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How does salinity affect the bonds of an enzyme?
According to my textbook, "Too much or too little salt can interfere with the hydrogen bonds that hold an enzyme in its three-dimensional shape". I know that NaCl is held together by an ionic bond, meaning that one atom is strongly positive (in this case sodium) and one atom is strongly negative (in this case chlorine). I would guess the polarity of salt has something to do with its effect on hydrogen bonds, which consist of a hydrogen atom which bonds weakly to a strongly electronegative atom, resulting in a similar behavior to its ionization in glass of water, since water molecules are also polar and form hydrogen bonds with one another.
My question is, how exactly does salinity affect the bonds of an enzyme?

I can't find a good reference for this, but I know the DNA double helix is only stable in the presence of cations such as Na+, K+, or Mg2+. The cations help neutralize the negative charges on the phosphate backbone and prevent repulsion. This allows the bases to form hydrogen bonds and hold the structure together. Without the cations the hydrogen bonds wouldn't have enough strength. Something similar may happen in proteins, where ions help to neutralize charges or bridge certain amino acids together and allow the hydrogen bond to form.

@user137 In the presence of water (which is the usual state in living cells) there are no ions bound to DNA.

@Chris But there has to be some interaction, when using RNA I have to use a 150mM NaCl buffer to get Poly A and Poly U to bind well.

@user137 I am not saying that there is no interaction (which is of course present), but not in the form of "bound" positive ions to the DNA backbone.

Sodium Chloride is not "polar". It is an ionic compound and dissociates into the respective ions in water (because of the latter's high dielectric constant).
Hydrogen bonds are similar to of dipole-dipole interactions (van der Waals) but much stronger and are therefore classified as a separate type of bond. However excess salt can lead to ion-dipole interactions (which are stronger than H-bond) that may prevent the formation of the hydrogen bond.
Ions such as Cl - can act as chaotropes (cause disorder)[ref]. K+ is also chaotropic while Na+ is kosmotropic (reduces disorder). However both Na+ and Cl - affect the entropy of water very slightly. So the effect of NaCl should be mostly due to ion-dipole interactions.


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How do catalase and other antioxidants neutralize free radicals?
In learning about how cofactors are essential to proper enzyme function, my textbook mentioned catalase and its relation to the human body. According to my textbook, catalase is similar to hemoglobin in that it has 4 hemes which cradle an Fe (iron) atom; the iron atom is used to neutralize free radicals when it "pulls on the substrate's electrons, which brings on the transition state" after catalase is holding a substrate in its active site. I already know that free radicals have one or more unpaired electrons which make them dangerous as they "seek out" an electron to complete its pair on any molecule, atom, or ion it can find, perhaps causing significant tissue damage in the process. I also know that the transition state is a key point in a reaction in which the activation energy required has been met and the reaction will continue spontaneously until it ends.
My question is, what exactly is happening here that helps to neutralize a free radical, and what is the part after the transition state doing?
If I had to guess, based on that cofactors generally can be affected during a reaction, perhaps Iron somehow binds with the free radical and share its electrons, effectively neutralizing the unpaired electron as well as using up the Iron atom? I imagine the "pulling" in the book could fit a description of a weak chemical bond/attraction, but I'm still unsure.

Catalase (hydrogen peroxide oxidoreductase) does not actually quench free radicals. It catalyzes the conversion of hydrogen peroxide to water; the former is a source of a free radical, not a free radical in itself.
This is the proposed mechanism of action of catalase: First one of the oxygens is deprotonated by at the active site of the enzyme. Then the Iron atom that is bound to heme forms a co-ordination complex with the deprotonated oxygen and pulls it away from the other oxygen. As a result the O-O bond breaks.
Free radical quenchers/antioxidants react with the free radicals and form non-toxic products.

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How many cells are there in the apical meristematic tissue?
How many cells are there in the apical meristematic tissue?
Looking at this picture...

, I would tend to think that there are few hundreds cells in the meristem tissue. But I guess this is a picture of a root tip and the answer will be much different if we look at big branches and big trunks of roots. Also, the answer will probably differ between monocots and eudicots.
Roughly speaking, how many cells are there in different apical meristematic tissues (root, branches, trunk, different species)?

