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Analogous organs: coevolution or opportunism?
The question reads as: "The lens of many vertebrate eyes is a crystallized form of a protein that also functions in digestion as a metabolic enzyme. This shows that
A. Vision and digestion co-evolved
B. Digestion necessarily evolved prior to vision since it is a more basic function
C. Evolution is opportunistic
D. Vision and digestion evolved around the same time"
My approach: Based on the given information it appears the protein might have given rise to analogous organs. I don't feel B has to be true in all cases. C is a good candidate but its meaning isn't clear. I'm not sure about D. To me the answer appears to be A but I would be happy to be have this confirmed.

If you think your question has been answered, you can click on the check sign next to your favourite answer.

I think the question you have to answer is a bit badly phrased. Overall, I mainly agree with you, except for point A. Here are my comments for each points:
A
co-evolution is defined for the evolutionary dynamic between two lineages. It is typically not used to talk about two body parts. Consider for example the definition from Understanding evolution:

The term coevolution is used to describe cases where two (or more) species reciprocally affect each other's evolution.

, wikipedia

In biology, coevolution occurs when two or more species reciprocally ("co-") affect each other's evolution.

or dictionnary.com

evolution involving a series of reciprocal changes in two or more noninterbreeding populations that have a close ecological relationship and act as agents of natural selection for each other, as the succession of adaptations of a predator for pursuing and of its prey for fleeing or evading.

I would note that the term coevolution can sometimes be used in its border line case as in this paper for example. It is particularly confusing as the term co-adaptation is sometimes used to talk about the interaction of two phenotypic traits. But stil, I would NOT check A
B
I agree with you! The conclusion is not valid from the premise (which means that it is not necessarily true, so even if the conclusion may be true, it cannot be concluded from the premise)
C
I agree with you! The statement is a bit unclear.
Typically, evolution is opportunistic would mean that throughout evolution history, a lineage may well evolve to reuse an existing gene for another purpose (neofunctionalization for example) which is very likely what happened here.
D
I agree with you! The conclusion is not valid from the premise.
In short
I would check C.

I would say C is the right answer. Here, "Evolution is opportunistic" means something like "Evolution is a process that re-uses structures and mechanisms".
The question is about what you can conclude from the information given. The other three answers (A, B, D) are about the relative timing of when these functions appeared. Only C talks in more general terms about re-use of an existing protein for another purpose.
Of course, it seems reasonable to suppose that digestion evolved before vision - however, we can't really conclude that from this one example.

As a side note, I did a project a while ago about eta-crystallin, which is thought to have been an aldehyde dehydrogenase that is 'moonlighting' as a structural protein in the eye lens.
See : Crystal structure of eta-crystallin: adaptation of a class 1 aldehyde dehydrogenase for a new role in the eye lens


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What are the exact reason causing missing calls in a VCF file from exome sequencing?
My data is a VCF file from exome sequencing variant call. I'm not very familiar with the sequencing process and variant calling process. I noticed that there are some missing genotypes, which is recorded as "./." at the GT field. From googling I learned that they're not homozygous reference genotype ("0/0"), but missing calls due to some sequencing ignorance.
In order to make my data "cleaner", I thought it's better to filter out the loci with missing calls if there're not too many of them. I also checked the corresponding "DP" of the loci with and without missing calls. For example:
chr1:123 GT:DP 0/0:2 1/1:4 ./.
chr1:234 GT:DP 0/0:10 1/1:11 1/1:20
chr1:345 GT:DP 0/1:40 1/1:37 0/0:78
chr1:456 GT:DP 0/1:7 0/0:23 ./.
chr1:567 GT:DP 0/1:34 1/1:39 0/0:58

In the above toy example, there're 3 people and 5 loci. I checked the mean DP of all 5 loci and I found that the mean DP of loci with missing calls (1st and 4th loci) to be significantly lower than the mean DP of loci without missing calls (2nd, 3rd and 5th loci). Is that a coincidence? Or are there any specific reason that the loci with missing calls have lower coverage than the "normal" loci? Thanks!

Have you looked up in the software that made the vcf what ./. means?  I would guess it means 0 coverage in that sample at that locus.

Not that this isn't a useful question here, but there's a newly-started Bioinformatics SE that might like to have a whack at this: https://bioinformatics.stackexchange.com/

@swbarnes2 In the documentation, "./." simply means no call. In literatures, there're several different reasons causing this. This could be due to 0 coverage, and also other reasons, which I'm not so clear about. But let's assume that they're caused by 0 coverage, I still don't know the answer to my question. Do you have any ideas?

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Term for timespan between generations
Is there a terminology for the average timespan between generations, like ΔG ?
I mean by that the time from the parental generation being mature to the filial generation being mature.

Note that $\Delta G$ sounds more like a time difference in generation unit like $\Delta G = G_1 - G_0$, where for example, $G_1$ could be the generation at which the state of your model has reached a basin of attraction (or whatever) and $G_0$ could be the initial generation. $Delta t$ would sound a little bit like an actual time (in years or whatever) between two generations (although often the unit of $t$ are defined to the generation time). +1 anyway

You mean generation time?
There are several definitions in use, but one is "the average difference in age between parent and offspring" (or "age at which members of a given cohort are expected to reproduce") which would be the same as the time period you're asking about.
(The difference between these two depends whether the population is at equilibrium or not.)
The two above are 'shortest generation time'; a third definition (which is the first in the link) is a little more complex but is more useful where individuals reproduce over a prolonged period.

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Can I pellet DNA back from dissolved state?
I have a dissolved plasmid pellet in water. Can I pellet it again by centrifuging it at 13000 rpm? If not, why?

Only by centrifuging?

Is this a homework question? have you done any research on this? Could you share your findings here?

Hi Alex, It wasn't homework question. After centrifuging a while, the concentration of the plasmid reduced a bit.  (1.7 ug to 1.35 ug). Couldn't find a proper literature on it. So I thought it is worth asking.

No, you cannot pellet dissolved DNA with ultracentrifugation.
Yes, you can recover a pellet with additional treatments, similarly to how you got it in the first place; only instead of your input being homogenized cells, or tissue, or extract, or whatever you used to obtain your DNA, it would now just be your aqueous solution of DNA.
For instance, you may have performed a TRIzol extraction to separate your DNA into an aqueous phase, prior to spinning it through mini prep columns to elute your purified DNA in water. You could perform the procedure again and you'd have your pellet once more after the final alcohol (ethanol or isopropanol) precipitation step.
The key idea with pelleting DNA (or any nucleic acid) is to make it insoluble; this is achieved with by using alcohols and salts. If it is soluble, nucleic acids cannot 'come out of solution' to form a pellet.

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How to differentiate male and female mosquitoes at pupal stage?
There are many differences between male and female mosquitoes in their adult stage. But for my experiment, I need mosquitoes before they mate. So I need to sort them before they develop in to an adult. The best option is to sort them in their pupal or larval stage. I tried to search the differences, but most of them were very general. So, if someone knows about it, please share your answers.

Male and female pupae are consistently slightly different sizes. This isn't particularly obvious to look at them, but allows them to be sorted mechanically by using two sheets of rigid, waterproof material (aluminium, glass or acrylic) fixed at a slight angle to each other, and washing the pupae down between them until they get stuck. The pupal sorter in most common use is described in this paper and you can buy one commercially here:
http://johnwhock.com/products/laboratory-equipment/larval-pupal-separator/
I think I've seen a video of one in use at Virginia Tech somewhere online but I can't find it right now; I'll edit it in later.


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What hold and inject pressure to be used in microinjection?
I am planning to set up micro-injection apparatus in our lab. Normally what hold and inject pressures are used to inject DNA in fly embryo? I couldn't find in any literature as far as I've come across.

It depends on volume that you want to inject and the width of your needle! Try to optimize the pressure by measuring the volume that you inject in mineral oil (I use grid in the objective to measure the drop size). You will decrease the volume by decreasing the injection pressure, of course. I work with zebrafish embryos so I am not sure if it is the same since it's in the water, but for DNA injection (1-2 nL) I normally use Hold Pressure 2 kPa and Injection Pressure 20-30 kPa.

That sounds similar to what I was using. We pulled our own micropipettes from borosilicate glass though, so had total control of the size. Edit I think we used 40kPa for 50 microseconds maybe, or milliseconds, whichever sounds more normal.

@Tamara Spika, I standardized the parameters (Micropipette size, inject and hold pressure) according to my need. But most of the time, when I try to inject in mineral oil, the water does not come out. I mean, the needle gets clogged. Do u have any idea about how to solve it?

@Mosquitoman Did you try to increase the pressure (like 10 fold) and press  once just to clear your needle and then try to inject again?


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Breeding mosquitoes at lower temperature
It is well known fact that, to slow down the growth of drosophila, they are grown at 18-19 degree Celsius. It helps in maintaining stocks for longer time without frequent change of food. Is it applicable to mosquitoes? especially Aedes aegypti?  can we slow down its growth by growing them at lower temperature?

I think there are 2 questions : temp for breeding and, temp for growing larva. I see larva dormant at about 45 F, then at 60+ F they are active.  again.

@blacksmith37 Possibly even three, as written - temp for maintaining larvae, and temp for maintaining adults. I'd suggest editing out "breeding" from the title, unless you really want to know about this, but I think effects on larvae and adults can be answered as two parts of the same question.

Check "breeding temperature" and similar obscure phrases for the search.
There's a study on physical aspect of mosquitos bred in cold, they perhaps didn't note any significant metabolism change, you can read the articles, they mostly cover wing length scales and follicles.
There's a study on lave development speed which passes over breeding temps, it may however cover "egg temperature".

