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What is the lowest pressure at which plants can survive?
What is the lowest pressure at which plants can survive? How the plants behave in a Martian-type atmosphere? Is there any plant that can survive such atmosphere?
Can a lichen grow at Martian pressure?

Are you referring to total air pressure or partial pressures of oxygen and carbon dioxide?

Lichen is not a plant though.

I like your question!
Low surface pressure on Mars (averaging 600 Pa or about 1/170 of Earth's at sea level) is only one difficulty that an organism would have to contend with. In addition, mean surface temperatures are ~210 K (- 63 °C), the surface ultraviolet flux is extremely high (no ozone layer) and an aridity comparable to the Atacama desert. On the plus side, a 95% CO2 atmosphere might promote photosynthesis.
So, higher plants are extremely unlikely to prosper on Mars. Purely in terms of pressure, experiments suggest that at 1/10 Earth atmospheric pressure vascular plant transpiration increases significantly. So much so that they enter into a drought response which often leads to plant death.
However, lichens may be another matter. These are often adapted to low precipitation/pressure environments such as high mountains. Indeed, this article addresses exactly your question (sadly it is not open access). The authors suggest that the lichen Xanthoria elegans experiences no loss in vitality after 22 days exposure to laboratory Mars-like conditions (low pressure, low temperature etc.)!
Having skimmed this article I am frankly amazed (and slightly dubious) at the result. However, it should be noted that they only ran the experiment for 22 days, applied no ionising radiation (to simulate the high UV flux) and make little mention of the precise metabolic state of the lichen. If it has entered into cryptobiosis (cessation of metabolic processes) then it can't exactly be regarded as prospering.

de Vera et al., 2010, Astrobiology, 10, 2, Survival Potential and Photosynthetic Activity of Lichens Under Mars-Like Conditions : A Laboratory Study

Short answer : around 0.47 atm
World's highest plants discovered growing 6 km above sea level
If this Air Pressure Calculator is to be believed that should be 0.47 atm, so for plants 'the lowest pressure at which plants can survive is around 0.47 atm' seems to be your answer.
The air pressure on Mars is 0.00628 atm, so no, plants can't survive on Mars, if they could then we'd certainly find them far above 6 km on mountains on Earth.
Howsoever
It does seem that some of Earth’s toughest life could survive on Mars.
The life in that article that (not only) survived (but flourished in) the environment in the chamber (which included the atmospheric pressure of Mars) where Lichens & Cyanobacteria.
Neither of those are plants though.

Cyanobacteria are bacteria.
lichens are a composite organism incorporating a fungus & algae or cyanobacteria.
Algae are plants, but it's in a lichen, not a standalone plant, it's not clear from the article any of those lichens were algal rather than ones with cyanobacteria either.

But (that bit of pedantry aside) it would seem the answer to your second question is yes.
A lichen can grow at Martian pressure.
So there are examples of life that clearly can survive lower pressures than 0.47 atm.
But actual plants don't seem to be among them.

No, the lowest pressure at which plants can survive is not around 0.47 atm.
It is 0.07 atm or less in the case of ryegrass. And it's the total pressure. Not partial pressure of one of the constituent gases.
See this article:
https://ntrs.nasa.gov/archive/nasa/casi.ntrs.nasa.gov/19860010460.pdf

... almost 8 years later..
A newer experiment with a timespan of 1.5 years on another one lichen species suggests that there is

.. a minor resistance potential of the lichen Buellia frigida towards
  Low Earth Orbit and Mars analogue conditions effecting the survival
  potential and the resistance of the symbiotic organism

due to a DNA damage.
Source: "DNA damage of the lichen Buellia frigida after 1.5 years in space using Randomly Amplified Polymorphic DNA (RAPD) technique" Backhaus et al, 2019 Planetary and Space Science
So the answer is possibly "no" until we find some Martian lichen.

It looks like this study is mostly showing the effects of radiation exposure in space rather than atmospheric pressure.


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Stabbing muscles when flexed and when relaxed
Just a random question, would a sharp object pierce your muscle more(stabbed with the same amount of force) when the muscle is flexed or when relaxed?

I would say that it would depend largely on the muscle.

lets say any large muscle, abdominals, hamstrings, shoulder, etc @RoryM
Edit: or are you talking about the muscle density?

Depends on the stabbing force and how sharp the object is.

I suppose in theory the density of the tissue has increased during contraction if you stab in the middle so (preparing for a possible physics disaster) that would mean less penetration for constant force from an identical object

Well, if we look in very basic detail at how muscle contraction works within a myofibril of the sarcomere:

N.b. this isn't on a loop and only plays through seven times
The red lines represent actin filaments whilst the blue lines represent myosin filaments.  During muscle contraction the filaments move over each other:

As shown in the above diagrams the "more contracted" a muscle is then the smaller the size of the H zone (the area where there are just myosin filaments).
So if we consider a penetrating impact that went through a plethora of identically aligned sarcomeres (obviously this is not the case in nature) then we could presume that (et ceteris paribus) the object would not penetrate as deeply into a contracted muscle as it will hit more tissue on its route than in a relaxed muscle.

Thanks for a very detailed and clearly explained answer! Pity i didnt take Bio during high school...interesting stuff

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How strong is spider silk?
Spider silk is pretty darn strong and all sorts of comparisons are made to steel. I'm more curious about the various moduli of spider silk and how it compares to other materials. What is the Young's modulus of spider silk? What is the bulk modulus of spider silk? What is the shear modulus of spider silk? In general how do those moduli describe the material properties of spider.
A simpler way to ask the question, what does it mean when it is said that spider silk is strong?

I do recall that (at least some) spiders produce two variants of silk, one sticky and one not - the latter being used in construction of the web.

Wikipedia has a remarkably well-cited article on the subject of silks and their various biological isoforms and mechanical properties. With respect to tensile strength, spider's silk is as tough as high-grade steel.
Explcitly, dragline silk was measured by Pérez-Rigueiro at al. to be 600 ± 50 MPa with a comparison to silkworm silk.
Reference:

 Pérez-Rigueiro J, Elices M, Llorca J, Viney C. 2001. Tensile properties ofArgiope trifasciata drag line silk obtained from the spider’s web. Journal of Applied Polymer Science 82: 2245–2251 [pdf]

I hate to admit that wikipedia does pretty much answer this question. Followup question. What does it mean?

You can think of tensile strength as how much pressure you need to exert pulling along the long axis before causing failure in the material, and it snapping. Pressure here means force applied over surface area of the face, or cross-section, of the material, with SI units of 10^6 Pascals, or MPa.

I do also hate to refer people to Wikipedia in most cases, but they do a good job of the fundamentals. Who knew it was such a hot research topic.

Why is everyone so down on wikipedia, even though everyone uses it?? As a jumping off point for research into a topic you are unfamiliar with, it is excellent. Once you know more, you can then cite the appropriate original papers and will be able to sift the good from the bad (and downright ugly).

Poshpaws I completely agree, and that's why I thought it was suitable in this case to refer to the Wikipedia page. There are many pages there however that are poorly cited and even though the information may be accurate, many people take what is documented as factual and authoritative. It is an invaluable tool to explore areas with which you have little familiarity.

While the Wikipedia page does have good information, the purpose of SE is not to provide links to information, it's to provide answers. You didn't actually answer the question here, hence, -1.

This answer isn't an answer, it would have been more appropriate as a comment.

Edited to reflect a concrete answer.

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How does one calculate the resolution of a crystal structure?
Considering that I have a diffraction pattern of a crystal, how would I calculate the resolution of a structure in Angstroms? How does that value differ from the information that I would get from the beta-factor?
I'm aware that the resolution can be calculated by Bragg's law but how does that provide details for the entire structure?

Excellent question for the upcoming Chemistry beta. This should be moved once the proposal reaches beta.

I guess the answer is very different for NMR then. Time for a new question.

Hi sorry i missed this one - not too hard for "biology"
If you look at a protein crystal (or any crystal really) in an x-ray beam, it scatters lots of spots (diffraction reflections).  If you look at a picture of crystalline diffraction, at larger angles from the center of the x-ray beam, the reflections get weaker and weaker and basically just stop, if the wavelength is short enough (in all crystallography labs its plenty short - from 1.5 to 0.9 Angstroms).
The resolution is marked by the angle of scattering to the last measurable spot (aesthetics can vary here, but there is little variance from personal judgement here).  Once you have the angle of scattering, you can calculate the resolution from the Bragg scattering equation:
lambda = 2d sin(theta)
which is rearranged to solve for 'd'
d = lambda / 2 * sin (theta)
where lambda is the wavelength of the incident radiation and theta is the scattering angle.
d = the apparent width of the 'slit' which caused this highest resolution reflection is called the 'resolution' of the X-ray scattering experiment.
There is one part that's a bit tricky as in the typical diagram, depicting Bragg reflection/scattering, you would take the incident x-ray beam as first beam and the scattered angle as the beam of the high resolution scattering, which is more easily measured as 180 - 2* theta.

Does this mean that the resolution is an ensemble average?

Yes- The resolution is a result of the mean coherence of the crystal; if its disordered on the 2 angstroms, then the resolution peters out at that diffraction angle.  There are cases where diffraction in one direction is stronger or weaker than in other directions.  Such anisotropic resolution is not unusual and is described pretty literally "crystal diffracts to 4Angstroms along the a axis and 3Angstoms otherwise.

Resolution is a general metric, the quality of the x-ray structure, describing the amount of data collected for the structure.  The quality of the structure depends on how well the structure reproduces the data collected.


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Is bootstrapping an acceptable way to determine standard error for binding constants?
I'm measuring binding constants my system and I appreciate the usual methods of using replicates to measure standard errors and using those errors to calculate propagation of error. I'm curious if bootstrapping is a reasonable alternative to calculate uncertainty?

This is probably more suitable for stats.stackexchange.com, or do you think biological assumptions will influence the answer (I'm not familiar with binding constants)?

