do only a few viruses successfully become variable? Is it because their receptors allow flexibility, or their glycoproteins have sophisticated conformations that allow more mutations?

The high mutation rate is only a small part of the reason it's hard to make vaccines against those RNA viruses.  The real problem is not that they mutate rapidly, but that they can tolerate high levels of variation in their antigenic regions without losing fitness.  Viruses like polio and measles, as you say, have mutation rates easily on a par with influenza or HIV, but when they mutate antigenically significant regions, those new viruses are much less capable of infecting and transmitting between hosts.  Vaccines therefore either block the virus replication altogether, or force them into a much weaker form that is much less infectious.
Why do some viruses tolerate antigenic changes better than others? It's not known, but presumably there has been selection for it in those lineages.

I can't give an upvote because I am new to here. Your answer is right.

It seems that influenza and HIV have employed some sophisticated mechanisms of immune evasion(I don't know the case of HCV). For example, they use a pocket like structure to protect their vulnerable parts. But these are just guesses.

Every single modern virus has an array of sophisticated immune evasion mechanisms, being the descendant of a billion years' worth of ancestors that successfully evaded increasingly-sophisticated immune systems.  Influenza and HCV are not particularly noteworthy in this respect.

I see, thanks. BTW, can you give me some "noteworthy" examples of the viruses sophisticated at immune evasion? I shall read about them.

The most sophisticated at immune evasion are probably the herpesviruses and poxviruses, large DNA viruses that encode multiple genes specifically targeting the immune system. Here and here are starting points


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What really is color and how do we perceive it?
How do our brains actually transform the information that the cones in our eyes  receive into the different colors that we can see and imagine?

Related: http://biology.stackexchange.com/questions/39882/are-some-animals-like-dogs-and-cats-color-blind-and-how-do-we-know-that/39890#39890

Despite its simplicity, this question demands a so complex answer that we can start by saying:
We still don't know.
Because you are talking about the colour as a sensation, as something that I feel and that I (literally) see. And here is the problem: as such, the "colour" is not a physical reality.
Some people may disagree here, but colour is not a physical property of any material. Light is a physical property. The wavelength, the energy, the frequency of light are all physical properties. Even the crazy quantum nature of the photon with its restless existence is a physical property. But not colour. Colours are creations of my mind, my nervous system, my idiosyncratic consciousness.
For instance, It's simply impossible to know if the red that I see in my mind is the same red that you see in your mind. The fact that we both call it "red" or the fact that we both agree that the colour of the blood is the same colour of the wine doesn't help at all: this is a problem of qualia:
http://plato.stanford.edu/entries/qualia/
https://en.wikipedia.org/wiki/Qualia
And the same goes for all other conscious experiences derived from the exteroceptors, such as "taste" and "sound". What I feel is particular and nothing can guarantee that another person feels the same, even if the stimuli are the same and the nervous impulse to the CNS are the same.
To finish, I'd like to propose a thought experiment, for you to understand the subjective nature of the colour:
We tend to imagine that the world is the way we see it (as primates, we value the vision very much). But we have only 3 different cones, giving us roughly 1 million (100$^3$) different colours. Reptiles, as the birds, have 4 different cones, and some of those reptiles, as pigeons, have 5 different cones, giving them the ability to "see" 10 billion colours (100$^5$). This is hypothetical, of course, to really perceive all these colours the animal needs a huge brain cortex, but let's suppose that they see (perceive) all these 10 billion colours.
Now try to imagine these 10 billion colours, you, who are an organism that only perceives 1 million colours. It's impossible. And it's impossible for a talking pigeon to explain to you how he/she sees the world, how all these 10 billion colours are, the same way that it's impossible for you to explain to an animal with achromatic vision what is green, purple, orange, cyan, magenta etc...
This is what we call qualia.
But, as someone that loves cognitive ethology and science in general, I don't think that this is something beyond the realm of sciences, something impossible to know... this is a problem that can be scientifically addressed and, with the ingenuity of the neuroscientists and other biologists, we can someday understand the "redness" nature of the red we see.


