text:
What is the term for all of the RNA in a cell at any given time?
Question is asked above, simply put.

Transcriptome..

@WYSIWYG, I think that is more like the RNA profile, as opposed to total RNA?

@AliceD It means all RNA. When you want to imply profile you usually say transcriptome profile or transcriptome profiling (the process of finding the profile). For miRNAs they say miRnome profiling. Also terms like dynamic transcriptome etc have been used.

You have to clarify your question: in what context do you want to use the term? Total RNA as a term is used generally in the sense of RNA isolation but not in the sense of cellular processes i.e. you won't say we studied the effect of stress on total RNA. Total RNA is used when you mean all RNA lumped as a whole and transcriptome is used in the sense of collection of all RNAs.

@WYSIWYG it's not just the transcriptome (mRNA), as there are also transfer RNAs, micro RNAs, ribosomal RNAs, etc.

@MattDMo Transcriptome includes all RNAs, not just mRNAs (anything that is transcribed). People usually are not interested in rRNAs in their analyses; so they exclude them. That's why probably most readers may have an impression that transcriptome means just mRNAs.

@WYSIWYG you're right. My bad :) When I think of transcription, for some reason I only think about protein-coding genes, which are transcribed and processed into mRNA. I'm more protein- and cell-focused than gene-focused, which probably explains why. I forgot that every RNA is coded in the genome. TIL.

I'd agree with WYSIWYG. The two are usually used in a different sense. Total RNA is typically used when referring to the sum total mass, as in RNA isolation, but not the composition (on the level of specific RNA expression patterns). Transcriptome is typically used when referring to the relative expression of each individual RNA transcript within a cell.

Qiagen and Life Technologies call it  RNA content, total RNA, or total cellular RNA.

i hear 'total RNA' often


text:
Skin extra sensitive to heat after burn
I just got my finger burnt (first degree burn $\Rightarrow$ I didn't even bother to bear the wound). It didn't hurt much, even when I pressed the wound.
However, when exposed to heat (hot water, but not so hot to hurt undamaged skin), the pain became at least nasty.
Is it an evolutionary adaptation to avoid hot objects not to get burnt again?

All traits that you observe have accumulated because of evolution. Is your question on enhanced sensitivity of burn area about its "how" or "why" ? Your reasoning on "why" is plausible and there is nothing much to say about that. Most "why" questions tend to have a philosophical aspect to it because we can at best, only make sensible guesses.

The burnt skin is extra sensitive because it is injured, just like a broken bone or a cut - it is the body's way of saying be gentle. The general evolution of pain, and sensitivity, acts to teach us to not repeat dangerous/harmful things, but this does not explain particularly why a burnt bit of flesh is extra sensitive.

Local inflammation (nerve receives inflammatory signaling molecules from its local environment) and direct injury can both increase the sensitivity of nociceptive (pain/noxious stimuli sensing) nerves. This sensitivity can drive animals to guard the injured area. This may be beneficial to survival. Persons unable to sense pain often accidentally self-injure, perhaps further sensitization helps protect the weak/injured area). So it's plausible, but as WYSIWYG said, we cannot prove why this behavior arose. We can only make reasonable conjectures.

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Need some good resources to learn about Protein function and structure
I'm taking a course on biochemistry at edx.
Since I'm a computer science student, I'm having some trouble in understanding many biochemical concepts. While the first module was just fine, I found the second module really hard to understand. I have problems to learn and understand about amino acids and proteins, so I would like to study apart from some good resources.
Which is a good resource to learn about amino acids and macromolecules?
Also, please let me know if this book is up to date?

Lehninger Principles of Biochemistry is a good text book.

Hello George. It would be much easier for others to answer your doubts if you ask about a specific doubt. There are a lot of things to know about proteins and we cannot know what the second module has that you do not understand. See the tag-wiki on book recommendation. You should address all those points otherwise we cannot suggest a good book as per your requirement. Alternatively, you can ask clarification for your doubts here but make sure that you do not ask too many questions in a single post.

If amino acids and macro molecules are what is troubling you, then just read any biochemistry textbook printed within the last few years.

I personally prefer Berg Stryer Biochemistry alot compared to Voet Voet Prat. There's also the lectures from Kevin Ahern. and there's a book by Ahern as well. As you see these preferences depends on each individual even though a particular text book can be recommended by a course. Another reference is "The Cell" since biochemistry is a study at molecular level and provides indepth explanations on DNA and Protein synthesis.

https://en.wikipedia.org/wiki/Ramachandran_plot

Given your background (not a biologist or chemist) you would probably find the introductory material in a biochemistry "lite" textbook more accessible/useful than a hardcore text for specialists.  As a co-author of a biochemistry textbook, I can tell you that there are essentially three different classes, or types of texts.

Comprehensive textbooks, of which I think Voet & Voet is an outstanding example, are designed for biochemistry majors who will be taking a full year, in-depth course, typically in the 3rd year of their undergraduate studies.
The general introductory texts are usually thinner, and are designed to whip through the same material in half a year--aimed at life-science students in other majors. Some of these books that I described as "lite" are further targeted to, for example, nursing, medical, or dental school students.
The third category of text tries to be multi-purpose, and appeal to both markets. The current versions of Stryer and Lehninger fall into this class (they are both excellent in my opinion); the instructors can cherrypick the readings if they want to use the book for a half-year course.

Voet, Voet, and Pratt (mentioned in the comments above) is a very good diluted version of Voet & Voet. As you can also tell from the comments, different texts have different flavors, and so which one is best depends on the reader.
It sounds like a more general "concept" based book might be useful for you (to provide background and context). The very thick "Molecular Biology of the Cell" by Alberts et al., has a lighter cousin named Essential Cell Biology which would be well worth looking into.
Keep in mind that when tackling a university-level biochemistry course the instructor has to assume that you have passed university level introductory courses in general chemistry and in organic chemistry. Biochemistry majors typically complete full year courses in both these subjects, as well as a watered-down version of physical chemistry.

I want to add a book to the list that may be easier for you since it takes it from the perspective of Physics:
Finkelstein & Ptitsyn, Protein Physics, Academic Press (2002). ISBN 0-12-256781-1.
It covers structure, thermodynamical processes in proteins, mechanism of folding, function, a bit of bioinformatics. It is designed as a master level course in Biophysics, but it takes most things from the beginning: it even explains what the partition function is (but it helps if you know it already). No prior knowledge in biochemistry is required.

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Negative association between habitat quality and reproductive success in birds
I'm looking for bird studies that have found either a negative correlation or no correlation between habitat quality and reproductive success.
Or in other words, bird studies that have found that reproductive success was lower in lower quality habitats. Or, that have found there was no difference in reproductive success between habitat classified as high quality and low quality.
Can anyone help?

Do you mean studies where the habitat quality was assigned before gathering data on reproductive success (i.e. based on other data sources)? Habitats where the reproductive success is low is often considered to be "poor" habitat post-hoc.

Yes where habitat was classified as low quality before high reproductive success was found

I've been part of one paper that estimates habitat-specific survival rates and population growth rate (to evaluate quality), with habitats relating to field-layer height, where there was a rather clear idea of what should correspond to "good" and "bad" habitats, see Arlt et al (2008). Habitat-Specific Population Growth of a Farmland Bird. PlosOne. Does this seem like a suitable study to your question?

Google Scholar pulls up some useful looking options


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Book recommendation on the human muscle system
I would like to learn more about the exact mechanism behind our movements, especially about what happens during intense training when anaerobic state arises.

You can get reviews on those topics. What level of information do you expect?

@WYSIWYG I would like to dig really deep into this topic, so something around university level would be excellent, if that's what you meant by your second sentence, but I'm afraid, I didn't understand it.

You answered my second sentence. I think reviews would be also good.

1. Fundamentals of Anatomy & Physiology by Martini and Campbel Biology are quite useful. 2. Have you seen this one? Muscle: Fundamental Biology and Mechanisms of Disease


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How does decreasing surface tension of lipids help to emulsify them?
According to my chemistry book, water has higher surface tension than lipids. But in my biology book it is written that "the gall forms an emulsion of water and lipids by lowering the lipid's surface tension". This will increase the difference between the two substances even more. How can this be beneficial?

Edited to "surface tension" as the original phrase appeared meaningless in context. If I have missed something, please do revert it.

This is essentially a physical chemistry question.

lipids have surface tension - and that's a good thing since it helps hold the cells together!  - that seems like biology to me.  its not clear to me what the 'gall' is but i imagine a non polar or amphipathic (polar and non polar) additive to the mixture will increase the solubility of the lipids in the mix

@shigeta I believe the "gall" means bile. https://en.wikipedia.org/wiki/Gall_%28disambiguation%29

Yes, gall is bile . I am not a native english speaker.

There appears to be either a typo or transcription error in your textbook.
According to this Nuffield Foundation and Royal Society of Chemistry article

Molecules of most detergents and soaps are long chain hydrocarbon
  molecules with an ionic group at one end, usually carrying a negative
  charge, thus making it an anion. This charge is balanced by the
  opposite charge of a soluble cation, for example Na+. The long
  hydrocarbon chains do not interact well with water molecules, and many
  of them are effectively ‘squeezed out’ to the interfaces between the
  water and the air or the glass sides of the beaker. The effect of
  these molecules on the water surface is to considerably weaken the
  forces between water molecules there, thus lowering the surface
  tension.

Soaps, detergents, and bile (all examples of amphiphilic compounds) act to reduce the surface tension of water, not the lipids.

Now it makes sense to me! Thank you for help!

That is why they are called "surfactants"

Surface tension is about how much energy you need to create new surface between not mixing materials e.g. water and lipids. Surfactants like bile makes this easier (lowers the energy required). So they can form small bubbles of lipids: micelles, which can be handled much easier by the digestive system. Another usage of surfactants to make foams, creams, etc... physical-chemistry / surface rheology is all about them.