I approve this move. @fileunderwater Please let me know how to make that transition. I was under the impression that this was a fairly regular question that was relevant to the biochemistry community?

I've flagged it asking for migration, but I don't know if it is possible. This is not my topic, so I cannot say anything about methods/problems in biochemistry. To me, it feels like a clearcut statistical issue though.

My understanding of bootstrapping is that you may estimate variance (and thus standard error of the population mean) iff your measurements are independent and have the same population distribution, in which case a number of sampling-with-replacement calculations can be done. I suspect that this method of estimation would be less desirable with small n values because of the effect that outliers or large standard deviations may have on the calculation. If you have a large dataset then it shouldn't be an issue.

What is the definition of independent in this case? Does running a dilution series maintain independence? Now I'm even more curious how legitimate this is.

Independent really depends on the context of the experiment. If you are doing a serial dilution then I would consider those to be dependent on each other since the lower concentrations derive from the larger. This would be better analyzed as a replicate.


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Ideal low-protein binding membranes
I'm looking through the literature on the topic. It seems like hydrophilic PVDF membranes are ideal for low-protein binding but it also sounds like Regenerated Cellulose is an appropriate substitution.
Looking at one resource (http://www.zellnet.com/elispotplatescolumn/)

When PVDF filter plates were introduced, some investigators chose to use PVDF plates and some continued to use NC.  The reasons for choosing one plate (membrane) over the other are highly varied and won’t be addressed in detail here.  The fact that some laboratories and individual researchers feel strongly that one membrane is superior to the other runs contrary to the large body of Western blotting experience:  Despite some clear-cut differences in how each of the membranes can be used, there is essentially no reported difference in terms of detection sensitivity or signal to noise on NC versus PVDF in the Western Blotting application.  This having been said, it is clear is that the two membranes and their properties are quite different.

The assay that I am looking at in particular is protein/nanoparticle binding to mammalian cells. I am looking for a balance that will enable me to remove free protein without fouling the membrane and/or killing my cells.

May I ask why you need this? Are you a grad student, is this for a high school project, hobby?

@CHM Grad student. I do this for research and the greater good of mankind.

Apparently poly(ethylene oxide) is a biologically interesting polymer, with minimal protein interactions.
The apparently means that I haven't tried it myself, but my polymer teacher told us so.
http://www.sigmaaldrich.com/materials-science/material-science-products.html?TablePage=20204110
http://en.wikipedia.org/wiki/Polyethylene_glycol
Nomenclature seems to favour poly(ethylene glycol). I prefer poly(ethylene oxide), because then I know from what monomer the polymer was synthesized.


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What is the least costly method to generate sequential amino acid deletions?
I'm looking to generation sequential deletions from a gene of interest. The total size of this region is 8 amino acids. I'm trying to determine which portion of this region is necessary within the gene.
For example, if this is my sequence:

ABCDEFGH
I want to generate:

BCDEFGH, CDEFGH, DEFGH, and so on.
What is the least expensive way to do this (by minimizing primer use, enzyme use, etc). I already have this gene sub-cloned into an expression vector.
Thanks!

How big is your gene and your vector?

The gene is 600 bp and vector ~5 kb. My thinking is that I would need a whole new primer set for each amino acid deletion.

I'll consider this question answered. I gave @bobtejoe best answer because he broke down the costs and a suitable method for making the sequential deletions.
Amy gave useful considerations for using conservative mutations over deletions to preserve protein conformation and possibly function.
QuickChange is not the cheapest kit to buy, but the costs seem to be minimized when OE-PCR is used in conjunction with homemade stocks of reagents.

While it isn't the cheapest, it is certainly the fastest and simplest. I would quikchange out the amino acid. This would require no subcloning and only require

two ~25 nt primers ($10)
1 shot of pfu (~$0.25)
1 shot of DPNI ($0.05)
competent cells (~$5)
sequencing to confirm (~$4-6)

Overall, probably >$20 a mutant all in 2-3 days of waiting.
(edit) I'm going with quikchange rather than OE-PCR simply because it removes the cloning steps. You will potentially need to screen more colonies with conventional cloning vs. quikchange.

How would you quikchange out the last amino acid? Replacing with a stop codon?

If we're thinking about this problem from the context of traditional biochemistry, I would just have nothing. That is if your gene is XABCDEFGHY, you now have XY. You still have the context of the rest of the "gene" to observe. It should be a nice negative control.

@bobthejoe - this is what I am envisioning.
Also, what kind of competent cells do you use? We use JM109 from Promega and they're about $100/10 transformations. Do you know of a cheaper strain?

@leonardo the cheapest competent cells are the ones you make yourself!

I've always made my own competent cells (DH5alpha cells which is why I don't know the costs). I would assume that you would want to keep your vector in an expression strain so if you want to skip a step, I would transform straight into BL21.

Thanks @bobthejoe - I think this method will work. I've never considered making my own stocks of competent cells. Can this be done from an existing vial of competent E. coli? If so, is there a limit to how much E. coli I can produce and still have them retain chemical competency?

Probably deserves its own question. The answer is yes. I don't know how many passages E. coli can go through before they lose their chemical competency. One of these kits can make a couple hundred of shots. http://www.zymoresearch.com/e-coli/transformation-kits-accessories/z-competent-e-coli-transformation-kit-buffer-set

Also see http://openwetware.org/wiki/Preparing_chemically_competent_cells

If you are going to clone directly into BL21 - use one of the "gold" strains so you can pull the plasmid out later with less chance of random mutations.

Deletions may make sense if you are analyzing the N-terminus or C-terminus of a protein. If you are looking at an internal region however, keep in mind that the more AAs you delete, the more likely you are to disrupt the overall protein structure. If you delete any random selection of 8 AAs within a protein, there's a chance you'll knock out activity by changing the protein fold or stability. That's not useful information.
This question is usually first addressed by alanine scanning - sequentially or additively changing amino acids to alanine. This is much more informative than deletions. Even better, you can choose to replace wild-type AAs with other AAs of similar size but differing charge or hydrophobicity. Then you are most likely to change the function of a region without changing the structure.
The quickchange kit works great, but if cost is an issue you can do whole plasmid mutagenesis PCR with your own reagents. And make your own competent cells.
In my experience though, whole plasmid PCR can be tricky - if it doesn't work the first time it can be difficult to troubleshoot. If time is an issue, I'd recommend doing overlap extension PCR with the same mutagenic primers, plus one set of amplification primers at the 5' and 3' end of your gene. Make a large batch of digested vector, test as a negative control, and use it for ligation of all of your different inserts.

I recently made 6 different constructs (single and double mutants) using overlap extension PCR. It took me one week, including sequence verification AND was a fraction of the cost for a quickchange kit.

OE-PCR might be a good way to go too. I'll have to work out the primers that I would need.
I'm aware of the uses of alanine scanning and conservative substitutions, but for my purposes these amino acids are in an unstructured region, at the C-terminus and deletion will tell me more information about the localization of the protein rather than function.

I may be biased but there is an entire MATLAB toolkit developed for this exact purpose for highthroughput alanine scanning using overlap extension. The nice benefit is that your costs gets reduced to only 1 oligo rather than 2 oligo per mutant. https://simtk.org/home/na_thermo

@leonardo that makes much more sense if you're making truncations at one end. I'll add that to my answer so it is more broad.

@bobthejoe - wow I didn't know about that! I've been designing them by hand like a sucker. Thanks.


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Why do glial cells of the retina become more abundant the closer they are to the optic nerve?
I am doing a project on expression of GFAP in the zebrafish retina. GFAP is a marker for glial cells.
I have found that the glial cells are more abundant the closer they are to the optic nerve at the middle of the eye. This may just be because the cells are more tightly compacted here than at the edges of the eye...
But I am wondering if it may have something to do with the glial cells being involved with neuornal processes, and the optic nerve being the transmitter of signals from the eye to the brain?

Any particular glial cell you're noticing this with?
I know that Astrocytes modify Calcium concentrations in the synaptic cleft. Perhaps at places where there are more synapses, more Astrocytes must exist to regulate such thing? Here's an interesting paper on a possible role of Astrocytes on associative networks:
http://www.antanitus.com/

Glia serve the classic support role in the retina, similar to that served by neuroglia elsewhere in the CNS.  That role mostly consists of taking used neurotransmitters and recycling them such as in the glutamate-glutamine cycle.  As Preece suggested, glial cells are a heterogenous group, and with a general marker like GFAP you could very well be observing two different types of glial cell, one with a uniform presentation and one specifically in the central retina.
That being said, the most familiar type of glial cell in the retina is the Muller glial cell.  It is particularly interesting in zebrafish, where it has been shown to act as a neural progenitor cell upon tissue damage in adult animals  As you can see from that article, it fits your requirement of being GFAP expressing, although I couldn't find any good flat mount pictures showing whether it was preferentially expressed in the central retina.
So that gives us two potential roles for glial cells in the zebrafish: as potential multipotent retinal stem cells and as housekeeping neurons present to clean things up.  You could come up with reasons either of those might be important in the central retina, but for my money the arguments are all pretty hypothetical: "the central retina is more active and therefore has a higher requirement for removing neurotransmitter" or "the central retina needs to be protected from potential damage more than the peripheral".
One thing I think we have a good basis to rule out is that it's the optic nerve.  From a retinal point of view, you refer to the point where the optic nerve passes through the rest of the retina as the optic nerve head or optic disc.  Axons from ganglion cells all across the retina stretch out from their soma toward this single point.  By the time they reach the optic nerve, the vast majority of axons are far from their axon hillock.  That means that they're being propagated from one node of Ranvier to the next.  Because that process requires voltage gated ion and not neurotransmitter gated channels, there is no neurotransmitter release associated with that process and consequently no additional reason for glial cells to be present to clean up.
Reference:

 Bernardos RL, Barthel LK, Meyers JR, Raymond PA. 2007. Late-stage neuronal progenitors in the retina are radial Müller glia that function as retinal stem cells. The Journal of neuroscience : the official journal of the Society for Neuroscience 27: 7028–40.