Maybe:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3992806/ is a NIH paper that gives a quick overview on maintaining an A. aegypti colony.  From the description they are somewhat fussy, but some of the lines imply temperature sensitivity at least at certain stages.
try google 'protocol for maintaining mosquito colony'

Dear Sherwood, I hope u did not understand my question properly. I know the standard protocol for rearing mosquitoes. My question is whether rearing them will slow down their metabolism and thereby their growth? if so will rearing at lower temperature harm them in any way other than their growth? (like their survival, lifespan, mating behavior,egg laying behavior etc.,)

Also just wanted to comment that Aedes aegypti is widely accepted to be the least fussy mosquito species to care for. We have far more trouble with Culex and Anopheles than any of our Aedes.


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Difference between autonomic and paratonic movements in plants
I can't understand the difference be because both involvery the main cause that is an external stimuli, so how do they differ(

its about the gene that is involved in autonomic movements. while, there is no gene involved in plants for paratonic movements.furthermore, autonomic movements are presents in plants by birth, and paratonic movements are induced in plants by an external stimuli only and not present in plants by birth.

There is no need to post a second answer to supplement a previous answer you gave. Instead, you can use the edit button of your previous answer.

In other words for autonomic movements the plants use an internal cause( simply indicating to gene) and external stimuli both. while, paratonic movemens use external cause only( light, temperature,gravity etc.Hope you understand

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How Excessive masturbation can make a person unfit for army?
Recently I saw this news trending, I never heard single
disadvantage regarding masturbation.
But China Army considering it has danger for army.
So How Excessive masturbation can make a person unfit for army?

Maybe don't get your medical advice from the Chinese army.

Maybe step back a bit, and ask just what's an enlarged testicular vein, how it's detected, and (if such a thing actually exists) whether it is indeed caused by "excessive" masturbation?  Or maybe consider that it's just ignorant prejudice, like the Western ban on homosexuals that existed until fairly recently.

Well, using some common sense I'm pretty sure the reason is that a soldier who is busy masturbating won't be a good soldier. It's the same with any kind of addiction, causing the person to not perform the tasks they're supposed to do.


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qPCR (weird ntc curve, amplifies before templates and reaches plateau quickly)
I'm new to qPCR, and I’ve been testing the AR expression on canine tissues. I’m currently using a pair of primers that have been tested in other article for canines.The issue I’m having is  that I have very early amplification of ntc AR (before the amplification of cDNA templates) but also this amplification curve looks weird since it reaches quickly the plateau phase (flattened). This problem persisted even after changing to a much more specific cycling. If anyone has any tips, or ideas on how I may be able to explain this, I’ll be very gratefull.

The cause of the signal in the no template control will be contamination. It could be that the reason for the different plateau positions is the presence of reaction inhibitors, depletion of reagents, or possibly different binding efficiencies between template (and contaminating DNA) and the primers. I'm not sure about that last one but it kinda makes sense in my head: any contaminating DNA that binds to the primers probably won't bind as efficiently as the template that the primers have been designed for so the reaction is inhibited by accumulation of dsDNA faster.
Either way the cause is going to be excessive contamination. Try using more template in your samples (increasing you signal to "noise" ratio), or be more careful when preparing your samples.
There are extraordinary measures that can be taken to remove contaminating DNA (e.g. treating the water with DNase and then deactivating it) but these often aren't necessary and the added steps can actually increase contamination, it's usually best to keep it simple.


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Processing of speech/non-speech sounds in the human brain
I have a ""which came first: the chicken or the egg?"-kind of question regarding the processing and understanding of speech / non-speech sounds in the human brain.
I'm wondering whether speech and generic non-speech sound processing in the human brain are somehow related and whether one of the two is used as a "basis" mathematically speaking or a reference to understand the other.
Most people use "His voice/It sounds like .." to describe sounds/human voices, besides, we are able to tune out and block any non-speech acoustic activity surrounding us if we are not in a conversation which suggests that we have a special sensibility for hearing speech (or maybe our language or just our names if someone is calling us).
I've read an article which states that :

Knowledge of our mother tongue acts as a sort of auditory "template" that influences the way we perceive the sounds of other languages (scientists call this "native listening").

Hearing other languages differently than its native speakers is easy to grasp but is there any research that studies the difference in brain activity when speech / other sounds are heard and whether there is something special about hearing speech in particular.

"I'm wondering whether speech and generic non-speech sound processing in the human brain are somehow related and whether one of the two is used as a "basis" mathematically speaking or a reference to understand the other."
They both have in common acoustic energy - whose rate of change is information in itself. The mathematical basis of choice to compare each against the other, I think, is in how each relate that energy to the brain response - aka the forward model of the stimulus-response relationship.
In auditory studies you often get the (spectro)temporal response function (S/TRF) to estimate an approximate "summary" of this relationship. Note that traditionally, this is done independently, that is, either energy from speech or from other types of sound are separately investigated.
"is there any research that studies the difference in brain activity when speech / other sounds are heard"
There is a history of work contrasting the differential encoding of natural versus artificial sound classes (check out foundational work by Theunissen and colleagues). At these scales (neurons or neuron groups), the differences can be rather stark and happen in birds and mammals alike.
If you are more interested in these coding rules regarding "brain activity" at a larger scale, there are local-field-potential studies (e.g. Gaucher et al. 2012 J Physiol-Paris) that also relate mathematically to the S/TRF. However they are most likely invasive animal studies. Also I don't recall if they contrast speech S/TRFs versus other sound's. If you want something closer to human cognition, probably you might want to look at EEG or MEG studies also.
It turns out that finding similarities can be a bit harder than finding out the differences, maybe because the sounds are so different themselves. The mathematical relationship cannot escape this fact, and may then give distinct S/TRF patterns in return.
In a pre-print that seeks out similarities across stimulus types it is reported that certain information about the acoustic energy changes, in particular temporal onset edges, can be coded by the human auditory cortex, be it from speech, or music, or something else, in a more or less generalizable format across classes, at least qualitatively.  https://www.biorxiv.org/content/early/2017/07/27/168997


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What is ApoCas9 in the CRISPR-Cas9 system?
I am currently reading an article about a particular assay of Cas9 nucleases. In one of the experiments, they have used ApoCas9 (Apo variants of other CRISPR nucleases) as some sort of control.
But the whole article they have not defined ApoCas9? I did check online of definition and activity of ApoCas9, but came across without any fruitful results.
A universal method for sensitive and cell-free
detection of CRISPR-associated nucleases

In general, "apo" is used to indicate an apoenzyme — that is the protein part of an enzyme without essential cofactor(s).
This is actually defined in the Experimental section of the paper:

Cas9/Cpf1 without gRNA (ApoCas9/Cpf1)

So, in this case ApoCas9 is Cas9 endonuclease that is not bound to a guide RNA.

Thank you. I clearly missed that from the experimental section.


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How does chemical shift assignment from NMR spectroscopy is translated to three dimensional structure of protein?
I am currently involved in determination of protein structure using NMR spectroscopy. As part of structure determination I have finished the chemical shift assignment. The chemical shift information is submitted to specialized software/servers for structure determination.
My specific question is "how is the structure of a protein is determined using chemical shifts"? How do the servers translate the chemical shift information to determine fully fledged 3D structure of protein?

The chemical shift can be used to determine secondary structure, i.e. if a certain residue is part of a helix or a strand.
You’re talking about structure determination, so I assume you’re interested in obtaining the three dimensional or tertiary structure. For this, you will have to use proton-proton distances as restraints in structure calculations, not chemical shifts.


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A reliable source of Cas9?
I live in Egypt, and I do want to perform CRISPR-Cas9 genome modification, but there are no reliable sources of Cas9. I can order some Cas9 online from the US, but not much. So... my question is, is there any way I can replicate a small amount of Cas9 to get a bigger amount? Or maybe extract some from S. Pyogens? I've been searching about this for quite some time, so any support would be really appreciated.
Note: I'm not really the "Biology" guy, so please tell me if I sound ridiculous.

You could get a synthetic gene for Cas9 and overexpress it heterologously.

I'm more curious why you are planning to do some genome modification while not being the biology guy...

I might be wrong but I'd guess it'll probably be more expensive to figure out how to produce the compounds you need than to just buy them (esp. if you're not a "biology guy").

Well.. I can't exactly tell you what I'm working on because I signed an NDA, but what I can tell you is that I'm a programmer and I want to create bacteria that can pass information through controllable electrical connections(interfaced with a microcontroller).

@None Hi, would be interesting to discuss more on your project


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In humans, are diseases inevitable during old age?
Considering that dying "from old age" actually means that one dies from an illness related with aging, is it inevitable to eventually acquire diseases in old age?

The first part of OP (supposition that dying from old age means that one dies from an illness) isn't required for the very interesting underlying question, whether diseases are inevitable.

Aging is not synonymous with disease, and hence it is generalized as such, although vulnerability to diseases does increases over time.
Why is it not a disease? Well biological aging can be defined as:
A process of progressive, intrinsic, and generalized physical deterioration that occurs over time (begins at the age of maturity).
While a disease is:
An abnormal condition of an organism which interrupts the normal bodily functions that often leads to a feeling of pain and weakness, and usually associated with symptoms and signs.
Now let's look as to why we cannot live forever and as to why as we get old our disease susceptibility will be (in general) increased, meaning that yes the majority of the population will be dying from a form of a disease. If not a disease it will be a failure of the body system to maintain life.
I will be looking at this in the form of Natural Selection.
The force of Natural Selection declines with age. For example, a gene that is beneficial during young age, but bad during old age (such as making you susceptible to several diseases) will spread in the population because it will manifest after you've reproduced.
Example#1: A gene that helps achieve good blood coagulation and prevents hemorrhage in young people will spread in the population. However, in old aged people, it will cause an increased risk of stroke. Such associations have been previously found for many genes associated with blood characteristics.
Example#2: Overproduction of sex hormones in young age is beneficial for reproduction but will cause prostate and ovarian cancer later in life.
This is called Antagonistic Pleiotropy
In addition, Natural selection is not concerned with late acting mutations.
So as we age will we be afflicted by a disease? Most likely yes, it depends on the trends in disease prevalence which have changed throughout the years due to preventative medicine. If we do not acquire any death-inflicting (be it slow or fast acting) disease, our body will give up before we do get one.
If you'd like to look at disease prevalence, chronic illnesses throughout the years, or the specific trends in a year, just go over to the CDC's webpage.