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Physiology of tricuspid and bicuspid(mitral) valves
The tricuspid and bicuspid valves are atrioventricular valves. Both are valves that prevent backflow of blood pumped from the atria to the ventricles. However, the former has 3 "flaps" while the latter has 2.
Despite searching the internet, I could not find a biological explanation for this difference.
Might this be just a relic of evolution or some sort?

An interesting question. Someone has asked it over here and you may find it useful. From fluid dynamics perspective and given heart's mechanism, there might be a really awesome reason behind it.

During embryogenesis at the level of an atrioventricular canal there is so called endocardial "cushion" tissue. This tissue bulges to the left side more than it does to the right and contribute to the fusion of the valvular ring to a one leaflet, while from the remaining part of the ring develops the second leaflet:

AVEC = atrioventricular endocardial cushions
As has been stated, the cushion tissue bulges more to the left, thus on the right side where the tricuspid valve is forming the leaflets does not "merge" and develop into three-leaflet valve.
Interestingly, this left side "suture" might sometimes fail to develop with resulting three-leaflet mitral valve.


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Are grasshoppers monogamous?
Noticed two grasshoppers jumping together on the porch, and started wondering if they are monogamous? I am aware they have males and females.

Interestingly enough, there are insects that are considered to be monogamous, including cockroaches and other beetles. However, I couldn't find anything on grasshoppers.

which species - there are many grasshoppers, mating system could vary greatly within that.

Male grasshoppers often mate several times with multiple female, and some females will mate again after, and perhaps even before they lay their eggs. So no, they are not monogamous.
Rufous grasshoppers for example have a very special mating cycle, the male will attract other females, possibly more than one with "pursuit sounds". After copulation, he keeps her close to prevent other males from mating with her, and the females enter a defensive mode where they refuse intercourse from other males. After laying eggs however, she enters a "relaxed" mode where she is open to others for mating.
Sources:
jrank
Rufous grasshopper: inaturalist

"some females die after lay eggs. So you could perhaps consider them monogamous" - this doesn't rule out multiple mating by males so is not monogamy


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Is MHC1 knockout sufficient to prevent transplant rejection?
A few days ago I read about MHC1 knockout pigs for organ transplantation research.
I was just wondering, is it enough to knock out MHC1 in the donor (lets say from same species, pig to pig) for successful transplantation?
I understand that someone without MHC1 is more sensitive to  viruses, cancer, to NK and more. But the study pigs lived fine, so in theory it is possible to have knockout MHC1 and survive.
But is it enough for successful  transplantation from one pig (donor with knockout) to another (fully healthy, normal pig) ?

No, MHCII mismatch can also lead to transplant rejection, though through different mechanisms. CD8+ Tcells (that recognize class I) may become activated and directly kill donor cells*, and some NK subtypes can see the lack of self MHCI and also induce cell death.
MHCII mismatch on antigen presenting cells (APCs) brought along in the tissue may activate CD4+ (helper) Tcells, which do not kill directly. However, they can secrete a lot of pro-inflammatory cytokines which will make a generally hostile environment, and can also activate b-cells to produce antibodies against minor histocompatibility loci.
As to your other question, lacking MHCI entirely would be really rough on an animal in the wild, but under laboratory conditions where pathogens can be managed a bit more, it doesn't matter so much. It's the same reason we can keep mice that have gross immunological deficiencies alive, where humans with the same defects would be screwed.

What about MHCII ? It's not on the organ. Also you talking about " lack of self MHCI and also induce cell death" but that is not the question. Also it's wrong cause pigs live well.

It's rather snide to say "You're wrong they live well" without having ever linked the paper showing this. Without the paper we don't know how far out they were followed, what immunosuppression regimes they may have been given (or what pre-treatment of the organ, etc), or how closely related the pigs were. All of these factors and more can effect the probability of transplant rejection.
Also, the organs almost certainly DO have MHCII  on resident myeloid cells. Invading myeloid cells will also have MHCII and have the potential to initiate an adaptive response against the transplant.

@VGranin - you're right, MHCII isn't on the organ tissue cells, but it's hard to remove all of the APCs from a graft. Modern transplant protocols do work to remove some of them, but it's not 100%. You asked about using MHCI knockouts as donors, I'm saying that an organ that completely lacks MHCI may be targeted by NK cells.

As to MHCI part - you asked about using MHCI ko animals as donors. I'm saying that lack of MHCI on the donor tissue may cause it to be targeted by NK cells. Not sure what you mean by "it's wrong because the pigs live well." Could you clarify (and as @InactionPotential alluded to, link to the study in question)?

http://www.ncbi.nlm.nih.gov/pubmed/25339675

It's an interesting paper, but there are some limitations to your understanding re: they live well. The paper says at the time of publication they were 7 mo old. It does not describe were they are kept, but likely in a highly controlled research facility. For comparison, we keep a number of strains of immunodeficient mice in our facility that wouldn't last a week outside. They are at lower risk of serious infection than your everyday farm/wild pig.

Also, regarding NK cell killing and lack of MHC-I: NK cells undergo a maturation process to a so-called "licensed phenotype" (licensed to kill, ha ha). Immature NK cells are poorly capable/incapable of killing other cells. Maturation into an effective killer involves a process that requires MHC-I expression (based on numerous mouse studies, likely applies here). In animals that do not have MHC-I, the NK cells likely never develop the potential to kill MHC-I negative cells. So they are protected from their own NKs, but licensed foreign NK cells (as in a transplant) could still kill them.

@InactionPotential... Ok, but it doesn't meter how well 100% MHC1 knockout pig lives. Interesting only the transplantation of liver, for ex., with MHC1 knockout to a fully healthy pig. So the NKs of the healthy pig, will attack the liver because it's with no MHC1? But doesn't it will be better than foreign MHC1 that we have now in transplantations?


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Sex biased gene expression in the X chromosome
It has been shown that the X chromosome is frequently enriched for female biased genes, and has a deficit of male biased genes. For example in this paper, and this one.
However, I'm struggling to find papers which test the general distribution sex-biased genes. I am trying to find out if the X is enriched for sex biased genes, e.g. if the X hosts 20% of all protein coding genes, it would be enriched if it carried 30% of all sex-biased genes.
Are there any such studies?

I think I found an answer tucked in the methods section at the back of the Allen paper where 15% of sex-biased genes were X-linked, I'd suggest this means that 15.55% ($100 \times (\frac{1075}{1075 + 4938 + 4323})$) of sex-biased genes are X-linked - other examples are still sought:

"Genes associated with chromosomes 2 (4,323 genes, 37%), 3 (4,938
  genes, 43%), and X (1,705 genes, 15%) were used in the analysis; these
  chromosomes accounted for 10,967 (95%) of the genes... a further 547
  (4.7%) of the genes ... were omitted"

You can answer this question for yourself using the modMine data warehouse for modENCODE datasets.  All you need is a list of female-specific genes (using your identifier of choice, although FlyBase FBGxxxxxxxx are the simplest). You can use their list tools to upload your own list of identifiers, and then there are a bunch of widgets that will tell you things like GO Term enrichment, PubMed references, and one is a histogram plot showing the chromosomal distribution of your genes, and a second histogram showing the "expected" distribution. Access to many modENCODE sites can be found at www.modencode.org
Okay, I went and did this myself.  modMine was quite slow, but fortunately the intermine server at FlyMine is working fine.  I downloaded Supplemental table 25 from Graveley et al., Nature, 2011 and cut and pasted all of the "Female Biased" IDs for those rows that had FlyBase Gene Identifiers.  This figure shows the chromosomal distribution of the 928 genes:

The Labels on the X-axis do not line up properly (for some reason), so here is a table with the Chromosome names and the counts:
Chrom     Actual    Expected
2L:     157      169
2R:     176      186
3L:     143      173
3R:     174      217
4:       0       10
X:     264      150


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Can beavers control the direction a tree falls?
We humans can easily control the direction a tree falls by making a number of strategic cuts, essentially creating a hinge:

This prevents trees from falling on equipment and people and sets them up in a good location for the subsequent processing steps. I'm curious if beavers also perform directional felling and, if they do, how do they choose the direction (eg to fell the tree towards the damn, in a river, away from thick brush, etc)?

In this picture (and others), it appears as though the beaver has created a hinge. Is their any method to their technique or do they just start chewing and hope for the best?

As far as I know, beavers do not control this process.

It is difficult to find a scientific answer to this question, but let me insert this citation from a specialist site:

Contrary to popular belief, beaver cannot plan the direction in which trees will fall. Many trees become hung up in the branches of surrounding trees and are lost to the colony. In heavily forested areas, this loss may amount to one-half of the trees felled.

Another source says the same.

But scientists think beavers may actually plan the direction of falling:

By measuring the falling angle of 888 trees of a variety of sizes cut
  near 8 different dams in southwestern Saskatchewan, we tested the
  hypothesis that beavers (Castor canadensis) fell trees in a non-random
  direction. We predicted that trees would be preferentially felled
  towards the dam to minimize the costs of transporting materials to the
  dam and to minimize the amount of time beavers spend on land. We
  established a 150 m wide × 250 m long transect at each dam and
  determined the felling angle of at least 100 aspen trees cut in each
  transect. We found that trees were felled by beavers with a mean
  felling angle of 357.9°, a direction not significantly different from
  that of the dam. In all, 62% of trees were felled within 45° of the
  direction of the dam. While our data are consistent with the
  hypothesis, an experimental test is required to establish the
  reason(s) for the pattern we found.