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How to typeset gene regulatory networks
I have a relatively simply gene regulatory network I would like to visualize, complete with the common arrow and bar symbols used to show, respectively, which genes enhance or repress with other genes. Is there a way to typeset a gene regulatory network using something like LaTeX or Graphviz?
For very simple networks, I guess something like Photoshop or Illustrator would probably be the quickest solution, but these programs become very tedious as the size of the network grows even a little bit. What do people typically use for this type of task?

If you have simple 1:1 connections or can list your data in that manner, you can try Cytoscape (freely available). There are numerous plug-ins to customize what you have in mind in terms of visualization.

+1 for Cytoscape. I found it useful for looking at gene interaction networks pulled down from the yeast genome database.

Thanks. One advantage of Cytoscape is its flexibility, simply provide a bunch of A-B links. Those links can be classified - stimulating/inhibiting - but need not be.

I haven't tried it, but this StackOverflow answer suggests that you can import a GraphViz network into OmniGraffle (for Mac), which makes it very easy to produce a pretty network (much easier than Photoshop/Illustrator).

I've used the Omni suite before, it's quite well designed software =)


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Is there a binding affinity metric for interactions not in equilibria?
I am investigating the strength of binding of a small peptide to a protein by isolating the bound version and subjecting it to collisions with gas molecules (CID mass spectrometry) to dissociate the complex.
When I plot the collision energy against the proportion of bound and unbound proteins I get a curve that looks like a Kd curve.  However, as the interaction isn't in equilibria (i.e. it is in the gas phase) calculating the Kd value wouldn't be correct.
So is there another value I could calculate to describe the strength of the interaction?

Bobthejoe was pointing in the right direction  kcat and Km - Michaelis Menton parameters are measured to look at the relative rates of an enzyme in non equilibrium state.  Basically kcat is 'how fast does the enzyme work with little or no product in solution'. Km is 'how strongly does the enzyme bind the substrates that it uses.
http://www.pearsonhighered.com/mathews/ch11/c11kkkk.htm

You should be looking at the interactions in terms of kinetics and not thermodynamics. k_on and k_off should do the trick.

I don't think this is right because, k-on/k-off = Ka and Ka=1/Kd. So that would mean having K-on and K-off would allow you to calculate Kd, which is an equilibrium measurement... ah well thanks for trying!

Your basing your argument on psuedosteady state criteria and a constant concentration of your peptides and proteins. k_on and k_off are exclusively kinetic based terms that can be extended to thermodynamic terms when in equilibria which you're not in.


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How is the sequenced genome of a person useful to him in practice, now?
Currently it is possible and not so expensive for a person to have his genome. This is useful in general for understanding how life works. But, in practice, how is this useful for the specific person at this point in time?

A human genome sequence can uncover large deletions and insertions in the genome and would give the genotypes of both common and private (rare to very rare) small polymorphisms (e.g. SNPs) and SSRs (simple sequence repeats). From this information, one can learn about some curiosity traits (say, sensing asparagus metabolites in the urine, slow or fast twitch muscles, curly vs not curly hair) and, more importantly, about disease risk. Ancestry and family relationships can also be learned as in, for example, a half-sibling relationship.
As many diseases are polygenic with numerous loci each making small contributions to the variance, it becomes very difficult to fully describe the level of increased or decreased risk. In other words, we don't yet know all the players and so assessing their contribution to risk of disease can't be done with complete confidence. To further compound this problem are both epistasis and gene-environment interactions. Epistasis is a gene-gene (gene-gene-gene, etc) interaction, such that genes A and B separately make no contribution to the phenotype (disease risk), but do so in combination - say in ab/ab individuals. A gene-environment interaction can be described as when an allele associates with increased risk only when an environmental factor (e.g., exercise, fat in the diet, sun exposure, oxygen tension (altitude), etc), passes a certain threshold.
Still, the most powerful predictor of disease risk, onset and progression is family history. A genome sequence approaches that history (half your genome is from your mother and half from your father, of course), but remains fairly uninterpretable in terms of complex traits. You may carry a couple variants posing increased risk for heart disease, but what about the other hundred or so loci that also make small contributions to this affliction? Sure, if we knew exactly what those other hundred were and how much they each contribute and if they interact with each other or the environment. An incomplete picture emerges.
With rare diseases and altered genomes (say in cancer compared to normal) great strides are being made to either identify the small number of defective genes (rare diseases) or the commandeered pathways exploited for uncontrolled growth (cancer). In this regard, much can be learned and will have quicker, but still measurable in years, applications to the clinic.

This is a good answer, for sure, but my impression is that the OP wants to know what can the man of the street take home from having his genome sequenced. I think that it can do more harm than good, seen that the majority of the population -for instance- does not know the difference between cause and risk factor.

Therein lies the need for a genetic counselor, and thanks for the comment. I do think that cause and risk can be explained simply enough - one is less likely to die in an automobile accident if one does not drive, eg, whereas the cause of that accident could be an icy road + speed + inattentiveness (a combination of controllable factors).

How is the genome sequence useful right now? There are several tests out there that rely on identifying single mutations that will lead to diseases, or that are associated with bad response to medication. Having the entire genome sequenced allows identifying all of them at once, and is cheaper than doing these diagnostic tests one by one. Thus, sequencing the genome gives you information about whether to expect certain diseases, and a list of medication that you shouldn't take, sort of as an insurance.
Sequencing also allows you to learn about your ancestry, which may be of interest especially to people from countries with a long history of immigration, such as the US.
How is the genome sequence useful in the mid-term? Many diseases (including many cancers) are not caused by single mutations, but rather buy a combination of genetic and environmental risk factors that exceed some threshold. Thus, the genome sequence only allows to tell whether a person has increased risk for certain diseases, but not whether they'll get it. By itself, this information is not very useful. However, it has recently been suggested that blanket screening for cancer may not be the best idea due to bad side-effects and cost associated with treatment of false positives (which you'll get if you screen a sufficient number of people). Here, the genome sequence may help to identify who should get screened.
How is the genome sequence useful in the long term? The more genomes are sequenced, and the more phenotypes and diseases get associated with them, the better the predictions become, and the easier it will be for basic science to understand how mutations cause/influence disease. Thus, getting the genome sequenced now may be extremely useful and informative for the people who get their genome sequenced five years from now.

I assume some people would have their genome sequenced not so much for "My family has a history of heart disease - what risk factors have I inherited?" but for "I have my genome on this DVD - isn't that neat?".
The reason I suspect that is that I've heard that there are services that allow Europeans to find out which of the "Seven daughters of Eve" they're from, which seems to be more about curiosity than medical information.

Sure, there is this curiosity factor that is outside health. And such ancestry and other info is a lure that brings customers to 23andMe, eg, where there is a mix of health and ancestry info in the report returned to the customer. I do think more people are interested in real ancestry - land, race, ethnicity - rather than something like the "Seven daughters of Eve."


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Why can hair grow without limit while eyebrow cannot?
I cut my eyebrow and it grows until reach a certain length. Hair can grow without limit.
Why can hair grow without limit while eyebrow cannot?

Do you know it can grow without limit, or have you just not let it grow long enough to find out what its limit is?

Hair actually does have a limit to its growth. All hair cycles between periods where it grows, and when a new stand appears, which pushes the older, long hair out. Hairs that are generally shorter, like eyebrows or arm hairs, have a shorter growth period before a new hair pushes the old one out. The hair on your head actually grows much faster than many other hairs as well, so with the longer cycle and the faster growth, it can grow to be much longer before being replaced.
I remember hearing that for many women (the cycle does vary from individual to individual, which explains why some men can't grow beards while others look like ZZ Top) the growth cycle ends between the waist and butt.
My speculation would be that hair on the head could grow for longer because there are more capillaries in the scalp, which might lead to more nutrients, higher cell turnover (like you see in dandruff), and hence more hair. That's just a guess, mind you.


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Pancretic Acinar Cell - ATP, calcium concentration data
I need to find a decent source of data for concentration of ATP and calcium in the pancreatic acinar cell.
So far all I can find is ATP or calcium 'levels' based on fluorescence , which are not accompanied by a value of concentration in moles/molar.
Is it possible to find this information in a specific book or website, to avoid trawling though vast amounts of literature?

Have you tried asking on Biology as well? I'll have a look to see if there's anything around in the literature that I can find too.

See http://www.pancreapedia.org/tools/methods/measurement-of-intracellular-calcium-concentration-in-pancreatic-acini

In this study, even though they have used fluorescence based method, they have reported concentrations.

When we studied basal intracellular calcium concentrations in acini from control rats they were in the low nanomolar range (140 ± 5 nmol).

For ATP concentrations you can see here.

Is it possible to find this information in a specific book or website, to avoid trawling though vast amounts of literature?

There is the human metabolome database. However, it doesn't have data for all cell types. Either more studies are required or the database needs updation.
Similarly there is the yeast metabolome database (you may not require it for your query but just another piece of information that I thought is worth adding).


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Why dont "growing degree days" have units of degrees Celsius (or do they)?
From Wikipedia:

Growing degree days (GDD), also called growing degree units (GDUs), are a heuristic tool in phenology. GDD are a measure of heat accumulation used by horticulturists, gardeners, and farmers to predict plant and pest development rates such as the date that a flower will bloom or a crop reach maturity.

GDD is calculated as $\frac{T_{min}-T_{max}}{2}- T_{base}$ - so a quick check of the units would indicate that they are in the same units as T, i.e., degrees C. However, they are usually presented without units.
Why is this?

Actually, the units are °C days   or °F days. The units are mostly given in the typical name, Growing Degree Days where which temperature unit is meant is understood from the context.  Much more important is knowing the base temperature ("T_base") since this value can be different in different usages, even for the same type of organism.