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Does common X-like picture represent one doubled chromosome or two homologous chromosomes?
What is on common X-like picture of chromosome?
Here is the image from Wikipedia:

Are (for example) lower petals homologous to each other?
If yes, then why (1) is entitled as chromatid: one-half of two identical threadlike strands of a replicated chromosome? Homologous parts are similar but not identical.
If no, then why does human chromosomes are often denoted by Xs:

Do we have 23 Xs (females) or 46 Xs?

You should the wikipedia legends on the post

I have cited important one.

Sure, but if you give more info and thoughts, it might be easier for us to understand what is unclear to you. This seems particularly important as I don't understand your comments below my answer.

@Remi.b note that I am absolutely agree with your answer and this is my "zero hypothesis". But I am confused, that sometimes X-like patterns are apparently used to depict homologous chromosomes.

Ok. If the legend under the figure (wherever you found it) says that it displays homologous chromosomes, then the legend is wrong! A single X-like shape always represents a single chromosome.

Please indicate the source of your second image.

The "X" you see is a chromosome. The two strands that forms the X-shaped chromosome are called chromatids. As they are bound together (by the centromer), they are called sister chromatids. Note that chromosomes look like that only during the metaphase. Note also, that not all chromosomes have a centromer that is in the middle of the chromosome as it is obvious from the picture in your question.
Many species (including humans) have two sets of each chromosome. If you add the other chromosome in the picture, you would see a pair of chromosome. One chromosome of the pair is said to be homologous to the other one. Below is a cladogram during the metaphase of a human (I let you figure out the sex) showing each pair of chromosome.

Sister chromatids are identical (except for mutation during the last chromosomal replication). Homologous chromosomes are similar but not identical. Crossover occurs in between chromatids of homologous chromosomes.
Further comment on your figure
There are 23 pairs of chromosomes, that is 46 chromosomes. Your picture shows only one chromosome per pair, that is your picture shows only 23 chromosomes. In other words, your picture shows the haploid genome and not the diploid genome.

See the picture of human genome. It is depicted as 23 Xs (some not fully formed).

I don't understand your comment. Can you develop? Do you think I answered your question?

So, pictures, depicting 23-24 X-like feutures are just incorrect?

See my update. I have added a picture. These pictures are common. Search human genome in google images.

Sure, I see the picture. I don't understand what you think would be incorrect on this picture based on my answer. Can you please develop further what is unclear? Note that your picture only show a single chromosome (two chromatids) of each of the 23 pairs.

Regard object #1 on my picture. There are ~ 23 of such objects in my picture. Hence, this object is representing 1/23 of genome. Hence, it represents 2 chromosomes. Probably, homologous ones. This object is depicted as X. Hence, strands are homologous, not identical. But you said strands are identical (not regarding mutations).

Please see edit "further comment on your figure"  and let me know if it helps.

To whoever is concerned: Please leave a comment when downvoting. Such downvotes are really not helpful at improving the answer.

I didn't downvote

I never thought you did. No worries!


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From 46 human chromosomes, is each one from a single parent?
Humans have 23 pairs of chromosomes. Each chromosome in pair is homologous to another one in pair.
Does this imply, that the entire chromosome in any cell is obtained from only one parent? I mean entire single chromosome from one parent, and entire homologous one -- from another parent?
This is obviously true for sex chromosomes, especially in boys. They get Y from father and X from mother.
Is similar true for any other pair of chromosomes?
Or they are exchanging genes during mitosis too?
I.e. parents data is distributed grouped by chromosome or by gene?

See Mitotic Cross-over. I don't know what is the cross-over rate during mitosis though.

To be clear, are you asking specifically about events after fertilization of the egg? Your question about chromosomes obtained "from only one parent" suggests a more basic question of how meiosis works.