Their picture is better than thousands of words:

And another paper:

We studied patterns in the orientation of cutting when beavers (Castor canadensis) cut trees around Alum Creek Lake in central Ohio. For 462 trees, we measured the slope at the base of the tree, the orientation of the cut relative to this slope, the distance of the tree from the water, the radius of the tree, and the symmetry of the cut. The land around Alum Creek Lake generally slopes toward the water, so to direct the fall of a tree towards the water a beaver should cut a symmetrical tree from the downhill side. Cutting from the downhill side occurred for trees >9.0 m from the water. Near the shore, trees tended to lean toward the water and would fall toward the water regardless of the side from which the beaver cut. At distances <9-0 m from shore, beavers cut predominantly from the uphill side where it should be easy to sit and there is little danger of the tree falling on them. At all distances, beavers showed random orientation when cutting trees on shallow slopes (<20°), whereas on steep slopes (especially slopes >30°) they cut predominantly from the uphill side. Beavers cut small trees (<5.0 cm diameter) mostly from the downhill side, but tended to cut trees >5.0 cm in diameter from the uphill side. Overall, enough factors interacted that no single pattern of cutting existed for all trees.

@Remi.b I've mentioned the study that actually tried to check the theory. They found some correlation :)

@Remi.b this sentence relates to your point - that the actual studies are scarce. Of course, if we have some budget and grants we can check any theory we want $)

Thanks for the answer. Actually, that study did not conclude that the beavers planned the direction of fall, only that there was a correlation between the direction of fall and the direction of the damn. I'll wait and see if anyone else can dig up some more recent/conclusive study, but I have been unable to and will likely accept your answer later.

There's this paper, which finds that the direction a beaver cuts from is related to the terrain slope, tree lean and distance from the shore, which implies that they are felling directionally.

@llan Oh ok. Intuitively, in my head it sounded a bit like "testing is too complicated" rather than "probably nobody cared about testing this". All good then.

@canadianer yep, I mentioned it :)

Sorry, I meant to link to this paper: https://kb.osu.edu/dspace/bitstream/handle/1811/23987/V103N5_143.pdf?sequence=1

@canadianer Believe me, poor beavers do their best to fell the trees in a right direction. They just don't have sufficiently long arms to handle the appropriate axes as humans do. Thus, they have no choice - they use their teeth and lost directions because of dizziness caused by their circular movement.... $%))

This is exactly what would be expected: beavers would be expected to try to fell directionally (towards the dam or, if necessary, avoiding obstacles) as there is an advantage to the individual and therefore an evolutionary advantage. On the other hand (especially regarding obstacles) they would not be expected to show the same degree of judgement as an experienced human lumberjack.


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Sense and anti sense strand
Why the sense strand is only involved in transcription though the antisense strand just has the compliment strand of the sense strand?

I don't understand your question. The sense (coding) and antisense (template) strands are defined by which strand is transcribed.

Is there anything that always a particular strand is transcribed

I mean when the sense strand is being transcribed for one gene why can't the antisense strand can be transcribed simultaneously for another gene as both strands contain the same genetic material

Which strand is transcribed depends on the gene. The terms sense and antisense are only useful when talking about a single gene. Between genes on a chromosome, a DNA strand may be sense for one gene and antisense for another.

This paper presents an interesting idea that the 2 classes of amino acyl tRNA synthetases originated as 2 genes on opposite strands of a double-stranded RNA. This would be helpful in a primitive mostly-RNA world where making long RNAs would have been hard and overlapping the genes would save space.

The short answer is the transcription machinery will only bind on the correct orientation.  The binding of proteins and such to the promoter DNA strand is determined by the sequence of the DNA, the sequence is not correct on the anti-sense strand for a given gene.

One of the reasons why DNA is double stranded--this means DNA has sense and antisense strands--is to make a copy.
During transcription, RNAs are transcribed referring to anti-sense strand sequences--making base pairs with anti-sense strand. In other words, the sense strand does not do anything during transcription.

Either strand of DNA can be sense or antisense.  SWBarnes2 posts that the "transcription machinery will only bind on the correct orientation" and that is indeed what determines which strand is sense.  But note his important statement "the sequence is not correct on the anti-sense strand FOR A GIVEN GENE" (my emphasis).  As you move from gene to gene, the sense strand can swap strands.  Coding sequences can overlap running in opposite directions, making both strands sense; this is more commonly a viral trick.  Sense and antisense are defined by what sequence is found in RNA and so the map of sense and antisense strands on DNA is complicated. As you move along a strand of DNA one strand might be sense, then the other, then both, then neither.


text:
Peculiarity of chemo senses
We can easily recall our visual stimulus and auditory stimulus but why can't we recall chemical stimulus like smell and pain?
We can recall a song or picture but we can't exactly recall smell and pain. Why is that so?

This appears, at least to me, a very subjective question that would have to be discussed philosophically rather than with empirical evidence. An interesting topic nonetheless!

Olfactory memories are among the most powerful known. They are so strong that copious salivation occurs when people are directed to think of biting into a lemon or a sourball. What is the basis for your question?

I mean can you imagine a smell of jasmine as visualizing it?


text:
Can anyone Id this flower?
Small pink flower, started out as tiny buds, leaves look almost like Maple leaves..

Welcome to Biology.SE. Try to tell us as much as you can about this flower. In which country did you find it? Which environment? What season? Do you know if it is a wild species or an ornemental species?

Location information is extremely important to species id questions @LindaMarie

It's a mallow.

The leaves - they look like maple leaves - and the flower are identical.
Mallows are from the family Malvaceae, which includes food plants (okra, cocoa beans, kola nut), economic plants (cotton), and ornamentals (e.g. hibiscus) One species of this family (Althaea officinalis) is actually the original ingredient to make marshmallows.
I'm not sure which mallow it is (there are 243 genera with 4225+ species), but it's a common weed wildflower all over the world.

Nice answer - I agree on the classification, it's a shame theres so many species

@rg255 - Thanks. Yep. I've seen this one on my own property, and couldn't narrow it down further. There are so many. I've seen marsh mallow, rose mallow, and a bunch of others, but this one I could not identify.


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Color vision across species
Is it true that color vision is sex-linked for all species with binary sexes? Is there an evolutionary significance to the fact that color vision is X-linked in humans? E.g., only female humans can be tetrachromats.

Welcome to Biology! What exactly do you mean with color differentiation? Note that one out of three cone opsins is coded on an autosome

Thanks!  I just mean having fewer or extra cones in general, I suppose.  Since colorblindness and tetrachromacy are both strongly associated with a single sex in humans, I was just curious whether that was a trend in other species.

The cultural significance of X-linked color blindness would be POB, I would guess.

I agree with @anongoodnurse and have removed the cultural aspect from the question. Please feel free to roll back though.

Thanks for the edits.  But sorry, what's POB?

POB= primarily opinion based.

Short answer
Human females do not benefit much from an extra cone class, as color discrimination is hardly affected in most tetrachromats. In fact, tetrachromats often show increased error rates in their color discrimination. In dichromatic New World monkeys the heterozygous females do functionally benefit from their extra cone as they gain trichromatic vision.
Background
Anomalous trichromats have all of their three cone types to perceive colors, but one type of cone perceives light slightly out of alignment. There are three different types of effect produced depending upon which cone type is affected.
The different anomalous conditions are protanomaly (reduced sensitivity to red light), deuteranomaly (reduced green sensitivity - the most common type) and tritanomaly (reduced blue sensitivity - extremely rare). People with deuteranomaly and protanomaly are collectively known as red-green colour blind and they generally have difficulty distinguishing between reds, greens, browns and oranges. They also commonly confuse different types of blue and purple hues. Red and green cones are indeed coded on the X-chromosome.
One source of variation is the very common Ser180Ala polymorphism that accounts for two spectrally different red pigments and that plays an important role in variation in normal color vision as well as defective color vision. The most common source of variation is the existence of several types of red/green pigment chimeras. The red and green-pigment genes are arranged in an array on the X-chromosome with one red-pigment gene followed by one or more green-pigment genes. Recombination events have given rise to red/green hybrid genes and deletion of the green-pigment genes. Only the first two genes in the tandem are expressed. The severity of red-green color vision defects is inversely proportional to the difference between the wavelengths of maximal absorption of the photopigments encoded by these two genes.
Females who are heterozygous for red and green pigment genes that encode three
spectrally distinct photopigments have the potential for enhanced color vision, as they are effectively tetrachromats (Deeb, 2005, Neitz et al., 1991). However, sensitive color-contrast testing on 43 tetrachromats has revealed that most of these females have no deviating color-discrimination whatsoever. 8 subjects showed relatively small effects, while only one showed a clear increased sensitivity in a narrow range of frequencies. It is believed that the human visual system is not plastic enough to cope with the extra spectral input. In fact, in the group there was an overall increase in error rates on some color tests (pseudoisochromatic plates, and Nagel anomaloscope color matching) (Jordan & Mollon, 1993).
In New World Monkeys, however, the situation is different. Squirrel monkeys are basically a dichromatic species, but two-thirds of the females are heterozygous, and gain trichromatic vision by expressing two of three possible alleles coding for pigments in the middle- to long-wave range of the spectrum. X-chromosome inactivation serves to segregate the alternative allelic products in different subsets of cones. The visual system of the heterozygous female is apparently plastic enough to take advantage of the presence of three classes of cone, because heterozygous monkeys have enhanced color selectivity in the red-green range that are impossible for all males and for homozygous females. This advantage perhaps enables the heterozygote to judge better the ripeness of fruit, or to find fruit or conspecifics (Jordan & Mollon, 1993).
Note that the emergence of trichromacy in humans and some other primates was the result of the red/green gene duplication. Trichromacy in primates was evolutionary selected for likely because of the enhanced capability to discern (ripe) fruits (Lucas et al., 2003). It has nothing to do with sex-differences, because not many human females benefit from tetrachromacy in terms of enhanced color vision.
References
- Deeb, Clin Genet (2005); 67: 369–377
- Jordan & Mollon, Vis Res (1993); 33(11): 1495-1508
- Lucas et al., Evolution (2003); 57(11): 2636–43
- Neitz et al., Science (1991); 252(5008): 971-4
Further reading
- Is our color vision calibrated to sky, vegetation, and blood?


text:
Why are our bodies created to itch when histamine is released by our immune systems?
Why do bug bites and cuts itch when scratching them clearly doesn't help us survive? Did our early ancestors need to rely on this itching sensation, or is it just that the receptors for itches just happen to be stimulated by histamine?