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Which human body hormonal systems exhibit 24 hour diurnal cyclical activity?
I'm researching the possible connection between the dream content and the activity of various organ or hormonal systems within the human body. I'm looking for information on biological cycles within the human body that occur on a 24 hour cycle and may influence the sleep cycle, dream content or the overall state of awareness.
So far I was able to find:
Adrenaline, cortisol, testesterone - circadian endogenous cycle.
leptin, glucose, insuline  -  peak with awakening, decline with bedtime
What else within the human body is functioning on a predictable 24 hour cycle?
Thank you for any information!

Note that circadian cycle is not exactly 24 hours

Also, the fact that an hormone is produced in a circadian manner does not at all involve it in the sleep/wake cycle. I would be extremely careful in concluding anything about that.

I agree with nico on both points. Insulin, glucose and leptin (and many if not all the incretin hormones) are not circadian regulated to my knowledge. Insulin generally exhibits 3 major cycles through the day corresponding with 3 meals, and then is not secreted while fasting or sleeping because it is dependent on nutrient intake. Glucose as well, a sugar, naturally exhibits peaks after meals and lows when fasting. These cycles would just as easily be perturbed if I got up in the middle of the night to eat a meal and not regulated with any kind of circadian rhythm, only behaviour.

Thank you for great info! There's anectodal evidence that eating before bed has an impact on the dream content. Would eating within 1 hour of bed trigger insulin/glucose elevation over the course of the entire night?

@leonardo: the situation is complex and not completely understood. Infradian and ultradian rhythms are modulated by circadian clock genes such as Clock, Bmal, Cry1/2 both in the suprachiasmatic nucleus and in the peripheral organs.

@nico - I agree that it is a complex situation and even that organs (and systems) have their own rhythms, however I cannot understand the function behind regulation of incretin hormones to any infra-, ultra- or circa-dian cycle. If anything (in this context) ultradian cycles could only be consistent. The evidence as I see it in the realm of diabetes points to a (albeit complex) stimulus-response type of system. If you have some literature to the contrary I would love to read about it. :)

@leonardo: what I am saying is that just because an hormone is not secreted in a circadian manner it does not imply that its secretion cannot be controlled -or at least modulated- by circadian genes. A colleague of mine has recently published a review on the subject.

@nico: Thanks for the link. I'll keep that in mind for my own work. :)

The real answer is probably more than you want, but its easy to do better than the list above.
I took a look through GEO for human circadian expression data and surprisingly I only found 2.
Looking at GSE2703 - the rhesus circadian expression experiment, they have shown 355 genes that are rhythmically expressed.  This is not a great experiment because they only looked over a single 24 hour period.  Its only the adrenal gland.  Nonetheless they found 355 genes which seemed to be circadian.  the table is supplemental data to the article,  listed below.
I see a fibroblast growth factor receptor, some hydrocarbon nuclear receptor components, sterol regulatory factors, bone morphogenic protein 2, glutamate receptor, thrombonspondin receptor, ryanodine receptor 3 (what is that?) , lysophosphatidic acid G-protein-coupled receptor 2, purinergic receptor P2Y, G-protein coupled.  You might find more if you know what you are looking for.
The other circadian study was on human muscle, which will no doubt give different answers.  I imagine circadian behavior is highly tissue dependent.
Reference: Lemos DR, Downs JL, Urbanski HF. Twenty-four-hour rhythmic gene expression in the rhesus macaque adrenal gland. Mol Endocrinol 2006 May;20(5):1164-76

Don't forget that many hormones and cytokines are translated in inactive forms (insulin is a great example) and are later cleaved to release an active peptide. Thus, mRNA production may be constant while active peptide levels may cycle.

Maybe there is only 2 in monkey, but the amount of data on mouse is huge.

355 genes is quite a lot to process at once. Thanks for the GEO Ascension viewer link, I'll investigate that!

nico is right - mouse and rat are going to be the strongest organisms to look at...


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Regulation of chromatin structure
Recently, I reviewed the different levels of chromatin structure. The primary level is nucleosomes, where DNA is bound to histones, and has structural similarity to "beads on a string." The secondary level is a 30nm fiber, and the tertiary level is formed by radially looping the fibers.
I've also been learning about the histone code and how different modifications to the core histones relate to transcriptional regulation. Are these modifications the primary regulation mechanism for chromatin structure? In other words, does chromatin assume the most compact structure possible until histone modifications are made to enable transcription? Or have other regulatory mechanisms unrelated to transcription been discovered and characterized?

AFAIK chromatin would not assume the most compact structure without topoisomerase activity.

"Are these modifications the primary regulation mechanism for chromatin structure?"
It depends on how you define primary, we might currently think of histone modifications as primary because other regulatory mechanisms have not yet been well studied. Something else you can think of are the various regulatory proteins that interact with histone marks to modify chromatin.
I don't think you should imagine chromatin as assuming "the most compact structure possible until histone modifications are made to enable transcription" but rather histone modifications being a dynamic process with various transcription factors (a class of proteins) coming in and adding/removing histone marks as well as 'remodeling chromatin' (adding/removing nucleosomes)
As a sidenote, I don't believe much is known about the tertiary stage you initially mentioned so maybe that could play a huge role in the regulatory mechanisms of chromatin structure, it has just not been well explored.


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Percentage of genome devoted to regulating gene expression
Recently I've been studying the p53 tumor suppressor gene as a model for regulation of gene expression. It's amazing how many different post-translational modifications are known to regulate p53 activity, and how many different factors are involved in this regulation.
It is postulated that there are between 20,000 and 30,000 genes in the human genome. Is there an estimate for the percentage of these genes whose primary function is related to regulation of gene expression?

http://en.wikipedia.org/wiki/Transcription_factor

@Amy See my comment to Larry's answer.

I think you'll need to figure out a different way to phrase your question. "Gene expression" refers to transcription of open reading frames into mRNA. Post-translational protein modification is a separate cellular process and separate field of study with different terminology.

And I agree with @Shigeta - if you're getting into protein regulation and turnover, then you're pretty much just describing "life"

@Amy "Gene expression = transcription" is a very limited view of gene expression. The more widely accepted definition of expression is the derivation of a functional gene product from the gene. If the RNA itself is functional, then yes transcription is sufficient. But for protein coding genes "gene expression" definitely includes translation of the mRNA. Many proteins then require further processing to be functional, and one could argue that a protein is not fully expressed until it is functional. Whether one agrees with that or not, though, gene expression is not synonymous with transcription

@Amy Although I do agree that degradation and turnover unnecessarily broadens the scope of the question.

I'm saying that "gene expression" is separate from "protein expression." One refers to transcription and post-transcriptional modifications to RNA. The other refers to translation and post-translational modifications to proteins. And I strongly disagree with "protein is not fully expressed until it is functional" - there are plenty of genes that encode non-functional proteins. If they are translated, they are "expressed"

Okay, I'll take this out of the comments and put in an answer for all of us to work on.
To directly answer your question:

"Is there an estimate for the percentage of these genes whose primary
  function is related to regulation of gene expression?"

It depends on how you define "gene expression." And what cellular processes you want to include in that definition.
Larry's answer is the usual standard response, especially for people (such as me, ha) that have spent significant time studying transcription factors. About 1% of human genes have DNA binding domains and are thought to be directly involved in regulating the transcription of genes into mRNA - these are transcription factors (TFs). Closely related are cofactors, which regulate expression by binding to TFs or RNA polymerase machinery, but not directly to DNA.
Regulation of gene expression could also include modifications at the chromatin level - here you would include chromatin remodelers, histone acetylases, deacetylases, methylases and the histones themselves.
mRNA transcripts can also be regulated by miRNAs: post-transcriptional regulators that bind to complementary sequences on target mRNAs, which leads to translational repression or target degradation and gene silencing. So you would also include the proteins involved in this process, most notably the RNA-induced silencing complex, which includes Dicer.
There are also proteins involved in mRNA stabilization and turnover, which effects gene expression.
I'm not sure if anyone has added up all of the genes above to determine an overall percentage of the genome.
If you include in your definition of "gene regulation" post-transcriptional modification, folding chaperones, intra-cellular transport, extra-cellular and intra-cellular signaling, and so on - then Shigeta is right, you begin approaching 100%. In the most basic sense, life itself is gene regulation.

Yes, look at FANTOM and their work. There are about 2000 transcription factors and co-factors in the human genome. These are proteins, of course. If you add a couple (or few?) thousand microRNAs and a few dozen anti-sense transcripts, although small in size, you inch that percentage upwards.
With some 70% of the human genome transcribed, by some estimates, one could argue that many of these non-coding RNAs (short, long, trans-spliced) act in some way to regulate the DNA to mRNA to protein process.
(I can send you those 2000 or so FANTOM TFs if you wish. Contact me by email.)

Transcription factors are no doubt important in regulation, but my understanding was that TFs only regulate transcription. For many genes, post-translational modifications (phosphorylation by kinases, methylation by methyltransferases, etc) play an important role in regulating expression. I would like to include the genes encoding these factors in the estimate as well.

Just to be clear, by "regulation of gene expression" I meant to refer to anything that has to do with regulating transcription, regulating translation, regulating activity post-translation, and regulating degradation. Perhaps I should have worded that differently.

by these standards, the answer would be closer to 100% because any signalling protein would be involved, as well as the proteins that route signalling proteins around the various parts of the cell would be included. its hard to imagine a gene being deleted which would not affect the transcription of a gene under some conditions.  Even metabolic enzymes would probably count as transcription is often regulated by the concentration of metabolites in the cell.

@shigeta That is an excellent point. One reason I wrote the question in the first place is because I was beginning to wonder how such complex regulation schemes could be possible without the majority of genes in the genome being devoted primarily to regulation of other genes. And I understand that the question is complicated by the fact that proteins can have different functions in different contexts, which is why in the original question I used (perhaps naively) the words "primary function."