Yes, each single chromosome came from one parent.  However, it is not true that each chromosome came from one grandparent.  Due to crossing over in meiosis, the copy of Chr 1 that you got from your father is partially from his father, and partially from his mother.  And the same for all the rest of your chromosomes.  You will not pass on a whole chromosome as you inherited it onto your children, crossing over will happen in your gametes, so that your kid will get whole chromosomes that are part from your mother, and part from your father.  The sex chromosomes are exceptions, because in men, they can't do crossing over, since men have a mismatched pair.  (At least in biologically "normal" men.)

No homologous chromosomes do not imply that each cell has genetic information from only one parent.
Let's just talk about one chromosome - and call it Chr1. This chromosome has genes A, B, C, D, and E.
When an egg is fertilized by a sperm, the resulting egg will have a pair of Chr1. One of the Chr1 would have come from the mother (egg) and the other from the father (sperm). These two are a homologous chromosome pair and they both have genes A, B, C, D, and E.
The mother and father contribute different alleles of the genes. So the mother could contribute A.1, B.1, C.1, D.1, and E.1 where as the father could contribute A.2, B.2, C.2, D.2, and E.2.
Then the child has two homologous chromosomes A.1/A.2, B.1/B.2, C.1/C.2, D.1/D.2, and E.1/E.2.
Hope that is a bit more clear.


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What is the rationale behind IgM being the default antibody?
I know that the$\ C _\mu $ gene appears first in line for class switching and hence the IgM is the default antibody. But what is the rationale for it being so? There must be some advantage (evolutionary?) of having the IgM first in line over the IgG or so on.
The IgM is different from the IgG in being a cluster of five, better agglutination, having more avidity, and more cross reactivity (correct me if any of these is wrong). How do these properties help in containing the infection only for the very first time? Or, why is the IgG is not good for the initial response?

The answer is that the Cµ-C∆ locus is expressed in the precursor B-Cells. It is only after the B-cell has produced a functional B-cell receptor and has receive the proper stimulation from cytokines do you get transcription through the other constant chain loci, which then allows class switch recombination to occur.

When the Naive B cell gets activated and begins to secrete antibodies the affinity of the antibodies is low, as it hasn't yet gone through several cycles of affinity maturation. The increased avidity of the IgM balances the decreased affinity of these initial antibodies. If IgG were released at this stage, the body would have a much lower immune reaction to the antigen.
However after affinity maturation, the IgG has sufficient avidity and affinity to mount a stronger immune reaction than the initial IgM antibodies. If the body still produced IgM after affinity maturation, there would likely be a significant amount of crosslinking. This could potentially cause aggregates to form in the blood/lymph which could cause occlusions.
Edits:

If the affinity of the antigen-binding sites in an IgG and an IgM molecule is the same, the IgM molecule (with 10 binding sites) will have a much greater avidity for a multivalent antigen than an IgG molecule (which has two binding sites). This difference in avidity, often 10^4-fold or more, is important because antibodies produced early in an immune response usually have much lower affinities than those produced later. Because of its high total avidity, IgM—the major Ig class produced early in immune responses—can function effectively even when each of its binding sites has only a low affinity.

Molecular Biology of the Cell
The claim on aggregation after affinity maturation is speculation based on the crosslinking that occurs with IgA antibodies (e.g. Phlegm) when there are only two high-affinity Ig molecules joined together rather than five.

Thanks! Could you add a reference for your answer. I'd then mark it answered. :)

I do not really think this answers the question of Why IgM is the default antibody.

You are sort of explaining the rational behind Somatic Hypermutation, but not that well... The correct way to answer the question is to leave out the variable chain discussion altogether and explain the myeloid developmental program with regard to the Heavy-Chain Constant region and then discuss Class Switch Recombination in mature B cells.