There is a thought that aging itself should be considered a disease. In which case, death by disease is inevitable with our current level of medical technology.

During the last 25 years, by targeting the underlying processes of aging biomedical scientists have been able to improve the health and lifespan of model organisms, from worms and flies, to rodents and fish. We can now consistently improve the lifespan of C. elegans by more than ten-fold (Ayyadevara et al., 2008), more than double the lifespan of flies and mice (Bartke et al., 2001; Sun et al., 2002), and improve the lifespan of rats and killifish by 30 and 59%, respectively (Valenzano et al., 2006; Zha et al., 2008) (see Figure Figure11 and Supplementary Table 1). Currently, our treatment options for the underlying processes of aging in humans are limited. However, with current progress in the development of geroprotective drugs, regenerative medicine, and precision medicine interventions, we will soon have the potential to slow down aging (Bulterijs, 2011, 2012).

"Old age" diseases are fundamentally malfunctions because stuff breaks. Some blame this on shortening telomeres, although an equally big part of the problem is that there are way too many important pieces that are unable to regenerate themselves.
Think of it as a machine where you can't normally get replacement parts. Stuff wears out, goes off warranty, and breaks.
Experimental regenerative medicine is working on fixing that with 3 fundamental approaches:

Adult pluripotent stem cells/regrowth. Researchers are looking for growth/regrowth/cell proliferation and differentiation mechanisms that already exist so they can be leveraged to regrow stuff that normally doesn't regrow. The advantage is that all the parts are grown from your own DNA or cells which means minimal problems with rejection or incompatibility. As an added bonus it could be considered "all natural". The main risk is cancer due to misconfigured cell growth/proliferation.
Lab-grown or 3D-printed replacement. Higher risk of rejection and other problems but simple and cheap compared to the others. Some research includes growing human-cell transplants in animals which raises various ethical and safety concerns.
Cybernetics or machine implants. Probably the most expensive and works out the best... when it works properly. "Robot" parts keep getting better and better, and have the bonus that they are more readily reprogrammable than DNA and biochemistry. A prominent research area includes brain/nerve interfaces with machine parts - expect pieces that either adapt to neural outputs or connect to nerves so you can "learn" how to use them.
The main drawbacks of this approach other than the cost include vulnerability to EMPs (a massive solar flare or EMP attack will fry all unprotected cybernetics/implants/robot parts), being dependent on both electricity and regular food, risk of getting hacked, and general lack of self-repairability short of replacing parts that break (again). Alternately you could argue that the risk of getting hacked through cybernetic implants and robot parts is a fair tradeoff considering they're immune to organic viruses and infections (except if someone invents bacteria that eat through solid metal or plastic pieces)

Thank you for the detailed answer. But I still don't know if it's inevitable to eventually acquire diseases in old age or not. Could you clear this up for me, please?

If you wonder about the downvotes, I assume folks are missing references and sources. Further, you're talking about robots and so forth, while the question is on dinosaurs. And please keep your comments in check. Commenting is encouraged, but not mandatory when downvoting. Downvoting is an integral part of SE.

No one mentioned dinosaurs until AliceD pulled that #FakeFact out of nowhere. As should be obvious from my answer, stuff breaks over time so you're going to get "diseases" in old age if you don't implement any of the regeneration or replacement plans I mentioned. Finally, I refuse to be censored. I'm helping you all out and telling all of you how to avoid "diseases" in old age, the least you can do is post a thank-you. If you don't like it then I can stop contributing.


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Are all diseases caused by organisms (microorganisms)?
Are there other causes? Or is it correct to say that all diseases are in fact caused by organisms (microorganisms)?

It is not correct to say that all diseases are caused by foreign organisms. Counterexamples are:

Cancer is caused by random genetic mutations in the cells of our body. The mutations can be caused by many factors such as ionizing radiation, smoking, chemical toxins etc.
Diseases such as stroke or heart attack are caused by blood clots blocking the blood flow to essential organs.
Autoimmune diseases are caused by the immune system falsely recognizing cells of the body as foreign and attacking that tissue leading to a wide variety of symptoms.
Alzheimer's disease is caused by chronic neurodegeneration, meaning that the cells in the brain die. The causes are not quite understood but as Alzheimer's usually appears late in life it is likely related to ageing. Also, it is known that some genetic defects can lead to early-onset Alzheimers.
Prion proteins can cause diseases such as Creutzfeldt–Jakob disease also known as mad-cow disease.
Hereditary diseases such as early-onset Alzheimers or ALS are cause by gene defects inherited from the parents.
Toxins can cause chronic diseases such as lead poisoning.

The list probably goes on...
Please note that the first two on the list are the most common cause of death in developed countries.


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Is there a cellular physiological response to desiccation in animals?
There has been much research on the molecular effects of high levels of temperature for animals, specifically regarding heat shock proteins, protein denaturing and energy investment into stress tolerance.
I understand generally, the effects of desiccation with respect to the importance of moisture, specifically for aquatic animals (eg. oxygen uptake), but I can't seem to find much information on cellular-level responses to desiccation stress.
Are there are well established effects of desiccation on a cellular level or if there is a physiological response in the cell (eg. production of hsp)?

Try a search on Google Scholar for "cellular response to desiccation" - you might also try "cellular response to dehydration" or to "hyperosmotic stress."

I have searched Google Scholar extensively and found most research is on plants and algae. There is a bit on Drosophila , it seems sometimes desiccation results in hsp production but I've been reading up on but I'm pretty much stuck here.

What about my suggestions to look at dehydration or hyperosmolarity? I'm not exactly sure what's out there because I am more familiar with organism-level reactions to water stress rather than cellular adaptations but with 70,000 some results (although I agree, it looks like a lot of work on plants, which is why I was suggesting those other search terms) I'd expect you to find something in there.

Your over thinking it, search "Osmoregulation animal cells" here is two results. http://www.annualreviews.org/doi/abs/10.1146/annurev.ph.43.030181.002425?journalCode=physiol And  https://www.ncbi.nlm.nih.gov/books/NBK21739/

@BryanKrause "Hyperosmotic stress" has been effective as has "cellular response to desiccation". I think I was over-thinking it John.

What's protocol now, should I delete the OP


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Phase Shift in Grid Cells
I would like to fully understand the phase shift in the grid cell in MEC. From my understanding, since there is a hexagonal (i.e. equilateral triangle) lattice, and hence there are 3 $\phi$'s, I have the following questions in regards to that:
1). If there are 3 $\phi$'s, how does the phase shift happen in (I guess) 3 phases, i.e. why are there 3 shifts? I am just very confused at a fundamental level: why does the phase shift happen, is it because of the phase resettling in neurons?
2). As Wikipedia defines it: "Phase shift is any change that occurs in the phase of one quantity, or in the phase difference between two or more quantities", so my question is, what is the "quantity" in the example with grid cells or what is "the phase difference between two or more quantities" here?
In other words, why there is the 1st shift, the 2nd and the 3rd? Why do the second and the third happen? Is it because the pattern of grid cells is an equilateral triangle and the 1st type of signal produces the 1st grid field (the blob) and the 2nd type of signal produces the 2nd blob, here I edited this picture to illustrate my thought:

and we can see, if we model it with cosine, since

Can you include a reference you are basing some of your confusion on? My initial read through your question suggests that you might be mixing together a couple concepts but I'm not certain (and it's been awhile since I thought in depth about grid cells, but I don't know of a resident grid cell expert here on biology.se).

Or to be a little less vague...when people are talking about phases in grid cells I am most familiar with phases with respect to theta, an oscillation in time, not spatial phase. So there is no reason for those phases to be in particular unit steps, like pi/3. Maybe this is where you are getting your "3 ϕ"s idea from so that's what I am wondering about a reference for.

I think this is about soft matter physics + hexacon + phase shift. Can you please describe your wished area.

There are two phases I can think of: The time phase in relation to the theta rhythm, as mentioned by Bryan Krause and the spatial phase. If you change the spatial phase, it means you are shifting the whole grid in relation to the environment it encodes without rotating the grid. Apart from these two, I don't know what the third phase could be.

This might help:
http://www.scholarpedia.org/article/Grid_cell  (written by the Mosers themselves)
"The grid of each cell can be described by three parameters:
o) spacing (the distance between fields),
o) orientation (the tilt of the grid relative to a reference axis), and
o) spatial phase (displacement in the x and y directions relative to an external reference point)."

I do not completely understand your question. Are you talking abotu three spatial phases? Or about the three angles of the triangle? Or about three shifts of the same phase parameter? I'm no expert on grid cells, but I've learned my share about them and have seen talks by the Mosers on conferences. Once I understand the question, I'll try to formulate an answer (if still required at that point)

@atiger "o) spatial phase (displacement in the x and y directions relative to an external reference point)."-so the "external reference point" is the true location of the rat in a box (or whatever the environment of the experiment is)?

@jen the grid is fixed to the animal's environment (for our purposes right now). It does not move around with the animal, so the animal's position is irrelevant if we are talking about the grid encoding of the environment. the external reference point is in the environment. E.g, a corner of the rat's box, an item in the room or something like that. something that you can look at to determine where in the room6environment you are.


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Strain vs. Species
What is the convention between setting that this organism is a strain of a specific species and what are the considerations in saying that this organism is just a strain and not a separate species entirely?