@shigeta If you were to write an answer beginning with "No, there is not an estimate" and then provide an explanation based on your comment (or even just copy and paste your comment), I'm sure you would get some up votes! You would definitely get mine, and you might even get the accepter answer!

@Larry_Parnell +1 for mentioning transcription of the majority of the genome.

it seemed too difficult to put in an answer form.  "everything is everything" is a common mindset you can slip into with cell biology and gene networks, but thanks for the suggestion.  I have no real reference.  its sort of a truism in the work.


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How do ribosomes contribute to their own synthesis?
In other words, what products synthesized by ribosomes are actual parts of ribosomes (if any)?   How are they involved in their own synthesis otherwise? What is the cycle/chain of products starting with the proteins synthesized by ribosomes and actually ending with the synthesis of a ribosome?

The most important parts of the ribosome are not made by other ribosomes - 5 rRNA (ribosomal RNA) of the ribosome actually do most of the direct work of creating the protein and are made by RNA polymerase ( a protein, but not the ribosome).
Then there are 92 ribosomal proteins, which as a rule bind to ribosomal RNA to support their structure and keep everything going.  These are all made by ribosomes.  They are thought to have appeared later in the evolution of the ribosome though I imagine that it would not be possible to constitute a working ribosome without each one of them.
these numbers are for the eukaryotic ribosome, the prokaryotic ribosome has 3 rRNA and 52 ribosomal protein components.
http://en.wikipedia.org/wiki/Ribosome

Is it fair to say then, that a ribosome is really an RNA scaffold (or multiple, actually) upon which ribsomal proteins bind and collectively form active ribosome units?

Any hints to articles describing the RNA-P synthesis? ... or is RNA-P synthesized by ribosomes?

leonardo that was the most amazing result of the first ribosome structures - the chemical assembly of the peptide and codon recognition was done almost entirely by the rRNA.

pointernil - RNA polymerase?  its totally made of protein.  since it uses DNA as a substrate, it is a much more recent development.  the original RNA syntesis was probably done by RNA, but to my knowledge all those genes seem to have been replaced by protein mediated functions (hope i got your question right).

@leonardo that is the prevailing hypothesis.  This just out - another view of the ribosome challenging 'RNA World'.  I'm not a believer here, but its an interesting idea. http://www.sciencedaily.com/releases/2012/03/120312192839.htm


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How are antibiotic resistant bacterial infections treated?
For example, how are infections of antibiotic resistant strains of MRSA, Streptococcus, or Gonorrhea treated?

Welcome to Biology, this question is about treatment of disease, a purely medical subject which is off-topic here (see this meta post on our discussion on that. Questions about the biological basis of diseases are welcome, but questions about treatment are off-topic here.

lots of biologists and biochemists study this topic.  why be so over defined?  This question should be answerable here. in my opinion.  The first line treatment for such things is to use rare and expensive antibiotics that still can work like Vancomycin.  antibiotic resistant strains keep popping up because (among other reasons) people don't take all their antibiotics and this creates an environment for more antibiotic resistance to develop through selection.  SEe http://www.ted.com/talks/paul_ewald_asks_can_we_domesticate_germs.html

A second vote for reopening. The question is not "What drugs should I use to treat X", the question is how they are treated. That question is very much in the domain of microbiology and epidemiology, neither one of which are medical fields.

There are a number of ways to address antibiotic resistance in infectious bacteria. What one gets used depends on exactly what organism we're talking about. But below is a short list of some ways:

Changing the antibiotic being used. Not all antibiotics have the same molecular target within a bacterial cell. Some interfere with the formation of the cell wall, others interfere with protein synthesis, some mess with DNA replication, etc. Similarly, resistance mechanisms don't work equally well on all antibiotics. So often the solution is simply to switch antibiotics. Or, quite often, treating all infections with a combination of drugs that should get around most resistance. This is why you see people getting skittish about things like multi-drug resistant organisms - because it removes this solution.
This isn't as much a treatment as a preventative measure, but increasing antimicrobial stewardship and the appropriate use of antibiotics to prevent widespread resistance from arising in the first place.
The use of non-antibiotic antimicrobials. The most "common" of these is phage therapy - using preparations of bacteriophages that naturally prey on the infecting pathogen to help combat the infection. This was a major "contender" for how we treated antibiotic infections, but has fallen away due to a bad reputation early in its history (due to difficulties purifying phage treatments) and the discovery of antibiotics which were vastly easier to use. But there's still ongoing research, and it may pose a potential to help treat highly resistant infections in the future.

As a former icu nurse and also a molecular biologist who specialized in genes for antibiotic biosynthesis I can tell you theory is world's apart from practicality. New antibiotics are least tested agents and very expensive, often the patient suffers more from the antibiotics side effects than they do from the infection. Monotherapy is basically old hat now, use of a single agent to treat massive drug resistant infection only increasea the odds of  increasing drug resistance. The general rule now is combitherapy using two or more cheaper and better known antibiotics and save newer agents as a drug of last resort for future cases. We are rapidly evolving into a post antibiotic Era according  to Dr Stuart Levy https://www.amazon.com/Antibiotic-Paradox-Antibiotics-Destroys-Curative/dp/0738204404

see my common on your other answer... please include some references to back up your claims - thanks!

Combinations of antibiotics are now becoming essential due to quite widespread resistance to single antibiotics in bacteria such as MRSA, E coli, K pneumoniae and P aeruginosa. Physicians often give two or three antibiotics. However, few of the combinations used have actually been rigorously tested for safety and efficacy (hence widespread side-effects, as the former icu nurse reported above). The odd thing is that there is only one approved combination of two antibiotics available for Gram-negative bacteria, the combination of trimethoprim and sulfamethoxazole. This seems to be a very obvious gap that needs filling. Which other dual combinations would be very useful?

References for your claims are missing.


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How would a warm winter affect maple sap production?
The past winter (2011-2012) was warmer than usual.
Trees are normally tapped in late February when the daily maximum temperature goes above freezing. However, assuming that there have been relatively few days with a maximum temperature below freezing, how would this affect the timing and quantity of sap flow?

I don't know about quantity, but here in NH the sap has been flowing already -- a couple of weeks early from what I can tell.

This article has a clear explanation (backed up by good links) of the effects of climate change on maple sap production, including the following:

Maple trees produce the best sap on cool days preceded by freezing nights – the cold weather causes the sap in the tree to freeze, creating a low-pressure vacuum that draws more sap up from the roots. When temperatures rise the next day, the sap melts and oozes through the tree, making for easy collection. When temperatures stay abnormally warm, as they have been lately, this process does not occur.
Additionally, the warm weather causes the trees to begin to bud.  The hormones that trigger budding also decrease the sap’s sugar content and spoil its taste. This means that it takes much larger quantities of sap to boil down to a gallon of syrup.


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Why are some genes dominant over others? What is the mechanism behind it?
If I have a brown eye gene which encodes the protein that is responsible for the brown color and have a blue eye gene as well, what is the reason that my eye color is brown? How does one gene maintain dominance over the other?

You mean having two differently colored eyes?

Here is another that is now marked as a duplicate of this post and that contains answer that already received several upvotes and are therefore eventually worth checking

One version or allele of the gene for eye color may encode instructions to make the brown pigment, while the blue allele makes no pigment. Alternatively, it is possible, logically speaking, that the blue allele blocks the productions of brown pigment, but this is not the case.
Now, brown vs blue is not a case of one gene and two alleles. After producing pigment, it must be transported, deposited and such. Many processes are involved. So, the pigment deposition process may be functional or not, but as above, it is often found that a non-functional version is simply non-functioning and not actively inhibiting the process. There are numerous cases where an aberrant form of a protein, encoded by a variant allele, acts as an active inhibitor of a given biological or biochemical process.
The key to your question as written is blue eye color is a lack of pigmentation.

If recessive allele is non functioning then how is it possible for that trait to be expressed in case of homozygous recessive condition?

At the DNA level there are several mechanisms that  might be cited.
A mutation (change in the DNA sequence) of a gene may actually render one or both copies of the gene defective.  In the case of albino-ism, the skin is pink - no melanin pigment is made at all.  This is a case of both copies of a vital gene being defective and an ability lost completely. A "loss of function" recessive trait.
Blue eyes have no retinal pigment - they are a loss of function recessive. Some cases of genetically inherited diabetes (<1%) dwarfism and obesity are examples of this.  There are many others - many genetic diseases are like this.
This can be caused by a single mutation in each copy of the gene, and others an entire segment of the chromosome can be lost or disrupted by a new, often nonsensical sequence dropped into the gene region.
Other changes can affect the way the genes turn on and off. - similar sequence changes in the regulatory sequences next to the gene sequence will make the gene behave differently. Even babies of african descent may be born with blonde hair and blue eyes and get the darker pigmentation later.  this is genetically caused by a change in they timing of the genes for hair and eye color turning on at other times (blonde hair and blue eyes have little or no pigment, so if the genes are off, then this is what you get).  So when genes are active can cause dominant (always on) versus recessive (sometimes off) patterns. which are because one copy of the gene behaves differently than the other copy.
Sometimes a single mutation in one copy of the gene can cause rather interesting effects. A single good gene and a mutated, less effective gene might result in lost of activity because the mixture of the two genes is different between a wholly functional or wholly variant set of genes.
A classic example is the sickle cell Anemia.  two copies of sickle cell hemoglobin causes the red blood cells to be stiff and misshapen which in turn causes a painful condition in the carrier.  a person with a single copy of the sickle cell gene does not have this problem - is nearly asymptomatic. So we say sickle cell anemia is recessive for the HbS mutation.  but in reality there is plenty of the HbS version of hemoglobin (Hb) in the blood cells, just that the mixture of the two does not cause the anemia.
Much rarer is an additive function from a genetic sequence change.  The immune system is where you will most often see this.  Since the sequences that drive immunity vary widely, some immune sequences are rare - such as inborn immunity to HIV.