Well, it answers my doubts! I know the heavy chain order in the gene. I wanted to know why it is that way. @AMR

@Polisetty The avidity / affinity of the variable regions of the light and heavy chains of the immunoglobulin provides no insight into the order of the constant region of the heavy chain. Deficiencies, such as Hyper-IgM syndrome are related to defects in cell signaling. That alone should tell you that the reason for IgM being first is the result of the developmental state of the cell and the signals that it receives, which in turn control the Transcription Factors that bind to the locus and express Cµ instead of the other loci. You can also have SIgM disorders, which you can look up.


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How does RCSB determine the origin of the Cartesian coordinate system utilized in all PDB files
When perusing through the text version of a PDB file, I noticed in records that begin with "ATOM," there are x, y, and z coordinates for these atoms.
How is the origin of each molecule's Cartesian coordinate system determined by RCSB?

They are just arbitrary numbers, the only thing which matters are the relative coordinates. The relative coordinates themselves are determined mostly by X-ray crystallography or NMR.


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What is the mass of an E.coli cell?
I'm trying to get into Biology, reading introductory texts. A discussion on E.Coli estimates the mass of the cell from $$density =1g/mL=1g/cm^3$$ and $$volume=1µm^3$$ From this I get $$ mass=density × volume = \frac {10^{-6} g}{10^{-2}}=10^{-4} g$$ which is wrong since the answer is supposed to be $1pg$. What am I doing wrong? Thanks!

Its simple:
Mass = Density * Volume

= 10^3 (Kg/m3) * (10^-18 m3)

= 10^-15 Kg

which is equal to 10^-12 gram or 1pico gram

Wiki gives me micrometers to be $10^{-6}m$. And also that an $mL=cm^3$. Since I don't come from a background where units were ever used, can u please elaborate on how u got ur density and volume compared to mine? Thanks

@Craig Yes micrometers are indeed 10^-6 meters. But 1 micrometer^3 = (10^-6)^3 = 10^-18

10^-18 is in m3

Ahh... I should've paid attention in high school  physics


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What is the another use of de Bruijn graphs in bioinformatics except DNA assembly?
I implemented own generic de Bruijn graph, which I use for DNA assembly (alphabet: A, C, G, T). I try to find purpose of de Bruijn graph for another bioinformatics problems, if some exists. I want use/modify my implementation to solve this.
Are there another problems in bioinformatics which we can solve with de Bruijn graphs?
I found only RNA assembly, which is similar to DNA assembly.


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What does a climax community lead to?
Seral communities modify the environmental conditions in such a way that these are less favourable for itself and more favourable for the next community. Each community acts to end itself.
If the same is applicable to the climax community, what does it lead to?*

Could you please define 'climax community' for the purposes of your question? Dictionary.com gives: "An ecological community in which populations of plants or animals remain stable and exist in balance with each other and their environment. A climax community is the final stage of succession, remaining relatively unchanged until destroyed by an event such as fire or human interference", which suggests an answer by definition to your question: a climax community, without intervention, leads to ongoing climax community.

In addition to the comment by @bshane, note that the term climax community is somewhat obsolete, since also late succesional stages (e.g. old-growth forests) are now viewed as much more dynamical systems than previously thought.

As pointed out by @bshane it seems your question is answered by the definition. From the relevant wikipedia articles

"A seral community (or sere) is an intermediate stage found in ecological succession in an ecosystem advancing towards its climax community."

and

"In ecology, climax community, or climatic climax community, is a historic term that expressed a biological community of plants, animals, and fungi which, through the process of ecological succession the development of vegetation in an area over time, had reached a steady state. This equilibrium was thought to occur because the climax community is composed of species best adapted to average conditions in that area."

It doesn't lead anywhere, it is the climax. It is the state a community reaches when there is little change in the biodiversity as it because the community is composed of species at proportions that suit the ecology well.
However, in reality it seems that climax communities are rarely (if ever obtained) and, with increasing climate change and habitat invasion by humans, few communities will be in equilibrium. The adaptive landscape varies in time and space, thus while a community may be well suited to the current environment, it may well be poorly suited to future incarnations of that environment and will be undergoing constant change. As such, the term "climax community" is somewhat obsolete with it generally referring to old or established communities rather than those at a climax.