Generally strain is equivalent to sub-species or lower. but the exact usage varies depending on the type of organism.  in plants or unicellular organisms it indicated all the descendants of a single specific organism, usually becasue it possesses some unique feature. Basically it is just a clade. In animals it tends to be reserved for a group of organisms that have been interbred to the point of genetic uniformity.
Almost always a strain can still interbreed with the parent population it just has identifiable feature that unites it.
Consider an example, let's say I find or manufacture a mutant wheat plant that produces much larger seeds, and all of its offspring retain those giant seeds. But I can still crossbreed it with normal wheat. That would be an example of a strain.


text:
Database of time lapse stem cell differentiation
Currently I am working on a project about modelling the social behaviours of embryonic stem cells (or induced pluripotent stem cells). I need a series of time-lapse live cell images which recording the stem cells behaviours in cell culture, also with markers showing the differentiation state of each cell. I wonder is there public resources of this kind of data?


text:
Probability of carrier for recessive trait given parents are carriers and sister affected
I'm trying to understand more about inheritance of an autosomal recessive trait that runs in my girlfriend's family. How could I start looking at this?
My girlfriend's sister, C, is affected with a recessive trait. Her parents, A and B, are confirmed unaffected carriers. Am I correct to assume my girlfriend, D, is a carrier with probability 50%? Or must I take into consideration that we know the state of C given she is affected.
Furthermore, if I (E) have a child with my girlfriend, what is the probability that our children are either carriers or affected? My carrier status is unknown.

Welcome to Biology SE!  Although questions on human genetics are most welcome here, please note that we do not answer personal medical questions or give health advice at this site.  For advice on genetic testing etc, you should consult your physician.

@Roland Sure thing. More interested in the probability aspect of inheritance, and how it works in general

Real life is not always as simple as the paradigms you learn in high school.
However, the high school level answer is this:  Since you know your girlfriend is not affected, there is a 67% chance she is a carrier, and a 33% chance she is not.
The state of the sister is irrelevant, if you are sure both parents are carriers.
Without knowing the prevalence of the recessive allele in your population, it is impossible to know the odds of you being a carrier.  But if you are not, then your kid has a 33% chance of being a carrier.

Assuming the trait is caused by a single gene, she would indeed have a roughly 50% chance of being a carrier. If both parents are carriers but unaffected they will both be Aa (with a being the recessive mutation). For your girlfriend to be a carrier she will have to be Aa, of the 4 possible combinations her parents could have passed on (AA,Aa,aA,aa) two lead to this outcome, thus 1/2. If you are sure that she is unaffected the aa option is eliminated and she thus has a 2/3 chance of being a carrier.
If you are not a carrier but your girlfriend is it will be impossible for your child to express the trait (but would still have a 50% chance to be a carrier!). If you are both carriers you loop back to the original situation of her parents, your child would have a 25% chance of being affected and have a 50% chance of becoming a carrier. I must emphasize that real life genetic inheritance is more complex than these textbook calculations, chromosomal crossing over and whatnot can seriously alter these percentages.
I am not a health professional, consult your physician and/or get your girlfriend tested (if possible).

That calculation is only correct if the girlfriend does not know whether or not she is affected.

@swbarnes2 Yeah I apologize I misread carrier for affected.


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Genetic information storage and the extent to which it controls appearance/structure
So there are often articles about cloning from a small piece of tissue etc.
My question is (two actually) Is the Complete information about entire organism's structure stored (as in duplicated) all over the body? And is everything actually stored/based on DNA information, such as number of hairs you have including their position and texture. That would be a lot of information, I mean just taking hair as an example and its quantity and position, but there are also things about every aspect of structure, from bone composition, to position of organs, veins etc. None of it is random (ignoring mutations aspect) and all of it has to be "programmed" in initially. How can this be possible when the number of specifications is so huge?

The common phrase I've heard is "DNA isn't a blueprint, it's a recipe". More specifically, the nucleotides in DNA correspond to which proteins get made (coding DNA) and when and where (regulatory DNA). Just like a recipe doesn't specify the exact color of a cake or the position of each raisin, but does say "cook the cake for this long" (which will, in interaction with the heat of the oven, determine its color) or "put in this many raisins, at this general point in this general area", DNA doesn't contain the exact information of how you end up looking (hence why identical twins aren't really identical), but it does say how to make you how you are.
It also illustrates how much has to be "programmed" initially; how we are really needs to be understood as an interaction between DNA and the environment through the process of development, just as you can't completely understand a cake just from the recipe, you also need to know how chemistry and physics cause the things in the recipe to have the effects that they do. A lot of what goes on in development is cells growing, changing or dying depending on the chemical environment they're in, which includes what their neighboring cells are. The information in DNA basically consists of affecting that via what proteins get made when and where during development.
As for whether complete information about the entire organism's structure is stored all over the body, yes and no (but mostly yes). Yes, by default every cell in your body inherited its whole genome from the original zygote that started things, and you can indeed in theory clone a whole person from many random cells in the body. However in practice it depends on the cell: some cells lose their nucleus entirely, like red blood cells, so of course they don't contain the body's whole genome. Other cells could theoretically multiply or eliminate certain genes in a similar way as they specialize for the specific task they need to do, meaning they won't end up with the same genes as all the other cells in the body, but this isn't thought to be a common phenomenon especially in humans (cells will vary more in the expression pattern of their genes without necessarily changing the DNA sequence itself). This is also ignoring the ordinary mutation rates in DNA as the cell divides, which will yield differences between different cells of a given body even without that being a deliberate process. Hence cancer !
Some references on the possible variations of DNA in somatic cells (i.e. not ova or sperm)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497787/

It is commonly assumed that all healthy cells that arise from the same zygote possess the same genomic content, with a few known exceptions in the immune system and germ line. However, a growing body of evidence shows that genomic variation exists between differentiated tissues.

Elimination of actual DNA in nematodes and lampreys :
https://www.ncbi.nlm.nih.gov/pubmed/23123092
https://academic.oup.com/mbe/article-abstract/33/9/2337/2579241/Characterization-of-Somatically-Eliminated-Genes?redirectedFrom=fulltext
Quote from the first abstract:

Chromatin diminution is the programmed elimination of specific DNA sequences during development. It occurs in diverse species, but the function(s) of diminution and the specificity of sequence loss remain largely unknown.

I have found no mention of it happening in humans however.

Thank you for definitive answer to my first question, makes it clear now. However regarding the 2nd question (blueprint-related) I'm still not 100% clear (probably because I didn't elaborate enough). Using computer terminology, we can write a detailed Instruction that performs exact task, or we can use/rely on a Library that is "known" to accomplish a particular task. This library being Environment, the instruction would be Environment(Plant Hairs in area X). Two ways -- same result. To create the organism, DNA (or something else) must know how to use the Library. Please explain :)

I'm not sure quite what you mean by "know how to use". The computer analogy is a terrible one, but I'll try and explain as best possible in the frame you're starting from. Do you mean "know how to use" as in "is compatible with" (uses the correct syntax, etc) or as in "is aware of the adequation of the library to the program's ultimate goals" (uses a scipy library for science calculations, etc) ? In the former case, the library is the laws of physics and chemistry, DNA follows those by default because it exists in the world. In the latter case (...)

the "instructions" in DNA (also not a good analogy btw) don't come from an ultimate goal; it just so happens that various proteins being made at various points has an effect on the final organism (because chemistry and physics), and when that effect promotes the final organism's reproductive success the originating DNA pattern spreads through the population, until all organisms have it and it looks like it was put there on purpose to have that effect (which in a way it was for a certain understanding of "purpose": the effect had a causal influence on why that instruction is there now).

Still not 100% clear. Lets say initially these proteins started out at various positions and now we have a particular organism. Whatever the physics/chemistry may be, in order to survive, DNA needs to accommodate for these things. The closer the match the better success rate. Lets take an eye for example and try to design it in a biological 3D printer (if one existed) We need 1) "blueprint" or some sort of "instruction set" and 2) Something that has the ability to transform/delegate it into "design" stage.  Otherwise, why would cells just stick together forming an organ of such complexity?

@Emil the eye isn't designed in a 3D printer. Organisms are self-assembling. And there isn't a clear division between "blueprint" and "assembly", just like the brain doesn't have a clear division between "software" and "hardware". DNA isn't the passive repository of the information to build something; it is an active part of the functioning of the cell, given it's part of the production of proteins. And cells split and stick together depending on what proteins they're secreting in their membrane, and that's determined on which genes are expressed.

@Emil this is becoming quite the conversation, and I suspect you might be at the point where you'd need to post a new question, but I don't know what it would be. I would be happy to talk more to straighten out exactly what points you don't understand and why, but maybe the chat would be a better place for that: http://chat.stackexchange.com/rooms/1997/the-biosphere


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What is the mechanism by which quitting smoking causes increased appetite?
I guess it has something to do with  sugar regulation.
Does anyone know something more about this?

please feel free to add relieble source of information for your claim or i think your post is going to be close because now its too opinion based,

@L.Diago Every internet site which mentions symptoms when someone quits smoking (nervousness per example) mentions also increased appetite

http://www.eje-online.org/content/170/2/219.short

But still i would be rather skeptical about this than making some generalization about this phenomenon.

@LDiago weight gain is a clear and consistent finding with smoking cessation. Where are you reading that it causes appetite suppression?

What is the mechanism by which quitting smoking causes increased appetite?