I guess itching, just like pain, is a signal to the organism that some part is injured.

Scratching is getting potentially poisonous or at least irritant substances out and removes lodged insects like ticks.
Removing subcutane parasites like scapies mites is not feasible without scratching yourself bloody.
I don't see how "scratching them clearly doesn't help us survive".  Behaviors and skin reactions evolved way before our modern hygiene and parasite cures.

Please support your answer with references.

Can you please add some references to your answer?

Answer
While itching and pain are related, research indicates that these sensations are caused by distinct nociceptors. Essentially, wounds itch because histamine is released as part of the wound healing process, and histamine activates those itch nociceptors. So perhaps the more apt question is just "why does histamine cause itching?" (See also answer to What is itching?)
As of now, we might only be able to speculate.
Educated guessing
The following are a few hypotheses:

Selecting for more specific itch nociceptors, which would incorporate some mechanism to prevent itching of wounds specifically, doesn't help influence survival enough to be useful, or would impose a cost more severe than the benefit.
Itching wounds may have caused ancestral species to remove contaminants, IE by licking them.
It could be a vestigial adaptation, a simple signal saying to the original "something happened here, do something about it!"

References

New insights into the mechanisms of itch: are pain and itch controlled by distinct mechanisms?
The accelerating effect of histamine on the cutaneous wound-healing process through the action of basic fibroblast growth factor.
Physiology and healing dynamics of chronic cutaneous wounds.
Histamine-induced itch and its relationship with pain
Histatins are the major wound-closure stimulating factors in human saliva as identified in a cell culture assay.

Now I'm all itchy.

Some insects produce chemicals to induce itching in order to further spread eggs laid in the wound. Some micro-organisms do the same, a cut may be infected.
It's perfectly possible that the urge to scratch is not beneficial in all situations but simply a majority of them. This would be more than enough reason to have the impulse stick around, evolutionary speaking.
The body does not differentiate very often between externally and internally produced chemicals.
For example, I am diabetic and take insulin, a hormone related to blood sugar. It is introduced to my blood stream from without, but my body reacts to it as if my pancreas had produced it, which is what happens in healthy individuals.
In an organic system which coordinates internally via chemical signals (hormones), it is impractical for parts of the system to attempt to screen out externally introduced chemicals, such as from a bug bite.

Thanks for your effort on trying to answer the question. Can you add some external references to support the claims in your answer? We always appreciate external reference to support all answers/questions on BiologySE - thanks for your contributions!


text:
Why does bacillus thuringiensis produce bt toxin?
Background : B.thuringiensis produces an inactive crystalline toxin during sporulation which when ingested by an insect, gets activated and causes pore formation in gut , subsequently leading to death of the insect.
Question : What is the  role of the toxin in bacteria's own metabolism ? Does it "unintentionally" kill the insects or is there an evolutionary advantage gained by the bacteria ?

Apparently the bacterium is an opportunistic pathogen. See here.


text:
What are 'factors' in biology?
My question is what does the word 'factor' mean in words like transcription-factor or nerve growth-factor? What is similar between these different compounds such that they deserve the word 'factor' in their name?
Edit: My confusion comes perhaps from the use of the word 'factor' in statistics, where it refers to a variable that can take on discrete values (e.g., the factor Gender takes on values 'male' and 'female'). Here a different meaning of the word seems to be used.

I'm voting to close this question as off-topic because it is poorly researched. https://www.google.se/search?q=transcription-factor&oq=transcription-factor&aqs=chrome..69i57&sourceid=chrome&es_sm=122&ie=UTF-8

@rg255 - I think it is fine - your (Swedish :-) google result links to transcription factor. This question doesn't ask what a TF does, it asks for the broader interpretation of 'factor'.

I'd still suggests its poorly researched (https://www.google.se/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=biological%20factors) if the OP has done research and asked about what thye specifically don't grasp it would be on topic

@rg255 - you may be right. I'd say it's borderline. The voting system will tell :)

this is googling-based question. I strongly feel this type of questions should not be dignified with an answer. Otherwise bar is pretty low

@AliceD do you think it is OK to create a question for every entry from a dictionary?

I agree this is off topic. There is no special meaning of the word factor here, a dictionary could answer this question (and did). This is about English language usage.

Yeah you guys are right. Vote2close2

I'm voting to close this question as off-topic because of poorly researched

There are many meanings of "factor" in Biology. In the context where you place it, namely bio-active substances, such as hormones and enzymes I would go for the definition given by the Medical Dictionary:

factor [fak´ter] :
  an agent or element that contributes to the production of a result.

Within this definition, a transcription factor contributes to the transcription of DNA into mRNA, and nerve growth factor contributes to the growth and survival of neurons.


text:
Does anyone know what type of Cocoon this is?

I am really concerned with this since I've never seen a cocoon this color before and can't find it anywhere on the internet. I found it just laying on the ground not attached to anything, but it seems to be alive because when you touch it, it will wiggle abit. Any answers are appreciated.

If you keep it in a box or something, you might have better luck identifying whatever comes out. It probably won't be anything dangerous.

Adding your location could help a big time identifying

I think I may have found your cocoon: it appears to be a Magpie Moth (Abraxas grossulariata) cocoon:

According to UK Moths, it's common in the UK.

I don't usually do this, but if you think this answer is correct, I'd appreciate it if you accepted it. Since it's so old, I don't think you'll get a lot of other answers.


text:
How do t-lymphocytes become mature if thymus has lost its function?
The development of t-lymphocytes are done by thymus and we also know that the thymus degenerates before puberty and we also know the maximum lifespan of WBC's is 15 days. So, how do t-lymphocytes become mature if thymus has lost his function?

A few points, I'll expand on this later and add references if I have time:

The thymus starts degenerating at puberty but continues to function in thymocyte maturation for decades, albeit at a lower level
Many mature T cells can live for years
Through homeostatic proliferation, peripheral T cells maintain their population size
Immune surveillance generally decreases with age

Note that extended lifespans and homeostatic proliferation (points 2 and 3) don't contribute to TCR diversity but only maintain the existing repertoire.

The key thing is this: yes, the thymus involutes at puberty but that doesn't halt  thymopoiesis. The thymus continues to produce naive T lymphocytes throughout our lives (even up to 70 years of age-see references) albeit at a very reduced rate. This mechanism is very important for example in HIV-infected individuals who are still able to repopulate their immune cells through a combination of peripheral T cell division and thymic production of naive T cells.
References: Reference_1, Reference_2, Reference_3


text:
Are there journals for theoretical models of protein-protein interactions?
Are there respectable scientific journals for publishing models of protein-protein interactions obtained by docking simulations? I would also discuss the biological significance of the particular mode of docking that I found through the simulations, and how it is consistent with available experimental evidence. The point is that my paper wouldn't have any new experimental evidence. Rather, I analyze existing experimental evidence in the literature and demonstrate that the model of interaction I propose explains this data. Are there respectable journals accepting this type of research? Can you post some example journals like this?
Also, can you post some references to good papers like these, hopefully highly cited, if there are any?

Several journals accept publications like this. The questions to ask are which biological audience would be most interested in the results and the expected impact of the results. Once you know these it is easier to narrow the journal search.

@Darwin Can you put some examples of journals? (And, if you have it, along with the impact points)

@becko Be careful about relying too much on journal impact factors (JIFs): yes, Nature Cell and Science do publish great research, but an article isn't necessarily great (or even decent) just because it's in one of those journals.

@DanielStandage Of course. But the impact factor does relate to the visibility of the paper.

@becko only very loosely. Many people regard it as a made up number that's doing more damage than good. Even the chief editors of cell and nature are wanting new bibliometrics.

please, move off-topic discussion in chat or elsewhere.

Protein-protein interactions is an area of biophysics, so certainly Biophysical Journal (published by Cell) is a nice place to look.
PNAS has a broad range of areas and they pay a lot of attention to nice biophysics and modeling. But also they require (seems to me) experimental evidence.
The Journal of computational chemistry certainly about a lot of simulations and modeling, so see for yourself.
As for publications, the fact that you are asking for references makes me think you haven't done your homework on literature review, as it is always first and foremost job in a research project.

I'd also recommend having a look which journals of the papers you have read and are citing have been published in. You will probably have to make a call whether you want to publish in a more methods-based journal (bioinformatics in your case) or in a more topic-based journal (biology/biochemistry/biomedicine...)

+1 Good answer. I am still deciding whether I'll begin this research project and which direction to take. I haven't found papers that are entirely "theoretical", in the way that I describe (although they support available experimental evidence published elsewhere). If you know any please post the reference.


text:
Are these termites?
These are outside a window in Phoenix, Arizona. I looked on the internet for pictures and these guys looked very similar to winged termites.

Do you have any shots from above?

@Oreotrephes no, unfortunately not, they're just sitting on the glass

Based on the pinched waist, I'd say these are hymenopterans, not termites.

They could be halictid bees, possibly Agapostemon splendens.
Yours looks very similar to this picture

(by Bob Peterson)
Compare also with this one on bugguide and to the pictures of Agapostemon species in this National Geographic article.
Compare the metallic head and thorax (that's the middle segment), the striped abdomen (the last segment), the apparent large size of eyes and place of antennae attachment, and the 'buff' hindlegs.


text:
Can we change the direction of a neurological signal?
My question is can we change the direction of a neurological signal? When a neurological signal is generated it goes to the brain. Along the way it passes synapses. Can we make it change it's pathway to go through another neurone instead of the neurone it was going to ?

With an eye to doing what with the end result?  Theoretically it's possible, but in practicality, it would be extremely complicated (dealing with axon collaterals and convergence/redundancy in higher centers).

When you write "can we"--who is "we"? A neuroscientist administering drugs to an animal? A neuroscientist using some other technology on an animal? A person exerting their will to influence the activities of the brain? I'm trying to understand what you are imagining happening, and who is involved, when this alternate routing occurs.