+1 for the sickle cell example. However, the phenotype of misshapen cells is dependent on the oxygen loading of the hemoglobin - low O2 -> sickle-cell shape (Stryer, Biochemistry, 3rd ed).

Sorry to blockquote, but this note from wikipedia gets to the heart of the question:

Which trait is dominant?
The terms dominant and recessive refer to the interaction of alleles in producing the phenotype of the heterozygote. If there are two alternative phenotypes, by definition the phenotype exhibited by the heterozygote is called "dominant" and the "hidden" phenotype is called "recessive". The key concept of dominance is that the heterozygote is phenotypically identical to one of the two homozygotes. That trait corresponding to the dominant allele may then be called the "dominant" trait.
Dominance is a genotypic relationship between alleles, as manifested in the phenotype. It is unrelated to the nature of the phenotype itself, e.g., whether it is regarded as normal or abnormal, standard or nonstandard, healthy or diseased, stronger or weaker, or more or less extreme. It is also important to distinguish between the "round" gene locus, the "round" allele at that locus, and the "round" phenotype it produces. It is inaccurate to say that "the round gene dominates the wrinkled gene" or that "round peas dominate wrinkled peas."

Recommended reading for an overview:

http://en.wikipedia.org/wiki/Dominance_relationship
http://en.wikipedia.org/wiki/Dominant_negative

You can also look to "dominant negative" phenotypes to get a good idea of what "dominance" entails (this was the concept that really locked it in for me in college). One example is Marfan syndrome, where the mutant allele of FBN1 (fibrillin-1) produces a version of the protein that is antagonistic to the protein produced by the "healthy" allele.
Dominant negative and semi-dominant alleles can be seen when the protein forms dimers to function. Activin type receptors form dimers to transduce a signal from an extracellular ligand into the cell. A truncated receptor protein that has the dimerization domain but  lacks the intracellular domain necessary for signal transduction will act in a dominant negative fashion over the wildtype allele: Dimers are formed but the signal is not transduced. This has been implicated in hereditary colorectal cancers.

This is the correct answer here... the others don't really get to the heart of the matter: It's not that there is a dominant vs recessive trait it is - for symplicity sake here - that there are at least 3 versions AA Aa and aa and the first 2 produce the same exact phenotype (albeit they go about it slightly differently possibly) and the third produces a second thing. (didn't read any answer below-so those might be saying the same thing)

A gene is dominant (lets call it B) when its presence in combination with a recessive allele (heterozygotic Bb) leads to the same phenotype as homozygotic BB. A recessive allele leads only to phenotypic expression when it is present twice (homozygotic bb).
To illustrate this rather abstract definition of dominant and recessive alleles let's look at a striking example, namely a gene mutation responsible for albinism.
One of the causes that can lead to albinism is a mutation  in the gene that encodes tyrosinase (TYR). Tyrosinase is used by melanocyte cells to convert the amino acid tyrosine into the pigment melanin that colors the skin, hair, and eyes (Ballantine, 2009). Animals lacking tyrosinase have white skin and hair and red eyes, such as the kangaroo in the picture below (source: Listverse):

One functional gene (B) is enough to allow for pigmentation to occur and hence it is dominant. The other mutated allele (b) produces nonfunctional enzyme, but is recessive as one functional allele produces sufficient enzyme to allow for normal pigmentation in a Bb individual.
In your question you mention blue and brown eyes. AS @Larry_Parnell indicates, in blue eyes the eyes do not contain the pigment melanin and are therefore blue (the blue color is caused by non-pigmented optic effects). Brown eyes are therefore dominant as the melanine colors the eyes such that the blue color is masked (it is still there though). The phenotype of blue eyes is therefore recessive, as one allele for brown eyes is enough to bring pigment into the iris.
Note that other interactions also exist, such as co-dominance (e.g., the ABO blood group system where the genes for A and B antigens are both dominant over O) and incomplete dominance. I refer to the wiki page on dominance here, as the question is not specifically about these interactions.
references
Ballantine. Sci Am February 2009
Wikipedia - Dominance (genetics)

Below are some insights about the evolution of dominance. It does not directly answers your question but understanding how it is thought to evolve also help understand the mechanism governing dominance relationship between alleles.

There are several hypotheses about the evolution of dominance. It is important first of all, to note that empirical observations show that beneficial alleles tend to be more dominant than detrimental alleles. Among the two main hypotheses to explain the evolution of dominance, one has been formulated by Ronald Fisher and one by Sewall Wright.
Fisher's hypothesis
According to Fisher's hypothesis, between two equally beneficial alleles, if one is more dominant than the other than it's heterozygote carrier will have higher fitness. In consequence, beneficial alleles evolve to become more dominant while detrimental alleles evolve to be recessive (so that they can hide from selection in heterozygotes).
Wright's hypothesis
According to Wright's hypothesis, beneficial alleles are more dominant because of the kinetic of biochemical reactions. The rate of a biochemical reaction is a function of the concentration in the substrates of interest. The function is called "Michaelis-Menten function" after the name of the authors. The Michaelis-Menten function looks like this:

Think about a knock-out mutation. Such mutation will decrease by half the concentration of protein the gene in question produce in heterozygotes. Imagine, the concentration of proteins in the wildtype homozygote was 3 (see above graph). The rate of reaction of this homozygote is therefore about 3. The heterozygote would have a concentration of 1.5 and the rate of the reaction is therefore about 2.5-2.75. Assuming that the rate of this biochemical reaction is directly related to fitness, then a the locus of interest, benefical alleles are necessarily dominant and detrimental alleles are necessarily recessive. Selection for dominance is not involved in Wirght's model.
Is Fisher's or Wright's hypothesis correct?
Current state of the art is to consider Wright's model to be correct and Fisher's model to be wrong. In reality, the truth probably lies somewhere in between these two extremes. Note also that some other alternative explanations may exist in the literature but Wright and Fisher original hypotheses are by far the most considered hypotheses for the evolution of dominance. During my undergrad, I remember a speaker (but I forgot his name, sorry!) who showed that some alleles actually have some domain that are directly responsible for decreasing the expression of the other allele on the sister chromosome suggesting that Fisher's hypothesis might sometime be a good explanation as well.

There are 2 main mechanisms.
Case 1: active/inactive product. A gene with 2 alleles: inactive and active, that codes for a cosmetic difference. In the case you gave (brown over blue eye color), the brown coloring is due to melanin.
If you have 1 functioning copy of the gene for melanin in eye color, then this causes melanin to be produced and the brown color overrides whatever would have been there otherwise.
Case 1b: active/inactive paradigm and disease. A common examples are sickle-cell anemia and red-green colorblindness where you need just 1 functioning copy of a gene to avoid negative health effects. These are insidious for inheritance purposes as it can make people asymptomatic carriers of heritable diseases (even worse in the era before genetics and biology as a field of study since there would be families with widespread, unpredictable, unexplainable occurrences of various diseases - often explained as a "curse" by those who didn't know better)
Case 2: the spoiler. This dominance pattern tends to be associated with genetic diseases where a mutation causes a protein to go rogue and damage its host. Having even one copy of such a mutation is a bad thing, and worse because the chance of handing it down to the next generation is roughly a coin flip (if you have 1 copy) and guaranteed (if you have 2 copies).

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


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Human sleep cycles and dream times, what influences the timing and intensity? Sleep history included
I'm doing sleep and dreams research and have developed an iPhone application to help me track my bedtime, rise time, sleep onset and also mark dreams. The app also monitors overall activity overnight as an Actigraph, recording periods of elevated motion and inactivity.
I have a lot of sleep cycle data that I have trouble analyzing.
I know that circadian rhythm is at play with 90-110 minute sleep cycles ehxibited over the course of the night, each one is a progression of various sleep stages, from NREM to REM. REM is more likely to result in a dream reported if awakened during REM.
What I'm seeing is a bunch of orderly patterns, and a lot of chaotic behavior that I cannot explain. Particularly the times of going to sleep and awakening, while dreams exhibit more orderly behavior, with dreams reported at similar times on subsequent days.
I'm also interested in any insight as to what's causing me to wake up at certain times and report dreams. What could be involved in this kind of behavior? I saw research about deuretic hormones not being suppressed for the night, causing the urge to urinate to awaken the dreamer.
Right now I have 90 days of sleep onset and dream data that looks like this:

Complete 90 day sleep history

In this case, each black marker indicates the sleep onset time for
the night
The orange marker indicates the time of getting out of bed
The green markers are dreams that I report upon awakening from a
dream, so dreams occur prior to the marker's location.
Each green
    marker's brightness indicates more clear dream content remembered
    and    recorded.
Cyan markers are lucid dreams, where I was aware
    that I was    dreaming within a dream.
Cyan color of a marker
    indicates that I    could control the dream's content from within a
    dream.
Red markers    are periods of insomnia.
The cyan line is
    number of hours after    bedtime
The purple line is sleep cycle
    approximation (90 minutes).

The data is stacked with each row being a day of data. You will notice that your eyes start to automatically seek patterns within the vertical arrangement of markers. Because each marker is a dream reported upon awakening, they roughly trace the sleep cycles over the course of the night.
I'm interested in learning what influences the desire to go to bed at a particular time?
What influences the getting out of bed times?
is there some sort of analysis I can perform to understand the pattern within the sleep cycles as it evolves over multiple nights?
Any input is appreciated!

I'm interested in learning what influences the desire to go to bed at
  a particular time? What influences the getting out of bed times?

It is the circadian rhythm. Circadian rhythm is mediated by the suprachiasmatic nucleus of hypothalamus, which gets afferent nerves from optic nerve. So, the circadian rhythm is mediated by light. Initiation of the NREM Stage 1 sleep is controlled by the lateral preoptic nucleus, which is another area in the hypothalamus, so it is mainly the absence of light which starts sleep.