Research has generally focused on weight gain, rather than increased appetite, since it's a more objective outcome.
Smoking cessation has been clearly and consistently shown to be associated with weight gain, in both retrospective and prospective studies, and nicotine replacement seems to reduce some, but not all of the effect, at least while it's used.
There is an excellent, though now aging review of both the effect and potential mechanisms behind a paywall by Filozof. One of the most cited early articles is free at NEJM.
The mechanism of this weight gain is an active area of research, and, as discussed in Filozof, includes increased appetite with associated increase in calorie intake, decreased resting metabolic rate, and decreased physical activity.
Leptin, a hormone that increases both satiety and energy expenditure, is actually increased in people who stop smoking at the same time they are gaining weight. This finding has been convincingly demonstrated and replicated. Leptin insensitivity is a strong candidate for the primary driver of the increase in appetite (and weight gain) after smoking cessation.
Of course, since cigarette smoking causes profound changes in gene regulation, smoking cessation likely does as well. The full answer is almost certainly multifactorial.


text:
Database for drug-target relation
I'm writing a thesis on bioinformatics and looking for drug-target databases. I'm implementing a open-source application for a tool called Cytoscape and so far I've used a open-source database called DrugBank to retrieve drug-target data, but I've read a paper on a database called Drug2Gene that combines multiple open databases into a unified format. The paper is from 2014, but all websites are down and I was wondering if someone here knows of any other databases/resources that does this and is maybe up-to-date? I want to utilize as much open-source data on drug to target relation as possible to provide a simple way of accessing all these resources. Drugbank is regularly updated and a good source, but with so many different databases with a decreasing overlap of data I was happy to stumble across Drug2Gene database only to realize I can't get it and it's probably not up-to-date.
I will be very thankful for any tips as I'm purely a Informatician and feeling helpless in finding thing related to biology.
Source: Drug2Gene paper

There are quite a lot drug databases. I think DGIbd is a good place to start (see below). Further there are a lot of databases which describe drugs and their targets, take a look at these (and the links at the bottom) hopefully you can use several of these in your implementation.
SIDER

SIDER contains information on marketed medicines and their recorded
  adverse drug reactions. The information is extracted from public
  documents and package inserts. The available information include side
  effect frequency, drug and side effect classifications as well as
  links to further information, for example drug–target relations.

DrugCentral

DrugCentral provides information on active ingredients chemical
  entities, pharmaceutical products, drug mode of action, indications,
  pharmacologic action. We monitor FDA, EMA, and PMDA for new drug
  approval on regular basis to ensure currency of the resource. Limited
  information on discontinued and drugs approved outside US is also
  available however regulatory approval information can't be verified.

Therapeutic Target Database

Therapeutic Target Database (TTD) is a database to provide information
  about the known and explored therapeutic protein and nucleic acid
  targets, the targeted disease, pathway information and the
  corresponding drugs directed at each of these targets. Also included
  in this database are links to relevant databases containing
  information about target function, sequence, 3D structure, ligand
  binding properties, enzyme nomenclature and drug structure,
  therapeutic class, clinical development status. All information
  provided are fully referenced.

Potential drug target database (PDTD)
NOTE: I think this one is coupled to DrugBank however you can take a look here

PDTD is a dual function database that associates an informatics
  database to a structural database of known and potential drug targets.
  PDTD is a comprehensive, web-accessible database of drug targets, and
  focuses on those drug targets with known 3D-structures.

PharmGKB

The PharmGKB is a pharmacogenomics knowledge resource that encompasses
  clinical information including dosing guidelines and drug labels,
  potentially clinically actionable gene-drug associations and
  genotype-phenotype relationships. PharmGKB collects, curates and
  disseminates knowledge about the impact of human genetic variation on
  drug responses through the following activities: Annotate genetic
  variants and gene-drug-disease relationships via literature reviews
  Summarize important pharmacogenomic genes, associations between
  genetic variants and drugs, and drug pathways Curate FDA drug labels
  containing pharmacogenomic information Enable consortia examining
  important questions in pharmacogenomics Curate and participate in
  writing pharmacogenomic-based drug dosing guidelines Contribute to
  clinical implementation projects for pharmacogenomics through
  collaborations Publish pharmacogenomic-based drug dosing guidelines,
  very important pharmacogene summaries and drug-centered pathways
  Display all information on the website and provide comprehensive
  downloads

STITCH

To facilitate access to this data, STITCH (‘search tool for
  interactions of chemicals’) integrates information about interactions
  from metabolic pathways, crystal structures, binding experiments and
  drug–target relationships. Inferred information from phenotypic
  effects, text mining and chemical structure similarity is used to
  predict relations between chemicals. STITCH further allows exploring
  the network of chemical relations, also in the context of associated
  binding proteins. Each proposed interaction can be traced back to the
  original data sources. Our database contains interaction information
  for over 68 000 different chemicals, including 2200 drugs, and
  connects them to 1.5 million genes across 373 genomes and their
  interactions contained in the STRING database.

SuperTarget and Metador

An easy-to-use query interface enables the user to pose complex
  queries, for example to find drugs that target a certain pathway,
  interacting drugs that are metabolized by the same cytochrome P450 or
  drugs that target the same protein but are metabolized by different
  enzymes. Furthermore, we provide tools for 2D drug screening and
  sequence comparison of the targets. The database contains more than
  2500 target proteins, which are annotated with about 7300 relations to
  1500 drugs; the vast majority of entries have pointers to the
  respective literature source. A subset of these drugs has been
  annotated with additional binding information and indirect
  interactions and is available as a separate resource called Matador.

Pharos

Pharos is the user interface to the Knowledge Management Center (KMC)
  for the Illuminating the Druggable Genome (IDG) program funded by the
  National Institutes of Health (NIH) Common Fund. (Grant No.
  5U54CA189205-02). The goal of KMC is to develop a comprehensive,
  integrated knowledge-base for the Druggable Genome (DG) to illuminate
  the uncharacterized and/or poorly annotated portion of the DG,
  focusing on four of the most commonly drug-targeted protein families:
   G-protein-coupled receptors (GPCRs); nuclear receptors (NRs); ion
  channels (ICs); and kinases. For more information on opportunities in
  the druggable human genome see this poster

KEGG drug

KEGG DRUG is a comprehensive drug information resource for approved
  drugs in Japan, USA, and Europe unified based on the chemical
  structures and/or the chemical components, and associated with target,
  metabolizing enzyme, and other molecular interaction network
  information. All the marketed drugs in Japan, not only the
  prescription drugs but also the OTC drugs, are fully represented in
  KEGG DRUG and integrated with the package insert information (labels
  information). These include crude drugs and TCM (Tradictional Chinese
  Medicine) drugs.

The IUPHAR/BPS Guide to PHARMACOLOGY (database)

The information in the database is presented at two levels: the
  initial view or landing pages for each target family provide
  expert-curated overviews of the key properties and selective ligands
  and tool compounds available. For selected targets more detailed
  introductory chapters for each family are available along with curated
  information on the pharmacological, physiological, structural, genetic
  and pathophysiogical properties of each target. The database is
  enhanced with hyperlinks to additional information in other databases
  including Ensembl, UniProt, PubChem, ChEMBL and DrugBank, as well as
  curated chemical information and literature citations in PubMed.

DGIbd

The druggable genome can be defined as the genes or gene products that
  are known or predicted to interact with drugs, ideally with a
  therapeutic benefit to the patient. Such genes are of particular
  interest to large-scale cancer profiling efforts such as TCGA, ICGC
  and others that identify lists of potential cancer driver genes from
  high-throughput sequence and other genome-wide data. In cancer
  therapy, the increasing number of targeted drugs--those designed to
  inactivate proteins carrying activating amino acid changes as
  determined by mutational analyses--make more compelling the need for a
  searchable database of drug-gene interactions, available here.

There are a lot more databases, maybe these links will help you:

Drug to Target/Gene/Protein Interaction Databases
Question: Database Of Drugs Targeting Genes
Drug Databases


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Stink bug identification
This is a stink bug that I found in Indiranagar, Bangalore. It was dead at that time and had become stiff, so the following are the best pictures I could get. It is 2cms in length. I tried searching on the net on various websites but I didn't find a match for the colouration on the dorsal side. Also, I would like to know what those protrusions on the top half of the shield ( excuse me if 'shield' is the wrong terminology) are. They seemed to be quite a troublesome feature as none of the reference pictures I saw on the net seemed to have bugs with these 'protrusions' .

I agree, but none of the species (which I found on the net) of Euschistus sp. Have such pronounced protrusions. Maybe I'm missing something?

I looked through the appropriate volume of Fauna of British India but couldn't find a good match (not surprising; the volume in question dates from 1902 and illustrates 201 of the 542 species known at the time); at the time Euschistus had not yet been found in India, and the species of Halyomorpha illustrated is not a good match.

I've been searching for quite some time in different subfamilies of Pentatomidae and have to admit defeat. Until now I'm unable to retrieve any information about the marvelous bug you have found.
The pictures you took are really great, by the way!
Maybe you can ask Dr. Salini for help? :)
She studied 94 species of Pentatomidae according to the following website: http://www.nbair.res.in/salini.php


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Did the hyoid bone of Australipetichus afarensis have a hyoid bulla?
The hyoid bulla is present in Chimpanzee hyoid bones, and not in Humans. Does A. afarensis have a hyoid bulla?

Short answer:
Yes.
Longer but still short answer:
H. heidelbergensis and H. neanderthalensis have a modern human-like hyoid bone. A. afarensis has a hyoid bulla similar to modern chimpanzees.
The hyoid bone is thought by some to be important in human evolution because of its position in the throat and the possibility that morphological changes in the hyoid were important for the development of speech. However, this view is not without controversy, and it is probably not sufficient to use hyoid bone morphology as a definitive marker for development of speech similar to modern humans, though it may be suggestive.
Some quotes from two references on the morphology of the hyoid of A. afarensis:
Alemseged, et al. 2006:

[the hyoid of A. afarensis] "...is
  most similar to that of juvenile African apes, and unlike that of
  modern humans11,12. The exposed greater horn is slender, and the
  body is expanded anteriorly, forming a bulla that is deep relative to its
  breadth and height..."