And do you mean change it on the fly, or permanently? I am inclined to vote for closure when this question is not clarified and/or specified.

OK jonsca you said it theoretically can be done. Can you show me a refrence that describes it with details?

"Neurological signal", or as I would put it, action potential, or activity propagation can be modeled as current in an electrical circuit. Trick is that such a circuit contains a bunch of highly regulated and non-linear and non-static elements. Imaging bunch of potentiometers (variable resistances) in your circuit. And all of them behave depending on something else in the system. So certainly currents will go somewhere, but level of control and complexity is phenomenal.
An example that should let you appreciate possibility of rerouting is simple Pavlovian conditioning. Neutral stimulus (bell) that has no evident connection to stomach, after conditioning elicits response there. Even though circuitry is very complicated and signal propagation is hard to investigate, this is an evidence that changing path of signals is very possible in some way. (Of course, conditioning require changes in higher-than-stomach systems, some intermediate levels).
On more practical note, we can readout neuronal activity in region A (of brain, muscle or else) and rely it via electrical stimulation somewhere in brain or muscle or gland. Both parts of this are available technology. As of drugs, some people report "seeing" sounds while intoxicated, this might be an example of such temporary effects.

How can neural activity being relayed to a muscle or gland? This seems to be at the heart of the question and references are needed. Further, psychotropic drugs alter brain activity not by changing connectivity but by changing synaptic activities within existing connections afaik. Here too references are needed to prove otherwise.

Also, a potentiometer although having a resistance, is a recording device and it's neural representation is unknown to me.

potentiometer is variable resistance, it can be analog or digital. Neural activity drives muscle through NMJ. You can readout muscle activity through afferent cells. I am precisely not talking about connectivity, but about changing final route. You have roads around, but take different route every day, based on traffic. In neurosystem you can do similar things


text:
Would a person live longer, if such a person lived in a planet with lower gravity? (say, Mars)
I was wondering: some companies plan to colonize Mars, many of us know.
But if one were to live on Mars, would this person live longer?
It seems to me that a lower gravity would mean less overall damage to the body cells, so they could last longer: resulting in a longer lifespan.
Or maybe lack of gravity = lack of exercise = lesser lifespan?
I'd like the opinion of some expert in the matter. Thanks.

No, reduction of gravity causes bone decalsification. Also there will be no protection from the sun's radiation in space and on Mars and that has been an issue.

Probably not. There's a thing called Hayflick limit, which is basically a limit of life expectancy caused by a shortening of telomeres with every cell division. And since most of our cells complete cycles more based on time (life cycle of RBC 100 days), and not due to damages to a cell, our telomeres would still shorten at the same rate. Of course the gravity could play a small part once organs have started failing, but there are many other factors that affect how long it takes for everything to completely deteriorate, and wouldn't have a big role. In fact, it could even shorten life expectancy, seeing as how our bodies are currently built to live in our current gravitational field. Without gravity, our muscles could become weak, causing other problems, which is why people at the space stations have frequent dedicated times to workout, to keep their muscles fit.

It sounds reasonable that reducing the physical stress on a body would reduce the wear and tear, and thus increase the owner's lifetime.
However, it's just as reasonable that human bodies are designed to be under stress, and drastically changing the environment will harm the body in subtle and even obvious ways. For instance, some research shows that lung and heart cells won't grow properly if not cyclically stretched.
Until we get some serious long-term research, in space or on a smaller planet, we won't really know.

We don't know is a valid answer, but not without resources to support it, or evidence of effort in not finding anything on the topic.

Is leaving a reasonable question with no answer better than giving the best answer that you have?


text:
Does "squinting" make you concentrate better on a logic test?
We have all had those moments of intense concentration on some tough exam, perhaps a college test or whatever...
Why is it that when we squint, it feels like we can focus and concentrate better on the test, and get answers more easily?
Do we actually get a better mental performance when we are squinting?  If so, why?

Isn't it a social tool to show others you're thinking. Could you cite something that actually says it helps focus?

@GoodGravy the use in the situation you mention is correct. But and additional usage, at least for me, is when attending a lecture and if very sleepy, closing my eyes or even keeping them half closed reduces drowsiness and increases focus on the talk. My guess is it has something to do with reducing resource consumption. Or maybe an effect similar to what happens with blind people that get other senses enhanced. But these are just wild guesses, can't back them up.

@ddiez Sorry to be awkward, but when I'm squinting due to tiredness I'm straining to keep my eyes open, not enhance my focus! It's semantics sure, until you assume it enhances normal focus. If you don't think Ilan's answer is correct I think you're mixing up "enhanced focus" with something else.

@GoodGravy, OK. Are we talking about sight focus or mental focus? In my case I am talking about mental focus (i.e. the ability to enhance concentration). It seems to me that the OP refers to this meaning whereas Ilan's answer is dealing with sight focus (and in that regard it seems like a fine answer to me).

@GoodGravy To add a bit more detail, when tired, of course I also have to force my eyes open because they tend to close themselves. However, if I give up and close my eyes or put them half opened, then I somehow get a bit of relief and can concentrate better. Also, when thinking about some difficult problem, like mathematics, sometimes I close my eyes and that allows me to concentrate better in the problem. I have seen others doing the same... but maybe it is us! Again, all this refers to mental focus rather than sight focus.

The phenomenon in question is probably related to people with uncorrected/undercorrected myopia.
This "ancient" phenomenon is called stenopeic slit effect (a case of pinhole effect): when the person squints the visual acuity becomes better because of smaller blur circles: the "slit" between the eyelids is the key point improving blurring.
One can check if it works by creating slit in paper or plastic:

Some "charlatans/witch-doctors/quacksalver/etc" can "treat" refractive error with pinhole/stenopeic glasses:

It is known that children with refractive errors have attention issues because they cannot see the objects sharply (this is why they can be mistakenly diagnosed with ADHD), thus your concentration improvement related mostly to your vision improve and not a better "understanding".
If you mean by squint using mimic muscles and corrugator muscle the answer should point out that not a "squint" improves your concentration, but your attempt to improve your concentration causes this type of "squint".

Doesn't squint mean strabismus?

@WYSIWYG "squint" means strabismus (eyes misalignment), but also it means "stare" gaze: (google translater):verb
look at someone or something with one or both eyes partly closed in an attempt to see more clearly or as a reaction to strong light.


text:
Why can't diamine oxidase be supplemented?
I've read from an academic article that diamine oxidase cannot be supplemented  but it had no explanation as for why. I am curious as to why this?

Food rich in histamine or red wine may cause allergy‐like symptoms
  such as sneezing, flush, skin itching, diarrhoea and even shortness of
  breath. The suspected reason is a diminished histamine degradation
  based on a deficiency of diamine oxidase. As diamine oxidase cannot be
  supplemented, a histamine‐free diet was implemented to reduce
  histamine intake.

Proteins other than hormones in general are not supplementable. Think of genetic retinitis pigmentosa, metabolic diseases etc. They are digested when taken orally and won't reach intracellular targets when injected in the bloodstream or in tissues.

More recent research contradicts the statement that diamine oxidase (DAO) cannot be supplemented1.
This paper clearly supports use of DAO. However, Triptans like sumatriptans are typically used instead because of cost.
Note: Research is of 2018, so not your fault.
Reference:

Izquierdo-Casas, J., Comas-Basté, O., Latorre-Moratalla, M. L., Lorente-Gascón, M., Duelo, A., Soler-Singla, L., & Vidal-Carou, M. C. (2019). Diamine oxidase (DAO) supplement reduces headache in episodic migraine patients with DAO deficiency: A randomized double-blind trial. Clinical Nutrition, 38(1), 152-158.

The OP's linked article clearly states that DAO can't be supplemented. I'm guessing that what you mean by "The article" is the one you linked? I've edited based on that assumption, but please correct as needed. Also, can you elaborate on the statement about triptans — it isn't clear to me how that is relevant to the original question.

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text:
Would a human survive eating only living ants?
After reading an admittedly foolish question about 1 googol ants vs. 1000 humans, I had a question. Could a human survive solely on eating ants (common ants, not the stinging kind, or leafcutters etc.)

This study in 1984 suggests it's a bad idea and other sites have said eating ants is for weight loss.
The abstract says that it goes into detail about the problems associated with eating ants as well as their low nutritional value.
So I believe the answer is no. You could not survive long term on a diet of only ants.


text:
How do you identify a mosquito's sex without letting it bite you?
Are there any reliable indicators?

male and female mosquitoes are morphologically different. You seem to have shown no effort at all. Have you even checked the wikipedia page on mosquitoes? -1

I'm voting to close this question as off-topic because OP has shown no research effort

Males and females mosquitoes are morphologically quite different.
The majority of individuals you see are females. The males are not attracted to humans and so we see them less often.
The main obvious difference is the size of the antenna. When you see the large feather-like antennas of a male, you'll have no doubt; it is a male. The male also tend to be smaller than the female but given the inter-species variation in size I wouldn't use this criterion to tell the gender especially the antenna criterion is so obvious.

You can find many more pictures if you just google mosquito male female.
Why do males have these large antennas?
The male's large antennas are for sensing the females. There is a very important sexual selection among male mosquitos for accessing a mate. Female beat their wing at another frequency than males and they therefore produce different sounds when flying. So males compete on their ability to hear and recognize female. Females are attracted to CO2 and warm bodies but males are incredibly attracted to the sound of the female. During my Bachelor degree I once played a 440Hz harmonic to male Anopheles gambiae. It is surprising how quickly they respond to this sound and fly toward the speaker.


text:
Why does a gene have two alleles?
Why does a gene have two alleles?
When there is a gene for producing the color pigment for a flower, why are there there two alleles, producing either same color or different color (homozygous and heterozygous)?

Why does sexual reproduction exist? You need to answer that first, alleles are just a consequence.

To sustain our species

I'm not sure exactly what question you're asking.

Have you done any research at all?