I'm also interested in any insight as to what's causing me to wake up
  at certain times and report dreams.

Sleep is not equal to absence of consciousness, it is just an diminished state of consciousness. Sleep consist of mainly 4 stages, NREM-1, NREM-2, NREM-3 and REM. Every stage, the "depth" of sleep, or the level of the decrease in your consciousness changes. REM is the stage in which dreaming most frequently occurs, and also it is the sleep stage where your consciousness is highest, so you are more likely to awake because of the stimulus coming from the environment.

Circadian rhythms persist in the absence of light. Although light cues can entrain the rhythm, I would not say they are its mediators.

Light is not the only, but one of the main mediators of the circadian rhythm. There are many circadian rhythm abnormalities reported in totally blind people.


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What influences the timing of human bowel movements in the morning?
I'm trying to understand if the timing of human bowel movements in the morning is associated with the circadian rhythm, and can thus be used to make predictions about the circadian rhythm.
What influences the timing of bowel movements? Is it the timing of meals, caffeine intake or is it a biologically programmed time?
Thank you!

The bowel movements are influenced by a lot of factors. For example, when you eat a meal it induces a movement in your large intestines, to defecate and clear up space for new food.
Also, there is MMC, migrating motor complex, which is responsible for the bowel movements when you are fasting. It causes a flushing effect, which prevents bacteria to overproduce in intestines.
So, the daily bowel movements are mainly influenced by the timing and content of the food that you eat. But as I said there are many other factors. The gastrointestinal system has a very complex nervous system. Even psychological factors can effect the bowel movements greatly, for example extreme physical pain may induce the symphatetic system and cause constipation.
Also caffeine may affect it, like many drugs do.


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Auxotrophic complementation test with yeast
If auxotrophic strains grow on minimal media do they complement each other or not?  Also, is complementation the same thing as complementing each other?

If the yeast strain A is auxotrophic for AA 1 and the yeast strain B is auxotrophic for AA 2, neither would be able to grow in minimal medium by itself. But combined they complement the lack of AA1 in strain A by strain B and vice versa. That is metabolic complementation.


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Why is propanoic acid often added to the diet of C. elegans?
And what are its effects on C. elegans?
The paper is  Burnett C, Valentini S, Cabreiro F, Goss M, Somogyvári M, Piper MD, Hoddinott M, Sutphin GL, Leko V, McElwee JJ, et al.. 2011. Absence of effects of Sir2 overexpression on lifespan in C. elegans and Drosophila. Nature 477: 482–5.

Propanoic acid is toxic against many types of mold, fungi and bacteria (wiki), but same time has almost no effect to C. elegans ("fivefold less", reference). This is why propanoic acids and (more commmon) its salts are used as conservants for C.elegans cultures (as well as for other animals, like Drosophila).

Another anti-fungal compound we use in our fly lab is methylparaben.

We use nystatin. I don't think the use of propanoic acid with C elegans is that common. Fly people use it a lot.


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Why would we overexpress Sir2 by overexpressing its hypomorph (dSir2-EP2300) in C. elegans?
Can't we just overexpress regular Sir2 in the paper? Rather than overexpress a reduced-function gene?
The paper is  Burnett C, Valentini S, Cabreiro F, Goss M, Somogyvári M, Piper MD, Hoddinott M, Sutphin GL, Leko V, McElwee JJ, et al.. 2011. Absence of effects of Sir2 overexpression on lifespan in C. elegans and Drosophila. Nature 477: 482–5.

That's an interesting paper.

could you point out exactly where they say this is a reduced function gene?  it seems as if they are characterizing a worm which has many copies of the sir-2.1 gene.

I think hypomorph implies reduced-function?

I have had a little time to look over this paper.
They do overexpress a native sir2 clone in high doses, called sir2.1 OE.  Which seems to be native and also appears in high copy numbers. This strain was found in previous publication to have a high lifespan... that is old news.
This paper sees sir2.1 expression levels as an oversimplification of the causes of longevity.  When they create crosses of the sir2.1 OE strain with wildtype, you can see the Outcross, which is verified to have a high level of sir2 expressed no longer has an extraordinary lifespan.
This can be seen in Figure 1.  http://www.nature.com/nature/journal/v477/n7365/fig_tab/nature10296_F1.html
So this paper is now asking, if sir2 levels do not convey the information that creates an extended lifespan, then what does?  It must be some modulation of some protein that sir2 affects.  They implies that the actual cause of the lifespan increase may have been a mutation somewhere else in the organism.
"However, longevity was not suppressed by sir-2.1 RNA interference (RNAi) ... indicating causation by factors other than sir-2.1, either on mDp4 or elsewhere in the genome."
"This implies that lifespan extension is due to transgene-linked genetic effects other than the overexpression of dSir2."
In the second half of the paper (figure2) the investigators have moved on to drosophila work, where they look at how expressing constructs or inhibiting sir2 protein levels might affect lifespan.  Although the dSir(EP2300) / + construct (drosophila sir2) with a wild type gene promoter did not live quite as long as dSir2(EP2300) with a fancy promoter (dSir2(EP2300) / tub-GAL4), the promoter construct (tub-GAL4/+) alone also had just as long a lifespan.  How can this be?  Not sure, but the expression of sir2 is clearly not the panacea we had hoped.  Note however that the reduced power gene still gave the same boost to lifetime.   This shows dramatically that sir2 activity alone does not drive the longer lifetime.
Lastly, deletion constructs (dSir4.5/1.7) , which should have lower than wild type protein levels for sir2 had completely normal lifetimes.
So the answer to your question; you need to test a hypothesis going in both directions - does increase of the protein really create a strong effect?  Does decreasing it have a negative effect then?  There are lots of other reasons to use knockouts and non functional genes in such an experiment, but those are the broad strokes.


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When are population dynamics models useful?
When are population dynamics models useful? There seems to have been a lot of research about it, but how does it help? If I need data about how a population will evolve under what conditions, I need it because I need data for a decision (such as "can we kill 50% of population X without doing too much damage?"), right? But for that, the model needs to be aware of what causes what. And for that, I have to do experiments, right? Like "let's kill a significant amount of population X and see what happens in the next ten years". I really don't get it.

Population dynamics occupies a whole subset of mathematical biology. Perhaps the most pragmatic uses for modelling population dynamics come from the fields of epidemiology for modelling disease infection and transmission through a population (one such article), or ecology modelling things like forestation, fishing dynamics, predator-prey relationships (an example). Then there are more abstract uses, when you cannot measure a population to test a hypothesis because the labour is too intensive, or it's too costly, or no such surveillance mechanism exists. Theoretical models of population dynamics are built to gain an understanding of what the system as a whole may do under certain conditions. In this sense, population models are more of a theoretical exercise or a thought experiment.

How can you know what the system will do under certain conditions? I mean, you can't deduce that from the numbers, right? Sorry for these noobish questions, I guess I just don't get it.

It may be impossible to know the absolute truth of what happens in real life but model building let's you study the population dynamics with a specific set of assumptions (the model itself and the starting parameters). These are modelled on a computer and so it is easy to test the same model with many different starting parameters. Often what happens is an understanding of the underlying mathematics of the model as well as the computer modelled dynamics gives the author/reader a feel for the characteristics of the system (eg, is it exponential growth, does it decline, is the system unstable).

Many thanks - I think I'm beginning to grasp this. :)

You're welcome. It took me a while too. :)

Now I coded a little webapp for lotka-volterra-equations with the RK4 method, and I think I really get it now. My teacher was right, you just have to re-code stuff yourself to understand it. :)

That's great! That's the easiest way to learn in my opinion. Having a system that you can manipulate as you read along with a text (or just to explore) makes understand the system more intuitive.

Leonardo's already given you an excellent answer, but I thought I'd add my perspective. I'm a mathematical epidemiologist, so I'd at least like to believe these types of models are useful.
For me, there are a number of things population dynamics models are especially useful for:

Highlighting data requirements. Yes, models need data, as you've mentioned. But they don't need all their data to come from one source, one study, or even one field. Models are also profoundly useful for showing where we don't have the data we need to fully understand a system. "To make a model where we understand A, we need the values for X, Y, and Z. X is well studied, but Y and Z aren't - though it turns out when we look over the entire parameter space for Z, nothing really changes in our answer. But guys? We could really use a study on Y."
Eliminating guesswork. Models aren't perfect encapsulations of reality - there will always be some simplifying assumptions, etc. But it's better than "going with your gut" - especially for complex problems.
Impossible studies. A ton of what mathematical epidemiology looks at it is areas where studies are either impossible, logistically difficult, or unethical. It would be very hard indeed to only be able to study pandemic response plans, or vaccination strategy only when we had an actual outbreak, or while a new vaccine is being rolled out.
Highlighting potentially new directions. If you're considering an intervention, but no matter how effective you make it in your model it doesn't move the system much, it might not be worthwhile. Models can also highlight threshold effects - like the critical % of the population you'd need to vaccinate to achieve herd immunity.

This is a very insightful answer from someone that regularly uses these types of models. Thank you.

Wow, that's a really good answer, too! Thank you. :)

Two previous answers listed many applications of population dynamics models. I want to add that they are also important for conservation of endangered species. For example classical stage-class model (Crouse et al 1987, free copy) indicate that the most effective way to protect sea turtles is reducing mortality of large juveniles.
Moreover, you don't have to perform such drastic experiments as killing 50% of  a population to estimate your model parameters. Information about number of offspring, breeding success, natural mortality, etc can usually be gain without serious perturbation of wild populations. The number of individuals in every natural population fluctuates because of random reasons, so it is possible (but sometimes needs more field work) to calculate, (possibly nonlinear) regression between density of population and some demographic indicators and then extrapolate it to non-examined densities. For some small, short-living species it is sometimes possible to measure that correlations in laboratory or semi-wild conditions. For some long-living species, especially if they are sedentary, like trees, it may be better to compare specimens living in different distance from its neighborhoods. For poorly-known species it is possible to take missing information from related or similar species.