Steele, et al. 2013:

"...the Dikika juvenile australopith hyoid is deep for its height (Figure 9) and width and is morphologically chimpanzee-like. This similarity applies both when comparing only subadults from the three extant species (Figure 9A), and when comparing across all observed age classes (Figure 9B..."

References:
Alemseged, Z., Spoor, F., Kimbel, W. H., Bobe, R., Geraads, D., Reed, D., & Wynn, J. G. (2006). A juvenile early hominin skeleton from Dikika, Ethiopia. Nature, 443(7109), 296-301.
Steele, J., Clegg, M., & Martelli, S. (2013). Comparative morphology of the hominin and african ape hyoid bone, a possible marker of the evolution of speech. Human biology, 85(5), 639-672.

Is the A. afarensis hyoid bone in the Steele, Clegg, Martelli paper, from Selam (the 3 year old, aka "baby lucy") found in Dikika ? That's the only fossil remnant of an A. ararensis hyoid bone I've come across (https://www.nature.com/article-assets/npg/nature/journal/v443/n7109/images/nature05047-f3.2.jpg)
From the image, it's difficult to make out a hyoid bulla, and the Steele, Clegg, Martelli paper mentions that they "interpret the morphology", would you happen to know if they go by indirect evidence, and if so, what?

The Dikika specimen was a child also, 3 years old, and child hyoid bones have different proportions than adult ones (https://boneclones.com/images/store-product/product-223-main-main-big-1418687938.jpg)

I think that paper will be the best you get for an answer - as you say, if there are no other fossils, you aren't going to magically find one on Biology.SE. Steele et al. compare the Dikika sample to juveniles of the extant apes. The line about "interpret the morphology" has nothing to do with the type of evidence they used, they are just referring to comparison of all of the extinct samples with the extant species they studied.

A quote from the paper in case you cannot access it: "...the Dikika juvenile australopith hyoid is deep for its height (Figure 9) and width and is morphologically chimpanzee-like. This similarity applies both when comparing only subadults from the three extant species (Figure 9A), and when comparing across all observed age classes (Figure 9B..."

If the extinct sample is one, and its this one https://www.nature.com/article-assets/npg/nature/journal/v443/n7109/images/nature05047-f3.2.jpg
are details, like the hyoid bulla, preserved? just by looking at it, it looks like its not protruding at the anterior end, http://i.imgur.com/BYdjvHx.jpg

It looks to me like it is, clearly moreso than a modern human of the same age (from the article I referenced). Note also that your reference refers to it as a bulla as well. It's possible there is some disagreement in the field, but I see two published sources that agree with each other and no evidence otherwise.

the Steele paper says that "and one (represented by the body only) from the Dikika Australopithecus afarensis (Alemseged et al. 2006)"
while the Alemseged says "the exposed greater horn is slender, and the body is expanded anteriorly, forming a bulla that"
are they not contradicting one another? how can the greater horn be exposed, if only the hyoid body was in the fossil?

@homonidae I can't speak for the authors, but my guess is that Steele is referring to inclusion in their own quantitative analysis, and by their quantitative analysis only the body was fully present for quantification (I agree with you this is not clear in the statement you quoted). The qualitative description by Alemseged would not have that limitation (and Alemseged's own quantification also was based on the body I believe). All that said, your question is about a feature of the body, so I'm not sure why the presence of the horn is particularly relevant.

I'm interested in knowing about the fossil record.
The airsacs, as resonance organs, would have de-evolved as a pharyngeal acoustic chamber formed with the descent of the larynx.
I'm also interested in the semi-aquatic ape theory, and that the larynx descended for inhaling large amounts of air while surfacing. In that universe, the loss of airsacs could have been a later adaptation, as the expanded pharyngeal tract formed an acoustic resonance chamber.


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fermentation in soil bacteria
I am doing a project on microbial fuel cell. For the purpose of the efficiency of the question, MFCs can be summarized to:

Devices that use anaerobic bacteria as the catalysts to oxidize organic and inorganic matter and generate current. I referenced this article

While writing the analysis I was quite confused about the fermentation process in which anaerobic bacteria in soil undergo. Usually the fermentation process and its byproduct would be specified, however, in this case there are numerous bacteria that the soil contains.
I want to ask if there is a specified fermentation process that the soil bacteria undergo (which is probably not the case), or is it unknown so I should just talk about fermentation in general.
Thanks in advance!
ps. it would be greatly appreciated if a link to some websites or articles that would possibly help me is included :)


text:
Why is suicide inhibition considered a catalytic reaction when the catalyst is irreversibly modified because of the reaction?
I understand that this might be meaningless semantics, but I'm confused and would appreciate clarification.
I've always been taught that, a catalyst is, by definition, a substance that is increases the rate of a reaction but is not consumed by the reaction. Enzymes are a subset of catalysts, so all enzymes must share catalyst properties. From my understanding, suicide inhibition irreversibly modifies the enzyme and consumes it during its normal catalysis reaction.
How can an enzyme that is consumed during its normal catalysis reaction still be an enzyme? Wouldn't it make much more sense to call it a reactant?

People are people. If you give them strychnine they die, but they are still people. Enzymes are enzymes, if you poison them with inhibitors they ‘die’, but they are still enzymes. Yes this question is meaningless, and it hardly justifies the description of semantics. And next time you post, please read how to ask a good question first and quote your sources, not your understanding.

It's not clear what the confusion stems from, but perhaps it was from the first sentence of the Wikipedia article, which says:

Suicide inhibition ... is an irreversible form of enzyme inhibition that occurs when an enzyme binds a substrate analogue and forms an irreversible complex with it through a covalent bond during the normal catalysis reaction.

This might mislead someone by using the phrase "during the normal catalysis reaction", which I suppose could be interpreted as saying the enzyme only catalyzes reactions involving the inhibitor.  That is very much not the case.
The normal action of the enzyme is with some other molecule, the normal substrate of the enzyme, and the catalytic reaction produces and release the product, leaving the enzyme in its original form.
In contrast to this, the inhibitor is an analogue of the normal substrate molecule, that is to say, a molecule which is very similar (in the target region at least) to the normal substrate molecule.  Because of the similarity, the enzyme will cause the inhibitor to undergo the same chemical reaction as the normal substrate. However, the inhibitor will thereby become active in a way which causes it to irreversibly bind to the enzyme and thus, unlike the normal substrate, will never be released.


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The Water hyacinth and its ability to absorb pollutants from the water
What genes makes the water Hyacinth able to absorb pollutants from the water it lives in? (2) can this gene be successfully harvested? And how?

Genes don't necessarily work in isolation (most don't). An ability to absorb pollutants would likely be a combination of many genes.
Also, what constitutes a "water pollutant" is very broad - you could be talking about pesticides, heavy metals, fertiliser, organic waste... If water Hyacinth absorbs all of these, it could just be the result of absorbing more water than other plants (with pollutants accumulating in the plants). Who knows - you should state your source of information.
In terms of how to figure out what gene(s) are responsible, you could consider a radioactive tracer to tag the specific compound (or even element) that you consider Hyacinth to absorb better than other plants. This might give you some idea of how it's doing what it's doing. For example, if you think it's absorbing a compound, you can tag that compound with a radioactive tracer, see where it's being accumulated (even it's path), and from there figure out what's happening.
The fastest path to figuring out which gene(s) are responsible from there would be to build up a list of all the genes you think might be involved in this path and create an array of cloned plants with those genes removed. If you remove the correct gene(s) from the equation, the plant will have less or no proclivity for absorbing the type of pollutants in question.

Ronald Greeff thanks for your reply. I would like to start by informing you that I am not a biologist, so I may need a little more help.
(1) How would I build up a list of genes likely to be involved?
(2) And create an array of cloned plants with those genes removed?

@NnekaOnwuachi-Iheagwara (1) I would check the literature. Usually, you would knock a gene out then try to figure out its function by looking at the effect of the gene's loss. You could also search the BLAST database. (2) You should take a look at "gene targeting", specifically using Agrobacterium. I believe today most people would use CRISPR/Cas


text:
What is the reason behind that children can cry but can't laugh?
I have a cousin who is almost 1 months old. As a normal child of her age, she cries a lot. But I noticed first that she doesn't laugh. So I noticed and found out that other children of her age also don't laugh. So how is it possible that childs can cry but can't laugh? What is the explanation for this?

Because life isn't funny yet. Sometimes, though, they smile in their sleep very early on, and smile socially as early as one month of age. They laugh when they can appreciate something funny - a funny face, a funny sound, a funny feeling (a 'zorbit'). Discomfort is present from the beginning, hence crying.

@anongoodnurse Why is discomfort present from beginning?

Hunger is a kind of discomfort. Cold, or being too warm, intestinal gas, uncomfortably wet diaper, being alone, having a startle reflex triggered, ad infinitum. Discomfort likely begins in utero, but believe me, every baby I ever delivered cried on delivery; I never had to slap a single one (nor did I hold them upside down. Being born is uncomfortable. Is it really a mystery?


text:
Is a flower having 12 petals trimerous or tetramerous?
Suppose if a flower has 12 petals. Then 12 is a multiple of both 3 and 4. So which category of flower is it? Is it trimerous or tetramerous?

Suppose if a flower has 12 petals. Then 12 is a multiple of both 3 and 4. So which category of flower is it? Is it trimerous or tetramerous?