So which factor decides a specific allele to be expressed and the other allele to remain repressed

Allele is a variant form of a gene. How many alleles there are depends on number of copies of the gene and number of variants. In theory you can have 5 identical copies or single copy and single allele (Y-linked genes come to mind).
Regulation is very complicated, I'll refer you to reading on recessiveness, dominance. Barr bodies also have to do with various expression profiles in same thing.

A flower (or a person) has two alleles for a gene because it inherits one set of chromosomes from one parent and another, comparable, set of chromosomes from the other parent.  Hence there are two copies of each gene, and so there are two alleles for each gene.

So which factor decides a specific allele to be expressed and the other allele to remain repressed

In a heterozygous diploid cell, typically both alleles are expressed (parental imprinting is a well-known exception to this statement).  However, if, as in Mendel's pea plants, one allele is wild type and one is mutant, than whichever allele is dominant will be expressed (or in other words  have a visible phenotype that you can score).  Co-dominance is a rare exception to this statement--if two alleles are co-dominant then each homozygote has a different phenotype, but the heterozygote has a third phenotype. For example, the mating type locus in baker's yeast.


text:
Who compared developmental biology to crystallography?
I need to find out the name of a nineteenth century biologist who compared developmental biology to crystallography. His idea was that crystals are formed from 'cells' (defined molecular units) that bond together to form arrays. In living organisms cells are bound together but the rules that form the structures change as the organism grows, especially in animals, which is why we have different organs. In both cases you have units that coalesce undirected but according to rules to form structures. I remember finding out about this biologist from a documentary which also showed illustrations from the book he wrote on the subject. I can't find his name or that of his book using a web search because it's too obscure and that would only work with the correct terms. Does anyone know anything about this?

The idea to compare biologic cells and crystal is mostly related to a German physiologist Theodor Schwann (1810-1882):

His work "Microscopic researches on the Conformity in Structure and Growth Between Animals and Plants, 1839 relates to this idea.

He believed that new cells form principally outside pre-existing
  cells, and wanted to draw an analogy to crystal formation.

another source:

The cell is the unit of structure, physiology, and organization in
  living things. The cell retains a dual existence as a distinct entity
  and a building block in the construction of organisms. Cells form by
  free-cell formation, similar to the formation of crystals (spontaneous
  generation).

(other related scientists are Schleiden, Virchow, Muller).

I think that's him, his main book was Microscopical Researches on the Similarity in the Structure and the Growth of Animals and Plants. But the analogy with crystals breaks down when it comes to their origin - cells don't spontaneously generate, which he helped to prove.


text:
How do paper wasp larvae not fall from their nest?
There is now a paper wasp nest hanging from the eaves of my bedroom. Not very big, I supposed about a hundred chambers and about 7 to 10 adults in total. I observe it every now and then.
It just occurred to me that when the larvae first hatch, they are so small compared to the chamber diameter. So here are two questions:

How do they not fall off, being suspended and all?
Is there any known statistics of how often larvae fall off (for a particular species, let's say)?

Social wasp larvae hatch from an overhanging egg, and they grow up through a series of skin moults, typically 5 in number. The shed skins accumulate terminally behind their pointed anus, where the egg chorion peduncule remain. These wasps have a special body construction and skin texture (e.g. abdominal lobes, numerous spikes) that allows for pressing against the cell walls.
You can see these traits from high-resolution images shown in the larval descriptions:
Florida Entomologist, 95(4):890-899 (2012) https://doi.org/10.1653/024.095.0411
Sociobiology 63(3): 998-1004 (2016) http://dx.doi.org/10.13102/sociobiology.v63i3.988
Finally, it should be minded that gravity doesn't affect small insects in the same way it affect larger mammals like humans. This means it way takes less effort and sticky secretions for these bugs to hang onto walls than we typically imagine by common sense.
I don't know of any dedicated estimations on fallen larvae, but I guess the event isn't common, unless perhaps in abnormally structurally-challenged nests.

What I can say from observing an abandoned nest, larvae have a connection to the chamber ceiling. I don't know what it is, exactly, but looks like some form of glue.

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text:
Why did Opabinia have 5 eyes?
I recently read about a fossil called Opabinia. What intrigues me is that it had five eyes. I was under the impression that most features, such as eyes, ears and legs are always even-numbered, i.e., 2, 4, 6 etc. Why did Opabinia have 5 eyes?

Actually, even modern insects have two compound eyes and three ocelli. For example bees, wasps, and ants. The ocelli are "simple" eyes: they generally can't form clear images and their purpose is mostly light metering. From a mathematical point of view, having three ocelli might make sense if light metering is most useful for a 2D space coverage, relative to the posture of the insect in 3D space (because 3 points in a 3D space define a plane).

Short answer
The number of eyes are not always even-numbered. In fact, many present-day lower vertebrates feature an uneven number of eyes.
Background
Eyes can be generally defined as photosensitive organs. Besides the regular paired eyes, lower vertebrates such as fish, amphibians and reptiles feature an unpaired (single) brain structure called the pineal gland, or parietal eye. It is primarily a photoreceptor organ, and its electrical activity changes in response to environmental lighting (Fig. 1). The pineal does not mediate vision, and it is mainly involved in regulation of circadian rhythms (Deguchi, 1981).
Hence, many lower vertebrates can be considered to have 3 eyes. In fact, the blind cavefish Astyanax mexicanus undergoes bilateral eye degeneration during embryonic development. Despite the absence of light in the cave environment, cavefish have retained a structurally intact pineal eye. Hence, cavefish can be said to have a single eye (Yoshizawa & Jeffery, 2008).

Fig. 1. Reptilian parietal eye. Source: review of the Universe.
The mammalian pineal gland is a secretory organ only, and no longer responds to direct illumination. In mammals it is situated deep in the brain and the mammalian skull does not admit light into the brain. Instead, the mammalian pineal needs input from the eyes to regulate the circadian rhythm.
References
- Deguchi, Nature (1981); 290(5808):706-7
- Yoshizawa & Jeffery, J Exp Biol; 211:292-9


text:
Generate full dimer from monomer with C2 symmetry?
I downloaded a PDB file of a dimer, but it only contains the monomer, and it says that the dimer can be obtained from C2 symmetry. For an example see here: http://www.rcsb.org/pdb/explore/explore.do?structureId=2PJY.
How can I generate the PDB for the full dimer?
I am comfortable with PyMol, so an answer using PyMol is preferred.

Use SymmDock. It is very easy.

This article will probably be informative for you:
Looking at Structures: Introduction to Biological Assemblies and the PDB Archive
The PDB file contains the asymmetric unit found in a particular crystallographic study. The biological assembly is the quaternary structure known or predicted to be found in living systems. For many proteins (but not 2PJY), the biological assembly can be downloaded directly from RCSB. For other proteins, the PDB file may contain the transformation matrix used to create the biological assembly from the asymmetric unit. If you look at the file in a text editor, this information is found under remark 350:
REMARK 350 BIOMOLECULE: 1
REMARK 350 AUTHOR DETERMINED BIOLOGICAL UNIT: HEXAMERIC
REMARK 350 SOFTWARE DETERMINED QUATERNARY STRUCTURE: HEXAMERIC
REMARK 350 SOFTWARE USED: PISA
REMARK 350 TOTAL BURIED SURFACE AREA: 8880 ANGSTROM**2
REMARK 350 APPLY THE FOLLOWING TO CHAINS: A, B, C
REMARK 350   BIOMT1   1  1.000000  0.000000  0.000000        0.00000
REMARK 350   BIOMT2   1  0.000000  1.000000  0.000000        0.00000
REMARK 350   BIOMT3   1  0.000000  0.000000  1.000000        0.00000
REMARK 350   BIOMT1   2  1.000000  0.000000  0.000000        0.00000
REMARK 350   BIOMT2   2  0.000000 -1.000000  0.000000        0.00000
REMARK 350   BIOMT3   2  0.000000  0.000000 -1.000000        0.00000

Note that the actual biological assembly of 2PJY is a hexamer and the asymmetric unit in the PDB file is a trimer. You can see that the first matrix is identity (ie keeps the original asymmetric unit). The second matrix transforms the assymmetric unit to create the full hexamer. This matrix is both author and PISA predicted. You can actually go to the PISA website and have it predict the biological assembly of a particular PDB file, and it will spit out the coordinates of the hexamer (and other predicted assemblies) which you can then load into PyMOL.
PDB files may also contain a CRYST1 record, which gives information about the unit cell and space group of the crystal. Via the symexp command, PyMOL can use this information to recreate neighboring asymmetric units. By limiting the cut-off distance (and this requires trial-and-error), the biological assembly can be recreated. This script, for example, will generate the hexamer:
fetch 2PJY
symexp 2PJY, 2PJY, 2PJY, 2.5
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text:
Change Genbank entry date with Biopython
I can create a new Genbank record in Biopython with the following code:
from Bio import SeqIO, SeqFeature
from Bio.SeqRecord import SeqRecord
from Bio.Seq import Seq
from Bio.Alphabet import generic_dna
from Bio.Alphabet.IUPAC import IUPACAmbiguousDNA

my_sequence = "ATAGGGACUCATAGATA"
my_record = SeqRecord(Seq(my_sequence, IUPACAmbiguousDNA()))
my_feature_location = SeqFeature.FeatureLocation(2,5, strand=1)
my_feature = SeqFeature.SeqFeature(my_feature_location, type="CDS", id="Cre")
my_feature.qualifiers["foo"] = "bar"
my_record.features.append(my_feature)

print my_record.format("gb")

The corresponding genbank file then looks like:
LOCUS       .                         17 bp    DNA              UNK 01-JAN-1980
DEFINITION  .
ACCESSION   <unknown id>
VERSION     <unknown id>
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
FEATURES             Location/Qualifiers
     CDS             3..5
                     /foo="bar"
ORIGIN
        1 atagggacuc atagata
//

How can I change this bit UNK 01-JAN-1980?