Yes, and problems with the climax community idea definitely doesn't hinge on human interference. For instance, plant distributions in Europe haven't stabilized since the last glaciation and the dynamics of old-growth boreal forests depend on forest fire dynamics. There are even studies that argue that the diverisity of tropical rainforests (arguably one of the most climax-like habitats there is) are dependent on glacial refugia.

I'm aware of that - just pointing out that habitats change, especially at the moment, so there is little chance that a community can stabilise (because environments are unstable)

It wasn't really citicism, just an addition/clarification to your answer. As a sidenote, I find it amusing that we both independently used the exact wording "somewhat obsolete" to describe the term climax community (see my comment to the Q). Then it must be an accurate description...

haha, weird! must be a very good description of its somewhat obsolete nature

A somewhat vague description of a somewhat obsolete concept.


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Quantity of toxin release by pathogen in host
I came across these lines from this paper:

Pathogenic microbes exert a broader sphere of influence by releasing a bolus of toxin that can act upon many cells within a given tissue and/or diffuse away to modulate one or more types of cells at multiple locations within the host.

What does this line mean? Does it mean that the pathogen releases multiple types of toxins or does it mean that the pathogen releases just one type of toxin in a large quantity?

bolus: MEDICINE - a single dose of a drug or other medicinal preparation given all at once.

@MattDMo I want to know what the sentence mean from the view of the pathogen

As I commented, a bolus is a single (often large) dose of a drug or compound given (released) all at once. Please read the very next sentence after the one you quoted:

For example, the lethal and edema toxins of Bacillus anthracis disseminate within the host bloodstream and act upon both immune and nonimmune cells.

This gives an example of a pathogen releasing multiple toxins, although there are other pathogens such as Clostridium tetani which release a bolus that consists of only one toxin. So, it can be one or the other.


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What is the difference of function between palisade and spongy layers of leaf?
I was just wondering that, what are the differences between the spongy and palisade mesophyll cells?

Did you do any research at all before asking? Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Well I'm assuming that you already have a fair idea of the structure of a leaf (of course, why else would you ask this question), so I'll just come straight to the point.
The major difference between the two is that the palisade layer lies just above the spongy layer, and vice versa. That's understood.
So firstly, the palisade layer consists of closely packed cylindrical/rectangular cells, while the spongy layer has loosely packed cells with many air pockets.
Secondly, these cells mentioned above are cylindrical/rectangular in the case of palisade layer, and cells in the spongy layer are rounder in shape.
Thirdly, cells of the palisade layer contain more chloroplasts than the cells of the spongy mesophyll layer. A probable reason is that since the spongy layer is comparatively much further into the leaf, it doesn't get as much sunlight as the palisade, which is a lot closer to the surface.
Lastly, palisade layer helps in photosynthesis, (in fact palisade cells are the site of photosynthesis) while the air pockets in the spongy layer allow exchange of gases like CO2 required for photosynthesis. So there's a difference in function.
There are also other differences, since the spongy layer contains other components like  vascular bundles, but I believe these are the major ones.


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What is the evidence that mammals are unable to process excess sodium chloride?
I grew up hearing the mantra

excess salt causes heart disease

I had a vague understanding that it caused deposits in the body or something. Now that I give it more thought - I come up with three vaguely plausible explanations for this:

kidneys have a fixed limit on how much sodium chloride they can filter from your bloodstream in a day
excess salt has an effect on oxidation/redux reactions or acid/base levels that means your body's chemical reactions aren't performing optimally
the excess ions mess with other reactions in the body

When I take the 'devils advocate' argument in my mind - my plausible arguments are:

how can salt cause deposits in the body? It would simply dissolve in the bloodstream
surely the body has sufficient chemical mechanism to flush out surplus sodium ions

Now the author here makes the following claim:

The entire field of research around salt is a colossal [stuffup], for a fairly simple reason: sweat is salty. If you sweat, due to exercise or high temperatures, you lose about 1g/L of sodium. So right off the bat, all the research that's trying to find a population-wide correct amount of sodium to eat is on a wrong track, because there's no such thing.
But it's even worse, because most of the research doesn't measure the amount of sodium people take in through food, it measures the amount of sodium they lose in urine. This isn't their intake, it's what's left after losses, so it's confounded by exercise.
And it's even worse than that, because while the actual studies indicate that there's no benefit from cutting salt intake, some high-status organizations once said there was, and are acting as though they can't take it back without losing face.
The overall result is that there are a bunch of people shouting "less salt!" and a bunch of people shouting "the same amount of salt!" and no one has any model of how much salt they actually need, so they occasionally end up deficient.

In addition, the article here claims:

...there are the epidemiologists whose research appears to point in the other direction. They track the connection between salt and deaths from heart attacks and strokes, and their studies indicate that while heavy salt eaters did die sooner, there is little evident danger from the average American’s intake.

My question is: What is the evidence that mammals are unable to process excess sodium chloride?

Good question. I don't know the answer, but this article http://www.scientificamerican.com/article/its-time-to-end-the-war-on-salt/ claims that there is no consensus in the field that high salt intake has any adverse effects.


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Can animals also get Down syndrome?
I heard that animals cannot get Down syndrome or trisomy. Is that true and why can't they get it? They also have chromosomes.

Note that Down's syndrome and trisomy are two different things, where the former is a special case of the latter.

Animals can be generated with genetic defects similar to Down Syndrome, but not that exact condition, except in the case of great apes.
Down Syndrome is a kind of defect called a chromosomal abnormality, meaning that either there is an extra chromosome or an excessive repetition of the same genes on a particular chromosome. In the case of Down Syndrome, that repetition in on a region of the 21st chromosome. Similar abnormalities in other chromosomes are possible, such as the abnormality which causes Klinefelter Syndrome.
Although animals do have chromosomes, they have different chromosomes than human beings do. For example, a horse has 32 chromosomes whereas a human has 23. Apes are most similar to humans, having 24 chromosomes. Therefore, if trisomy is to be found, apes would be most likely to have it. Researchers have attempted to answer this exact question and there is a paper on the subject entitled "Conservation of the Down syndrome critical region in humans and great apes".
The result of this study was that the area on chromosome 21 in humans that is responsible for trisomy is found analogously on chromosome 22 in apes and that apes can, indeed, get Down Syndrome, if they have duplication of this region. There do appear to be apes that suffer from this condition. The band diagram for both chromosomes is shown below:

where "H" indicates human and "C" indicates chimpanzee.

It depends on the animal, some can get it, others cannot.
Down syndrome is the result of an extra copy of the twenty first human chromosome. So, it is a rather humanly genetic problem.
However, the closer an animal is to humans, the greater the chance of it being at risk of suffering from down syndrome.

There have been several chimpanzees found with Down Syndrome. As the syndrome is caused by an extra copy of a specific chromosome (chromosome 21 in humans) only animals closely related to humans have a similar syndrome. Extra copies of other chromosomes cause even more serious syndrome and most are not compatible with life. To study Down syndrome, scientists have created mice that have extra copies of the same genes found on human chromosome 21. These mice have some of the features of Down Syndrome.$^1$

There had been some uproar a couple of years ago around a tiger (they have 19 chromosomes) who supposedly had down-syndrome. The tiger "Kenny" was called the tiger with down syndrome, however that is not true. His appearance and mental retardation was due to aggressive inbreeding.

A great benefit of having two copies of each of our genes is that damaging recessive mutations are seldom expressed. However, where parents are closely related there is a high chance of them both carrying the same rare version of a gene, with a one in four chance their offspring will inherit it from both sides. With enough damaging alleles in common this becomes like a repetitive game of Russian Roulette.

References:
1. https://www.genome.gov/dnaday/q.cfm?aid=788&year=2008