Merosity, in the context of your question, is the number of petals in the corolla.
Refer to "Gray's Botanical Textbook: Structural botany", on page 176, section 322:

"322. To designate the particular plan, such familiar terms of Latin derivation as binary, ternary, quaternary, quinary, unary, &c., are sometimes employed, denoting that the parts of the flower are in twos, threes, fours, fives, or sixes. More technical and precise terms, equivalent to these, are composed of the Greek numerals prefixed to the word meaning parts or members, as Alonomerous, for the case of a flower of one member of each ; Dimerous, of two, or on the plan of two members of each ; Trimerous, of three, or on the plan of three members ; Tetramerous, of four, or on the quaternary plan ; Pentamerous, of five, or on the quinary plan ; Ilexamerous,$^{[1]}$ of six, or on the plan of six members to each circle. But, in Monocotyledons, so-called hexamerous blossoms are really trimerous, the sixes being double sets of three.
[1] These may be shortly written 1-merous, 2-merous, 3-merous, and so on up to 10-merous (decamerous), 12-merous (dodecamerous), &c.".

Because counting is done using Greek cardinals a corolla with 12 petals is dodecamerous. One with 4 sets of 3 is trimerous, and one with 3 sets of 4 is tetramerous.


text:
What is the weight of a single human sperm (spermatozoon) compared to a single human egg
While the difference in dimension is well covered, I have been unable to find the mass measurements of each.

Hey tohster! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

OK. That is new. I'm a member of quite a few stackexchange sites and I've not seen a requirement to document what efforts the user has gone through to answer the question. I used reasonable efforts to search online for an answer but was unable to find one, which is why I made the effort to post the question here so that others do not have to go through the same process.


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Emulsifying action of bile salts
n my book, It is given that the action of Bile salts (a part of Bile juice) is similar to the emulsifying action of soaps on dirt. The role of bile salts is to break down the fat into smaller globules.
I don't understand this and cannot find it on the internet. Can someone help me with this?

The Wikipedia entry on Bile says it all:

Bile acts to some extent as a surfactant, helping to emulsify the lipids in food. Bile salt anions are hydrophilic on one side and hydrophobic on the other side; consequently, they tend to aggregate around droplets of lipids (triglycerides and phospholipids) to form micelles, with the hydrophobic sides towards the fat and hydrophilic sides facing outwards. The hydrophilic sides are negatively charged, and this charge prevents fat droplets coated with bile from re-aggregating into larger fat particles.


text:
How different can the Tm be between 2 primers?
I have a forward primer with Tm 85 degree Celcius. I cannot change this primer. But I have two options for the reverse primer. One with Tm 65 degree Celcius (Annealing at 65 degree Celcius) and another with 72 degree Celcius (Annealing at 72 degree Celcius).
First of all, will either of the primers work for me?
If so, which pair would be better?

You should check with the manufacturer of your PCR kit. I use NEB and their online tm calculator warns you when tm difference is greater than 5C suggesting that 5C or less difference is best.

Simple: try both.

This really depends on your application, but from my experience 2-3 degrees with a max of 5°C difference usually works. The more the melting temperature differ, the more you need to optimize all the other parameters like salt and magnesium concentration, amount of enzyme, annealing and elongation times and so on.
85°C melting temperature seems very much for me, as you are 13°C over the optimal working temperature of the Taq polymerase. This willmost likely  lead to a lot side products with incompletely bound primers. You can change the annealing temperature by shortening the 3' end of your primer (I assume that you need a specific starting point) so you get down at least a bit. Then I would probably order both other primers and test which ones works better, but I wouldn't expect that this works immediately and will need at least some optimization.
Can you give some more information why you can't use other primers and on your application?

Thanks, Chris. I cannot change my forward primer as it incorporates a restriction site in 5' end and a point mutation near 3' end. I think i just have to try it out and play with the parameters. I will comment once I do my experiment. I welcome any other suggestions.

The default parameter provided by "primer-blast" is 3 degree (max difference between the melting temperatures of the pairs) .
that said I think it really depends on the application. in case of cloning (in my experience) you can allow wider ranges of delta Tm between primers (in this case I used to use the average Tm of the two primers as annealing temperature). you accept to have a bad efficiency but eventually you can pull out your insert from the gel and clone it in a vector for a prep.

Thanks, Pedrini. This is the case of cloning. With all your suggestions, I am just gonna try with the same primers.

@RKK what do you mean "with the same primers"? if none of the two reverse is working you can even redesign one by elongate at the 3' to match the Tm of the forward.


text:
How many primary oocytes in human female body at birth?
https://discovery.lifemapsc.com/library/review-of-medical-embryology/chapter-4-gametogenesis-oogenesis
In the above site, I see that:

About 2 million primary oocytes are found in the ovaries of a newborn
  femal Many regress during childhood so that at puberty about 30-40
  thousand remain. Only about 200-400 of these ever reach full maturity
  after puberty and are expelled at ovulation during the female's
  reproductive life

http://www.pnas.org/content/107/22/10280.full
Also, from this site, I see that

Human ovaries contain follicles as basic functional units. The total
  number of follicles is determined early in life, and follicle
  depletion leads to reproductive senescence. Human follicles begin
  development during the fourth month of fetal life, and each human
  ovary contains ≈400,000 follicles at birth.

From my understanding, there is one oocyte inside one follicle. So, two number should be the same. Why there is a big difference? Or my understanding is just wrong?
PS. I am doing research for my sci-fi, I didn't learn this topic in any college, sorry if this is a silly question.

keep in mind the body is capable of generating new oocytes and follicles, https://link.springer.com/article/10.1385/ENDO:26:3:301

@John definitely read about it in source 3 of the answer.

Short answer: The developmental process starts from oogonia as follows:

Oogonia(7million) in the foetus develops into primary oocyte(2million) in the foetus prior to gestation which again develops into primordial follicle(700,000-800,000)at birth.

From the second excerpt of your question I could understand that it said, "each ovary contains  approx. 400,000 follicles at birth." which is definitely correct if you consider that total number of follicles in both the ovaries would give 800,000.

Excerpts from the references that lead to the short answer above:

In the developing female fetus, oogonia become primary oocytes that begin the first division of meiosis. However, this division is not completed and the primary oocytes remain “frozen” in the prophase stage of the first meiotic division.
At birth, oogonia are no longer present. Each primary oocyte is surrounded by a single layer of squamous epithelial cells called follicular cells. The primary oocyte together with its follicular cells is called a primordial follicle. There are about two million primordial follicles with their primary oocytes in the ovaries at birth suspended in the first division of meiosis.
As the female grows, primary oocytes begin to die and disappear with their follicular cells. This process continues until puberty when there are only about 400,000 primordial follicles left in the ovaries. The primary oocytes continue the process of oogenesis after puberty begins.[Source]

The total number of primary oocytes at birth is estimated to vary from 700,000 to2 million. During childhood most oocytes become atretic; only approximately400,000 are present by the beginning of puberty, and fewer than 500 will be ovulated.[Source]

Primary oocytes reach their maximum development at ~20[6] weeks of gestational age, when approximately seven million primary oocytes have been created; however, at birth, this number has already been reduced to approximately 1-2 million.Recently, however, two publications have challenged the belief that a finite number of oocytes are set around the time of birth.[Source]

In the human embryo, the thousand or so oogonia divide rapidly from the second to the seventh month of gestation to form roughly 7 million germ cells.[Source]

REFERENCES:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0008772

"There are about two million primordial follicles with their primary oocytes in the ovaries at birth suspended in the first division of meiosis." doesn't this imply that there are 2Million follicles at birth, which clearly contradicts the information provided by OP?

@JM97 I want u to read source 2.that will answer ur question...

then add this point of source 2 :  "The
total number of primary oocytes at birth is estimated to vary from 700,000 to
2 million", could you provide any research paper/ or something more credible for that statement in second source? It would be much helpful.

Thank you @JM97 You make this question active again. lol


text:
Replication cohorts in microbial GWAS
Replication in an independent cohort is of course the gold standard in GWAS studies, and many high profile journals will now (quite rightly) not accept finding indicating a phenotype genotype association without evidence of replication.
However GWAS is no longer the domain only of human genetics and is being increasingly used on microbial species, pathogenic on humans, animals, and plants. However having read many of these studies (mostly in plant pathology) i can find no discussion of technical replication practices in their methods. In my own research I intend to conduct GWA between snps and gene presence-absence genotypes gathered by illumina sequencing, and phenotypes of virulence (as a continuous quantitative variable) when inoculated onto the host plant (which is wheat), of a large population of a fungal pathogen. i have inoculated 120 plants with 120 isolates of the pathogen, and i'm an additional replication cohort of 80 plants and isolates.
My question is, what is required to make these additional inoculations an 'independent' cohort?
The idea of independence in technical replicates is to correct for systematic bias present in the discovery cohort, I will likely grow these plants in a separate greenhouse bay for example (although since the different host-isolate combinations are randomised within the greenhouse even this may not be necessary); in a human GWAS different genotyping methods would be ideal in the replication cohort due to possible introduction of bias in the snp-chip, in my own study i'm unsure if this would be necessary as variants in my data will undergo stringent filtering prior to genotype calling.
If anyone could help point out to me what my possible sources of systematic biases are, i'd be very grateful.


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Investigating rare variants in ethnically different populations (European ancestry & African ancestry)
If you are investigating low-frequency and rare variants for a complex trait using exome sequencing, why would one consider using different populations (African ancestry and European ancestry) especially considering that the populations have different allele frequencies. Is the main object to see if they're could possibly be novel rare variants in each population at different allele frequencies?

Mainly you do this because these populations have segregated long time ago and developed differently. You will find rare SNPs for pigmentation in europeans that are not present in the more ancient african population (and must therefore be occured after the populations divided), examples are the so called "golden mutation" in SLC24A5 (rs)

Too long for a comment, but sort of:
Mainly you do this because these populations have segregated long time ago and developed differently, so it is more likely to identify these polymorphisms. It is also helpful to use populations for this which mixed not too much with other populations (thats why north-americans are usually not used here, as America was kind of a melting pot).
You will find rare SNPs for pigmentation in europeans that are not present in the more ancient african population (and must therefore be occured after the populations divided), examples are the so called "golden mutation" in SLC24A5 (rs1426654) or a polymorphism in IRF4 (rs12203592).