So, the problem is that you are probably using wrong class for your record. Compare Bio.SeqRecord class with Bio.GenBank.Record class. Reason why in your GenBank format you have this reference date (01-JAN-1980) is because your record has intrinsically no date attribute, so SeqRecord.format set undefined fields to default (look through the source code to see where this happens).
What you want to do for creating GenBank record is following:
$ python
Python 2.7.10 |Anaconda 2.3.0 (x86_64)| (default, May 28 2015, 17:04:42)
[GCC 4.2.1 (Apple Inc. build 5577)] on darwin
Type "help", "copyright", "credits" or "license" for more information.
Anaconda is brought to you by Continuum Analytics.
>>> from Bio import GenBank
>>> from Bio.GenBank import Record
>>> my_rec = Record.Record()
>>> my_rec
<Bio.GenBank.Record.Record object at 0x1030b1890>
>>> my_rec.sequence = Seq(my_sequence)
>>> my_rec.sequence
Seq('ATAGGGACUCATAGATA', Alphabet())
>>> print(my_rec)
LOCUS                         bp
DEFINITION  .
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
ORIGIN
        1 atagggacuc atagata
//
>>> my_rec.date = '13-JUL-2015'
>>> my_rec.features.append(my_feature)
>>> my_rec.data_file_division = "ROD"
>>> print(my_rec)
LOCUS                         bp                    ROD       13-JUL-2015
DEFINITION  .
KEYWORDS    .
SOURCE      .
  ORGANISM  .
            .
FEATURES             Location/Qualifiers
type: CDS
location: [2:5](+)
id: Cre
qualifiers:
    Key: foo, Value: bar
ORIGIN
        1 atagggacuc atagata
//

Notice, how print(my_seq) outputs data in GenBank format by default (since that is a GenBank record after all). I am sorry I cannot really talk on differences between GenBank.Record and Bio.SeqRecord and why/when use one object or another.
Anyways, looking up reference documentation is always a good habit: http://biopython.org/DIST/docs/api/Bio.GenBank.Record.Record-class.html

have you tried the code you suggest? appending my_record.date = "13-JUL-2015" or my_record.data_file_division = "ROD" does not modify my resulting record.

Many thanks! As a follow-up question, do you know how I could actually save a Bio.GenBank.Record object? The SeqIO.write(main_record, destination+".gb", "genbank") I used before gives me TypeError: 'Record' object is not iterable. The obvious solution, SeqIO.write([main_record], destination+".gb", "genbank") gives me TypeError: object of type 'Record' has no len()...

Actually, I turned that into a question in its own right.

For Bio.SeqIO.write(...)``` you have to give it SeqRecordobject(s), it does not understandBio.GenBank.Record`` objects.

Using the SeqRecord object approach with Bio.SeqIO, you would do something like this:
my_record.annotations["data_file_division"] = "PLN"
my_record.annotations["date"] = "24-DEC-2015"

Note that only valid NCBI GenBank divisions, or their EMBL equivalent, will be accepted.


text:
Do deaf people sleep better?
Since deaf people can't hear, is relaxing and falling asleep easier for them? In general, do they sleep better than hearing people?
Of course some hearing people have no trouble getting to sleep, but others awaken whenever they hear a sound.

I'm voting to close this question as off-topic because it's not biology

@rg255 - since when are sleep and sensation not Biology?

ok perhaps better to say I think it is trivial, does not deal with any kind of biological question or problem, and is unlikely to be of interest to the target audience (students, academics and active researchers)

You must also consider the reason for the condition. Are they deaf because of something mechanical in the ear? Something neurological? Maybe even psychosomatic? I would postulate that the total lack of one sense from birth would have no discernable effect on sleep patterns. As well, I would think that induced heading loss would harm sleep, because of the likely depression to go with loss of hearing.

Let's firstly differentiate deafness - profoundly impaired ability to hear, and other states where the subjects can still hear at different degrees.
Secondly, differentiate the congenital deafness & infantile hearing loss and hearing loss in adults who previously had normal hearing.
The subjects with congenital and very early infantile hearing loss would have better sleep characteristics (this state will affect psychological state in a lesser degree than one acquired in more mature & "conscious" state), while persons who have lost their normal hearing would have abnormal sleep patterns at least in the period when they have just realized that they are going to lose their hearing. After this "preliminary" period, the sleep pattern should be dependent on the person's psychological status and other similar factors.
Many persons will mention that while using ear plugs they feel that their sleep is better comparing with "un-plugged" sleep.
sources

Characteristics of sleep in deafness. Rev Neurol. 1998 Jun;26(154).
Non-scientific source.

Please pay attention that scientific sources are scarce, thus take the answer as one of limited evidence.


text:
Cell line immortalisation biosafety
Cell lines are often immortalised by artificial expression of proteins which specifically cause the knockout of important cancer suppression genes or the activation of proto-oncogenes.

Cellular immortality happens upon impairment of cell-cycle checkpoint
  pathways (p53/p16/pRb), reactivation or up-regulation of telomerase
  enzyme, or upregulation of some oncogenes or oncoproteins leading to a
  higher rate of cell division.

However, this would appear to fall under the purview of Biosafety Level 3 since the protein expression vectors are capable of causing cancer in the researcher when they infect the researcher. Cancer can certainly be considered a serious or lethal disease, and aerosolisation of the vectors, while rare, is not impossible (for example during a spill).
According to the biosafety definitions of Columbia University,

Agents: serious or lethal diseases transmissible via aerosols, e.g.,
  M. tuberculosis, SARS.  Recombinant DNA activities using genetic
  material from BSL-3 organisms or such organisms as host cells.

Why then, does the CDC classify cell line work, including work with viral production cells, as a BSL-2 activity requiring only BSL-2 containment levels, when the act of immortalising the cells would involve working with viral agents that can cause cancer?

Cells immortalized with  viral agents such as SV-40, EBV adenovirus or
  HPV, as  well as cells carrying viral genomic material also present
  potential hazards to  laboratory workers. Tumorigenic human cells also
  are potential hazards as a  result of self-inoculation.[...]
Human and other primate cells should be handled using  BSL-2
  practices and containment. All work should be performed in a BSC,  and
  all  material decontaminated by autoclaving or  disinfection before
  discarding. BSL-2  recommendations for personnel protective equipment
  such as  laboratory  coats, gloves  and eye protection should be
  rigorously followed.

Are the transformation cells (eg the 293T viral cells containing the transformant viruses) considered Level 3 biosafety risk, and if not, why not?

Work with vectors expressing oncogenes or knocking down tumor suppressor genes (particularly if vectors are based on lentivirus) is often done under "BSL-2+" conditions. This essentially means that personal protective measures required for BSL-3 are used, but the specialized ventilation systems and so forth of BSL-3 physical laboratory space are not required. That would seem to address the investigator-safety issues raised in this question. See the complete Columbia policy as an example of the details and the risk-assessment process.
As noted already, once cultured cells have been infected with these vectors the risks to personnel are substantially diminished if not eliminated, so less stringent protections are then required.

Maybe, cells should be contained under BSL-2 and agents (viral particles etc) under stricter BSL-3? That is, after immortalization you can keep cells under lower security.

Biosafety Level 2 builds upon BSL-1. BSL-2 is suitable for work involving agents that pose moderate hazards to personnel and the environment.
Biosafety Level 3 is applicable to clinical, diagnostic, teaching, research, or production facilities where work is performed with indigenous or exotic agents
  that may cause serious or potentially lethal disease through the inhalation route of exposure
CDC Biosafety in Microbiological and Biomedical Laboratories, Laboratory Biosafety Level Criteria

As of HEK 293 cells, check this out:

Biosafety level 2 practices and containment facilities for all activities involving HEK-293 cell lines.
HEK 293 Cell Line Risk Assessment - IBC

+1 for the possible interpretation of the definitions. However, do you have any examples of such viral transformants being actually kept in Biosafety Level 3 environments by an academic research lab?

my guess is that any research group will try to keep as low safety profile as possible (maybe, except NIH labs) to save money, or time, or stress. Low enough for NIH grants and publishing approval.

@aaaaaa : such work is regulated by institutional biosafety committees, which are in the best position to gauge the relative risks of particular procedures and the level of protection required. That required regulation is independent of funding source. Individual labs that do not get permission for the work or do not follow procedures can be shut down. There is more stress in working with such vectors without protection than is generated in the process of applying for permission or for carrying out the protective procedures.


text:
Difference between modules in KEGG Module
The KEGG module M00115 includes a set of reactions while M00542 does not have any; it just shows the list of enzymes. Is the reaction set for M00542 still unknown?

Module means, as defined in the KEGG Module page, a functional unit. So it can be anything, from groups of enzymes to genes to metabolites. About the two that concerns you:

Pathway modules represent groups of functionally related enzymes part of the metabolic network. I think this one is easy to understand because it represents the classical understanding of "module". The modules involve metabolites (compounds with id starting with "C"), enzymes (represented by KEGG ortholog ids starting with "K") and reactions (represented by ids starting with "R"). The reactions integrate compounds and enzymes in a particular step in the chain of reactions included in that module.
Signature modules represent molecules associated with a particular phenotype. In particular, the example listed in the KEGG page points to EHEC pathogenicity signature, Shiga toxin. The two molecules in module M00363 are associated with the phenotype, which is in this case EHEC pathogenicity. But in principle they do not necessarily need to be related to each other (in this case they are, but not in the same meaning as the metabolic module).

In your particular examples, M00115 is again a pathway module including enzymes, compounds and reactions, all connected in an integrated manner. Module M00542 on the other hand shows the proteins part of the T3SS (Type three secretion system) used by Gram-negative bacteria for infection. These are not enzymatic reactions, just proteins associated with the EHEC/EPEC pathogenicity phenotype. They are however related in that they form a protein interaction complex that mediates infection.
Other Module categories include:

Structure complexes related to molecular machineries.
Functional sets seems like a miscellaneous category.