I'll throw one more application into the pot. Population dynamics also forms the foundations of population genetics, population ecology, and more recently plays an important role in frameworks such as evolutionary game theory and eco-evolutionary dynamics.
Here the models are also used as a type of theoretical exercise or thought experiment (as a previous answer suggests). In the development of evolutionary theory we simply cannot observe the process over the timescales we require to test the hypotheses we make. Thus, the development of population models allows us to explore 'possible worlds', as Robert May once put it, to see what kinds of adaptations or population structures we would expect to see, given the assumptions we put in.
We are also seeing an increasing number of population models and dynamical models used in conjunction with experiments on microbes in the field of experimental evolution. Here we can observe evolution in real time, and many of the assumptions about well-mixedness and large population sizes that are often made in modelling populations are actually fairly accurate.


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Do white Australians have a distinct look?
Background
I've heard from many people working in tourism or similar industries that, white Australians can be recognized as Australian solely by their facial features. Being Australian myself I've heard variants of the claim quite often and lean towards the claim being at least, a possibility.
While it's true that people tend to see patterns when there are none or incorrectly attribute, why they correctly recognize something. I don't necessarily think that is the case here. Australians don't tend to dress in a distinguishing way when overseas, and people have recognized them before hearing them speak. Given the extent to which I hear this claim made, I can't completely dismiss it.
Examples of claims
This article from an Australian newspaper in 1943 interviews an artist who when asked if Australians have a racial type, says he thinks that it was generally possible to distinguish an Australian [from other Caucasians] due to differences in the nose and differences in the jaw.
Googling for terms like "look Australian" returns examples of the claims strewn around the internet, such as this forum thread and this blog.
Also of note is the art project to show the average face of Sydney, of which the following quote is relevant:

In many cases, however, the likeness is so strong that it's possible
to guess the nationality just by taking a cursory glance at the photo.

Reasons for thinking it may be possible
I'm fairly ignorant when it comes to biology, although there are a few reasons I think this might be possible. The (relatively) small gene pool from when Australia was colonized could have led to features from a small group being inherited in a large population.
There seems to be some evidence that environment can play a large role in influencing genetics more so than ethnicity. I can't find the paper investigating that, although will update this question if I am able to.
It seems possible to me that facial features belonging to the original colonists could have spread through subsequent populations, becoming a defining characteristic for some Australians.
I don't think most immigrants are relevant to this question as they will not have inherited distinguishing features (if they exist), nor will they or their parents/grandparents have been able to be influenced by the environment - if that is even a relevant factor.
So...
Do a significant number of white Australians, excluding 1st or 2nd generation immigrants, have distinct facial features unique or generally only found in Australia?
Is it reasonable that some white Australians could be recognized as Australian, going only by facial features?

Why the downvote? How can I improve the question?

Our brains are incredibly good at two things. 1) Seeing patterns, even when there is none 2) recording hits and discarding misses. It is very likely that the people who told you that had either recognized Aussies from other features (e.g. wearing flip flops in the middle of winter :P) or that they just recalled the times when they recognized Australians just by their looks, conveniently forgetting the times when they did not.

@nico that may be likely, although as an Australian who spent an inordinate amount of time overseas, I do feel like I can sometimes tell Australians by face alone. Aussies don't tend to dress like the cliche when overseas, so dress isn't really a distinguishing factor.

I don't understand the downvotes. I'm asking if it is possible or not. Is the question really so ridiculous that it doesn't merit an answer?

I actually upvoted it, I think it is a good question, too bad there is no Anthropology SE :D.

@nico thanks, I just get miffed when downvoters downvote without giving a reason.

"I do feel like I can sometimes tell Australians by face alone" -- and you can also sometimes tell what way up a coin is before seeing it. 50% of the time, in fact. Which is why the only way to answer the question is a study of the actual task, which is to measure whether anyone can distinguish between (for example) white Australians and white New Zealanders better than 50/50 :-) If we knew whether it was true or not, we could worry about whether it's reasonable and what facial features are involved.

@Steve, my claim on being able to identify some Australians by face alone is nothing like being able to correctly guess the side of a coinflip. I absolutely agree a study would be needed to see if there is anything to my question, however I thought a question checking the plausibility of my claim was in order first.

@SonnyOrdell: sorry, but if you only get it right 50% of the time when asked to state the nationalities of an evenly-mixed group of Antipodeans, then yes it is exactly like guessing a coinflip. So make sure that's not what's happening. Which is why I say that "sometimes" getting it right is worthless, that just means you don't always get it wrong. To protect yourself from the natural human tendency to perceive a pattern where none exists, you should establish that you get it right better than guessing.

@SteveJessop Your argument is based on a flawed assumption, that I only get it right 50% of the time. Try 90%. Note, I'm not saying I can identify all Australians by facial features, only those that I perceive to have facial features distinct to Australians.

I didn't assume anything, I merely said that "sometimes" isn't good enough. Most people would not describe 90% as "sometimes", but if that's what you meant then that's great. I'm not saying you can't do it, I'm saying that (until just now) you'd given no indication that there's any real phenomenon here. But fine, if 90% of Australians are recognisable to you as such because you perceive distinctive features, and the other 10% aren't because you don't, from a "big enough" sample, then that's an extremely strong result.

@SteveJessop fair enough, my apologies. That is a result of my trying to make the question more conservative so that it could even be asked on Skeptics.SE, although the mods at the time we rather difficult to work with so it ended up on here. When I worked in the tourism industry, it was pretty common to be able to spot Australians, something my colleagues do frequently also. They don't tend to be wearing anything that would signify Australian nationality and it is often before they speak.

I'm surprised this question has so many up-votes. The sources cited are forums, bad journalism, and an art project. The reason you might think there is a difference seems purely cultural. Even the studies cited below in answers have no empirical data, or are purely hypothetical, and the facelab haven't published anything on this. This is a very subjective question and I am going to open a close vote.

Sun exposure - Lots of it over years make people look distinctive.

Yes, it is possible (on some average basis, i.e. with chance better than random).
Take a look at average women faces from 41 different countries (AFAIK created with Face Research software; sadly no picture for Australia). Clearly, even from small and nearby European countries you can spot differences (which work on the average). I guess the case of Austriala vs other countries isn't an exception. Similar face averages are also on the project Face of Tomorrow.
However, when dealing with a single subjects it it may be not a reliable method to tell of his/her nationality or country of origin, as:

even within an relatively isolated group there is variance in genotype and phenotype,
people do move (especially now) and do mix (so unless you are comparing isolated islands you should't expect to have homogenous genotype).

Moreover, when identifying a person we may (even subconsciously) look at different features (including clothes, accent, behaviour, context, ...).

As much as I like that "average face" link, it only remains an exercise in style. Obviously averaging different faces will give different results. What you would have to do to make it meaningful is getting different subset of faces from the same country and show that all the subset give similar results (I guess we could call that face bootstrapping). Then, as a negative control, take various faces from different countries and show that those characteristics do not show up anymore.

@nico I am hoping that someone may explain why or why not what I propose in my question would be possible, although average a decent sample size and looking for patterns would also give a good indication.

@nico I agree with your scrutiny, as the result is not cross-validated. However, it is not hard to design a test when people see two faces (single, not averaged) and two countries (and their task is to match them). I bet that even for nearby countries (e.g. Germany and France) one can guess with >50%.

@Piotr Migdal: sure, that would also be another very good way to do it.

I think this answer deals with the general case of recognizing someone by their nationality and not Australia specifically. I think that Australia is a special case as most people would not believe white Australians could have a distinct look, as they simply look white.

@SonnyOrdell Yes, it is a general case and here is nothing special about Australians. Perhaps there is something special about Caucasian Australians but I doubt.

@piotr but that is the question I am asking is about, if there is something special about white Australians. Your answer should be specific to that, not a general case.

It seems unlikely, but it's possible.  The mechanisms that might occur (that I can think of) are:
1) if the Australians had some rare genetic traits that became more common in the australian gene pool than in the UK gene pool, it is possible.  This is what happened with eastern Asia and the Y chromosome, which something like 40% from a single individual.
For this to be the case, it would be necessary that:  Australia's gene pool must be isolated - very little immigration to the company and mixing with other gene pools.  (i think not- what do you say?)
2) the diet of Australians caused their general body or face to be distinctive.  As there is a lot of fast food in Australia now (and obesity) I'm guessing that this is simply not the case, at least compared to the UK and US.
Since there is no direct study (that I can find) all we can go on is anecdotal thought experiment.
As far as cognitive bias goes, I'm Asian American and I've heard many many (maybe most Asians say that they can tell one nationality vs another just by appearance).
Whenever I have tested myself or others I have not found anyone who can tell that i am 100% Japanese genetically.  This is probably because diet in the midwest where i grew up was so corn rich and I've been mistaken for nearly everything, including Latino backgrounds.  Most people think I'm Filipino, which is great except that I am not :)
Even when I ask Asians to look at other Asians and guess, it seems pretty rare that one can be consistently correct.  There has been a lot of gene migration between countries there, even though the national groups are much much older than Australia.  This is why I really doubt that Australians have been genetically isolated long enough or strongly enough for this to really be likely.
It would be pretty simple to get a bunch of pictures together, say 100, and test this if you really want to know.

Do you know about alllooksame.com?

ha - good one! I hope I wasn't trying to subliminally prove a point, but for faces I scored 6/16.  the average is 7.

Could you maybe expand on point 1 and 2 showing that what you say is possible? There is no direct study with Australians but there should be for your underlying points?

RE Australia's gene pool being isolated, it surely was at the formation of the country and likely stayed so for many years, perhaps this could have had an effect?