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What is the upper limit of number of SNP based mutation in any protein?
I want to know if there is any upper limit of, how many point mutation a protein can have because of disease or nsSNPs? The general studies only focus mostly on a single or double site mutation of any protein structure.

Aren't you limiting yourself to "one" (SNP)? The more mutations, the more likely the protein will not be functional. Theoretically, there is no upper limit. The more vital the protein, the more likely a SNP will adversely affect the individual, and the more likely more mutations will be lethal.

@anongoodnurse: Actually, I wanted to know same thing. If there is any method to determine, how many mutation makes it lethal (or in other words non existent).

Which protein are you wondering about?

Depends on the protein. Also depends on the kind of substitution that is happening. Some functional proteins can tolerate deletion of huge segments. Selection would happen only if the SNP has an adverse effect under the ambient conditions.


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Question regarding stop codon
I just wanted to ask that in a given RNA, If there is a start codon and no stop codon, is it still considered mRNA, I mean can it be translated to a protein ?

Possible duplicate of Mutation That Loses Stop Codon

@Adrian …and then again possibly not a duplicate, as the poster has given a single tag of DNA sequencing. Are you asking about interpreting the results of DNA sequencing? When you ask about a given RNA, do you mean mRNA? And are you talking about an actual case or a homework question or what? You have already attracted two close votes. If you want an answer I would edit your question quickly, before I add my vote as "unclear what you are asking".

Yes, this is still considered mRNA. A lack of stop codon is usually due to a so-called readthrough mutation, where DNA sequence changes within the stop codon and after transcription it can no longer be recognized by release factors. But yes, ribosomes still recognize the mRNA molecule and start synthesizing abnormal proteins, usually until the ribosome stalls on the 3' end of mRNA and can neither go further nor detach. There are various mechanisms converting this "stalling signal" to a chain of intracellular reactions that lead to degradation of that protein and that abnormal RNA.
Bacteria for instance have a very curious mechanism of solving that problem, namely a tmRNA molecule that is targeted to a stalled ribosome by some specific proteins and acts as an aminoacyl-tRNA as well as mRNA template. It resumes translation, allowing addition of a peptide tag to the malformed protein, which will serve as a marker for degradation. More on that here:
https://en.wikipedia.org/wiki/Transfer-messenger_RNA
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358797/


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Why introduction of an extra copy of a gene related to pigmentation causes RNA interference in Petunia?
RNAi became famous after Fire and Mello experiment in C.elegans; however, it had been observed before. In the 80's, Jorgensen was trying to increase pigmentation of Petunia flowers by introducing extra copies of chalcone synthetase gene, which encodes an enzyme involved in anthocyanin synthesis.
However, this experiment lead to post transcriptional gene silencing (PTGS) by a mechanism that was not understood at that time, called RNA interference.
Here
you might find more information about the experiment (including the vector used to introduce the gene).
I know how RNAi works by the classical pathway; however, I didn't understand how an extra copy of the gene could generate gene silencing. Introducing of DNA sequences has been used to knock downs target genes, however, generally these sequences are planned so that they will form a hairpin which is recognised by Dicer; probably, the researcher did not use such a sequence. Moreover, exogenenic genes are widely used without resulting in unplanned RNAi.
Does someone know more information about what possibly happened in the experiment to produce RNAi?

The answer is in the slides you provided a link to. The key fact is that Craig & Andy did careful controls to show that it was the presence of dsRNA in both the sense control, and in the anti-sense experimental sample that was responsible for the RNAi-mediated knock-down.  Actually, Ken Kemphues showed this earlier in a Nature paper (the control also knocked down gene expression) but did not pursue the mechanism.
Therefore, I infer that the transgenic gene expression construct introduced into the petunias must also give rise to dsRNA. I am less familiar with the consequences of introducing foreign DNA into a plant cell (e.g., does a single copy become integrated, multiple copies?, is it maintained extrachromosomally?)


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Is it possible to isolate and analyse intermediates of protein folding?
I would like to know if there is an assay which could allow us to analyse a protein before it has assumed its 3D functional form.
While studying structural biology, I only came to know the forces that stabilize the structure, but not the gap between the original random coil and the protein in its native form.

http://en.m.wikipedia.org/wiki/Protein_folding#Experimental_techniques_for_studying_protein_folding

Sometimes multiple techniques are combined, such as in intrinsically disordered proteins, like so.

This is difficult. You need to use stopped flow methods(CD, fluorescence, NMR) or single molecule methods. What exactly do you want to know about the protein? I mean, it would be hard to get the complete accurate 3d structure, as you can't crystallize an intermediate. Apart from that, if you have an accurate folding simulation for that protein, you can of course see what the common intermediates are. I am sure that if you have the Rosetta protein folding algorithms, you know the final structure, you can calculate likely intermediates with some accuracy. Then you may be able to use stopped flow methods to try to refuse those findings. If that fails, you may be able to make a convincing case that you found those intermediates.

Can you add sources or references to your answer?


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Examples of how the presence or absence 2'-hydroxyl groups influence physicochemical properties of DNA and RNA
I know, for instance, that RNA is much more succetible to alkaline hydrolysis than DNA and this difference is determined by the presence of 2'-hydroxyl group in ribose.
I have also heard that "DNA is more stable" and thus was selected as the repository of genetic information. Though, I still haven't understood why the lack of just one hydroxyl would lead to more stability...

@Chris ok, I will actually delete the other because something similar has already been asked

My answer to this question may interest you, specifically the part about sugar pucker: http://biology.stackexchange.com/questions/19115/what-makes-dna-helical

From a chemical point of view, the phosphate can form a bond with the 2' hydroxyl, forming a cyclic structure and breaking the bond with the next nucleotide, thus breaking the RNA backbone.

As user137 said, the general base abstracts a proton from the 2'OH and subsequently the 2'O- renders a nucleophilic attack on the δ+ Phosphorous, leading to the hydrolysis of the phosphodiester bond. There can be slight variations in the mechanism and the intermediates; for details see this review.

After hydrolysis both 2'- and 3'- phosphates can form.
RNA is not thermodynamically unstable; apart from being unstable in the presence of a strong base RNA is biochemically unstable too. This is because there are several RNAses and most of them degrade RNA by a mechanism similar to alkaline hydrolysis (they cannot act on DNA). Also see this post.


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What network motifs or other mechanisms can make the expression of a gene invariable to the environment?
Next to double positive feedback loops and chromatin modification, which other mechanisms can make a gene susceptible to a certain environment in one cell-type but not in another?

This phenomenon of being insensitive to certain fluctuations is called robustness. The fluctuations can be of two kinds for an input-output device such as a gene that is activated by a signal:

Fluctuations in the signal
Fluctuations in the intrinsic parameters

Signal fluctuations can be temporal but parameter fluctuations are not (parameters are supposed to be time invariant). Parameter fluctuation can exist in a genotypic space or a population of cells because of variation.
Some motifs are robust to signal perturbations whereas some are robust to parameter fluctuations.
Negative feedbacks and incoherent feed-forward can confer robustness by correcting the output fluctuations because of fluctuations in the input.
When an all or none sort of (binary: one state need not be smaller in magnitude than the other) behaviour is important, then positive feedbacks confer robustness to such systems because of their property of bistability.
I cannot recall any particular motif that is robust to parameters. There are certain cases though (I am still working on that!! :P).
In any case environment can be thought of as an input.  For your question "what mechanisms can make a gene susceptible to a certain environment in one cell-type but not in another":
There can be a heterogeneous population of cells which can arise because of bistability or even otherwise, due to stochastic effects. If the gene that is in one of the two states (expression levels) in these two sub-population of cells, and this gene is responsible for the expression control (the controller gene in feedback), then one sub-population will be sensitive to the environment while the other will not be.
For more information on biological robustness read this review.


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Potato with purple veins!
Today while cooking with potatoes when I cut open a potato(raw) which was looking perfect from the outside showed purple veins. I threw it in my kitchen garden but than I wondered what it could be

Questions

Why did my potato developed these purple patterns?
What could be that purple pigment?
Are such potatoes Edible?

PS: The potato was not old. It was quite fresh.

The potato developed this pattern because it's (probably) natural to cultivar you're growing or due to cross-pollination.
Purple pigment is anthocyanin. It's perfectly normal and considered as more healthy (as those varieties of potatoes contain more antioxidants and vitamin C) and even 'gourmet'.


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Why is cholera toxin added to certain culture media?
I was reading an article [1] where they cultured SEB-1 human sebocytes in DMEM F12 + FBS + EGF + adenine + hydrocortisone + insuline as well as cholera toxin. Why is cholera toxin added to the media? Will the toxin not initiate some kind of unwanted immune response?

https://www.ncbi.nlm.nih.gov/pubmed/25647437/

It is used to generate cAMP which promotes sebocyte growth

Empirically, it can improve growth of cell cultures (https://www.atcc.org/Global/FAQs/C/C/Cholera%20toxin-541.aspx).
It furthermore has the potential to make cell populations more homogeneous by selectively binding to gm1 containing cells that can arise from spatial inhomogeneities among cultured cells. Snijder er al. Nature 2009 (https://www.ncbi.nlm.nih.gov/pubmed/19710653)

A quick check on Wikipedia would have answered your question.

Applications
Because the B subunit appears to be relatively non-toxic, researchers
have found a number of applications for it in cell and molecular
biology. It is routinely used as a neuronal tracer.[15]
Treatment of cultured rodent neural stem cells with cholera toxin
induces changes in the localization of the transcription factor Hes3
and increases their numbers.[16]
GM1 gangliosides are found in lipid rafts on the cell surface. B
subunit complexes labelled with fluorescent tags or subsequently
targeted with antibodies can be used to identify rafts.