You could argue that the T3SS is a molecular machine and should be classified in the Structural complexes category. Indeed, something important to remember is, as stated in the KEGG module's page:

KEGG MODULE is a collection of manually defined functional units [...]

As anything manually defined, there is some degree of arbitrariness. Use the information in KEGG modules as far as it serves your needs, but it would be better not take it as written in stone.

M00115 is a pathway module (NAD biosynthesis) whereas M00542 is a signature module (EHEC/EPEC pathogenicity signature).
From the KEGG page on modules:

pathway modules – representing tight functional units in KEGG
  metabolic pathway maps, such as M00002 (Glycolysis, core module
  involving three-carbon compounds)
signature modules – as markers of phenotypes, such as M00363 (EHEC
  pathogenicity signature, Shiga toxin)

Can you please explain the difference? The reaction for the M00542 is unknown right?

what is meant by signature module?

@Rishika I have mentioned in the answer what signature module means. It does not have reaction pathways. It just has a set of biomarkers for a phenotype.


text:
Can roots have cuticle, especially aerial roots?
In my school biology book, it is written that cuticle covers the epidermal cells in aerial parts of plants and root epidermis doesn't have cuticle. My question is that whether aerial roots, in plants like kalanchoe, also not have cuticle?
Do all kinds of roots not have cuticle?

I don't believe that any class of root has cuticle tissue. The cuticle is special layer designed to work with the mechanical transport of leaves etc, which roots don't have. Different types of roots have different methods for absorbing and retaining water.

According to this article, Selaginella aerial roots have a thick root cap that possesses a cuticle. Roots that have breached the soil do not have cuticles.

Basically roots don't have cuticle while stem and leaves contain cuticle. As roots have to absorb water cuticle is not present in them


text:
What information does the KEGG Module statistics page show?
While browsing through the home page of KEGG Module, I clicked the button named Module statistics.
Can someone tell me what does these numbers signify? What are they the statistics of?

My understanding is that these statistics show the coverage for each KEGG Module in the particular phylogenetic group. For example, M00001, is found in 275 of the eukaryotic organisms in KEGG (which represents 90.5% of the eukaryotes in KEGG). The same logic applies for other groups.
An quick example demonstrating this hypothesis, done with the Protists group found in KEGG Organisms (since it is easier to count by eye). There are 43 protists, and in the statistics it says (as of 2015/7/9) that module M00001 is found in 33 of them, hence: $33/43=0.7674419$ which agrees with the 76.7% shown.


text:
Could viruses be used as antibiotics?
Could we use viruses that only affect bacteria to act as antibiotics?
The more bacteria, the more times the virus divides, so the stronger it gets. Is this practical?

Look up Phage Therapy, that's basically what they're doing. In fact, it's used in many cases where antibiotic resistance is high. My  college lab was actually researching the use of Phage Therapy with E. coli infections.

Yes, it is practical. Assuming you have or create a virus that attacks the bacteria you want to destroy, the nature of the virus should wipe out the bacteria. The problems that could arise, as with any genetic manipulation, are the potential for an out of control mutant.

You may already be eating cold cuts that are treated using this method.

Could we use viruses that only affect bacteria to act as antibiotics?

Yes. The specific class you're referring to is called a "bacteriophage".
There's quite a bit of research going on surrounding phage therapy as a stand-in or replacement for traditional antibiotics. Here's a Nature Biotechnology article from 2004 that discusses your very topic.
It is practical, carries some risks (mutations being a known and accepted risk), and I wouldn't be surprised to see phages in practice now or sometime soon.

Yes you could.
It used to be a big deal before antibiotics were discovered, and continued for a bit in the Soviet Union.
However, due to the success of antibiotics, it fell out of grace. Due to the lower level of applied research in the Soviet Union (not research itself, although equipment might have been often outdated a bit and the Soviets did isolate themselves quite a bit, but a great deal of research originally discovered behind the Iron Curtain was actually commercialized in the US, such as contact lenses; many Soviet research projects are actually getting rediscovered, such as the great experiment about the domestication of foxes), it never became the thing, and after the fall of the SU, it was nearly forgotten.
However, now it is becoming trendy again. There are several reasons:

resistance against antibiotics have grown out of proportions
it is quite trendy to use "natural predators" against pests

https://en.wikipedia.org/wiki/Phage_therapy

In fact, you could say that_ there's a phage for that_. They take water from a river, for example and see which phages feed and reproduce on the germs you are targeting, and cultivate them, benefitting from artificially induced natural selection.


text:
shRNA knockdown not showing with Western
I've recently been performing shRNA transfections and was hoping to get some advice on why I'm not seeing any knockdown via western blot
I transfected by MDAMB468 breast cancer cell lines with shRNA against PTEN from the pLKO.1 lentiviral vector. I selected for the transfected cells using 1ug/ml  puromycin for approximately 6 days. During this time there was very few cell death amongst the cells compared to my control plate (untransfected cells with 1ug/ml puromycin), suggesting that the transfection was successful.
After the 6 days I harvested my cells for protein and RNA extraction. I performed a western yesterday to assess knockdown, but noticed that there was hardly any differences (if any!) compared to my shGFP control. I haven't done a qpcr yet but I plan to this week.
I was wondering if anyone has experienced something similar, especially when working with PTEN? could it be that the cells need to be selected for a longer period (i.e. more than a week) before assessing protein knockdown?
Thanks!

I don't know much about this protocol, but is it possible that you transfect enough for antibiotic resistance expression, but not enough for shRNA to actually work?

I assume that you transfected the plasmid directly not producing viruses. If you want stable transformants, you might want to subculture them and maintain a bit longer. It is because efficiency of integration of plasmids into genome could not be that high--less than 0.1% of population obtain stable resistance by integration into genome. After 6 days, cells were still healthy in your case. This means you might get good transfection efficiency and after several times of cell division, your plasmids were diluted and the effects might be low even if cells maintain resistance against puromycin.
If transient expression (KD) works in your experiment, you might want to check expression level of your target at day 2 or 3. If you prefer stable cell lines, you can increase puromycin concentration, and if you agree, you pick up single colonies after cells not having plasmids in genome are dead. Among these colonies, some have more plasmid copies other have less. You can choose cells least expressing your targets as well as moderately expressing cells if you want. Because you might want to see expression level dependency.
For some cells, 5ug/ml puromycine is used according to this link.

thanks for the suggestions. I don't have much experience with shRNA transfections, but do you think it's possible that the protein (PTEN) is quite stable and the cells would need to be cultured for longer (what would you recommend, 2 weeks?) to see the knockdown? I'm interested in doing the qPCR to see how the mRNA knockdown looks...

@tolo9397 Try that qPCR. It is possible that your shRNA sequence is not binding like you wanted it to. Have you verified that this shRNA actually knocks down your gene of interest?

@tolo9397 As you mention, in general, KD effects could be delayed from a shRNA expression peak because of protein life time. So, cells may be cultured one or two more days compared with protein expression vector transfection. If the delay is more than that, you might want to transfect shRNA expression plasmid again several days after the first transfection to keep shRNA effects high. If you need stable transformants, this is not the case, though.

@tolo9397 PTEN is a popular protein, so you could find KD experiments published like http://www.nature.com/nm/journal/v17/n4/full/nm.2309.html#supplementary-information


text:
Why do skinny people live for shorter than the norm even though calorie restriction extends life expectancy?
If I understand correctly, calorie restriction may extend life expectancy slightly (not proven exactly how much for human). But according to the statistics, skinny healthy people have even shorter life expectancy than healthy, slightly obese people. Could you explain why this is not considered as contradictory?
(Reference)

Could you include a link to these statistics?

The original source is written in Japanese, so I cited the following page written in English.
http://phys.org/news/2009-06-japanese-overweight-people-longest.html

Could be cultural differences. Young people die alot due to car deaths.

rate of ageing and age at death are influenced by many things, calorie intake is just one tiny factor.

Interesting point. Note that it is "calorific restriction" in the animal experiments, not fat vs skinny mice. Skinny people don't necessarily eat less than average, and I imagine smoking is a big factor (makes you skinny and sick). I wonder if the original study controlled for this.

"Slightly obese" means that they weight more than a standard reference weight for their height. If these people are more healthy than most this only means that the standard reference weight is wrong.

Well fed people are happier, and happy people live longer?

This is an interesting point you raise, and as the study you linked to states, "the link between physique and life expectancy is not clearly understood," which is certainly true at the moment. The relationship between BMI and lifespan in humans is a very different story to controlled dietary restriction in model organisms.
Dietary restriction is defined as "undernutrition without malnutrition" [1], and by definition model organisms live in controlled environments. In contrast, humans have confounding factors that may reduce weight and health (for instance smoking status, early-life diseases, malnutrition, etc) that are not modelled in these experiments.
In addition, the relationship between BMI and mortality is complicated in older humans, known as the 'obesity paradox'; overweight and obese elderly hospital patients have a lower mortality risk than low-normal weight patients [2]. There are a number of hypotheses regarding this, but the favoured one appears to be that the association is not actually paradoxial, but that higher BMI only appears protective because losing weight is associated with many diseases of ageing, so after accounting for many of these confounding factors (e.g. dementia, cancer, etc) high BMI no longer appears protective.
Therefore the study you found only appears to be contradictory to the dietary restriction experiments; in human populations the situation is much more complicated. Additionally, there is conflicting evidence as to whether dietary restriction even works in primates [3], let alone in humans (the largest effects are observed in worms and drosophila).

Weindruch et al. The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake. (1986) J Nutrition; 116(4):641-54
Yamauchi et al. Paradoxical association between body mass index and in-hospital mortality in elderly patients with chronic obstructive pulmonary disease in Japan. (2014) Int J Chron Obstruct Pulmon Dis; 9:1337-46
Maxmen. Calorie restriction falters in the long run. (2012) Nature; 488, 569

I started writing my own answer and realised you hit each of my points better! Again I would point out that (healthy) skinny people don't necessarily eat more. Although we know that they're skinny, did the study in question confirm that they consumed less calories?