Meristem size is a very controled, highly genetic feature. It doesn't change between big or small branch/root (The SAM and RAM are obviously different).
There are very levels of potency in the meristematic tissue, so you should explain more which section of the meristem is of interest.
SAM (shoot apical meristem)
In *Arabidopsis thaliana* there are 9 long-lived meristematic cells, 3 in each lineage (L1, L2, L3) (https://www.sciencedirect.com/science/article/pii/S0012160609013840)
But the whole meristem is somewhat larger. If you consider the organizing center and cells that react to wushell by creating CLV1, CLV3 you get a few dozens.
If you consider cells that express miR156, miR172 or AP2-like genes you can get a few hundereds.
The scale is similar between species but the number and genes used to asses it vary.
RAM (root apical meristem)
I know less about the RAM but we can consider there the Quiescent center and also the Intial cells togheter called the promeristem.
THe Quiescent center consists of 10-20 cells and there is one (sometimes more) initial per file of cells in the root giving 20-30 cells in the promeristem.
The meristematic zone is somewhat bigger than the promeristem but the cells are pluripotent with relative small mobility.
 Roughly speaking
The most meristematic zone of each meristeme has no more than 50 cells.
The full area considered a meristeme can have a few hundered cells, depending on the research goal.

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Is it one queen bee per hive or per colony?
I've come across lots of information on the lifecycle of bees, but I cannot find the answer to my question.
If a beekeeper had, say 6 hives, would there be six queens (one per hive) or one (for the whole colony)? Maybe they would be considered six separate colonies, I'm not sure, but that would be a different question.

Every beehive contains one colony, and every colony has one queen. (Of course there are exceptions, like if a queen dies or is about to be replaced, but I don't think that's what you're asking.)
A swarm is a specific thing, when the queen and part of a colony has taken off from the original colony to form a new one.
I think Wikipedia works well if you need more information on beekeeping terminology:
https://en.wikipedia.org/wiki/Beehive
https://en.wikipedia.org/wiki/Swarming_(honey_bee)
Edit: To clarify, I only have experience of keeping European honey bees (Apis mellifera).

I think this is species specific no? I have some memory of some species having multiple queens per beehive, but could well be wrong - it could be some species of ants or wasps!

@rg255 I don't know! I'm only familiar with keeping Apis mellifera. Hmm... Maybe someone else will show up and let us know.

@rg255 I found this: "in the Brazilian stingless bee Schwarziana quadripunctata, a single nest may have multiple queens or even dwarf queens, ready to replace a dominant queen in a case of sudden death."  But they aren't honey bees. Might still be other species that do weird things, though. https://en.wikipedia.org/wiki/Queen_bee

In honeybees, there is usually one queen per hive / colony. The original queen will leave with the swarm and leave numerous queen cells behind. Mostly one new virgin queen will hatch and kill the others or some of the worker bees kill the others by not letting them hatch or starving them, or breaking open the queen cells. However not infrequently there may be smaller cast swarms that leave a strong colony, each with one or sometimes numerous virgin queens.
If a establishes mated mature queen is damaged, I'll or running out of sperm, the workers will make one or more new queens. These will have to be mated and it is well known that the old and new queen can co- exist peacefully for a period in the hive.
We do not yet understand many factors influencing this.
Reference: The Buzz About Bees by Prof Jurgen Tautz ( original text in German ) Springer books 2nd den 2009 ISBN 978-3-540-78727-3

That's interesting about the old and new queen co-existing peacefully. There must be some sort of chemical signal given off by the old queen so the workers or new queen don't kill her.


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Workspace preparation and cleanup for DNA work
What steps should be taken in a molecular lab environment to help ensure that DNA samples/stocks are not contaminated, or contaminate other objects in the lab?

VTC because this question is identical to the later one, and the later one is better asked and has better answers.

From the comment section:
Mostly segregation of PCR-amplified DNA from non-amplified DNA. Typically no DNA or sample should ever enter a specific room designed to prepare the MasterMix for PCR (this is true for diagnostic labs, in the research one I never saw that). For the rest, following good laboratory practices (google that) should be enough.


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

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


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Do *Ambystoma macrodactylum* predate on *ceuthophilinaens* like the one I observed?
I observed this Ambystoma macrodactylum within half of a meter of this Ceuthophilinaen under an old board. I can imagine salamanders eating cricket-like things, but this question is far outside my expertise. This page says that long-toed salamanders prey on small crustaceans, dipterans and tadpoles at the larval stage, but doesn't seem to discuss their terrestrial diet. Not much about predators on the putative prey's page.
Do Ambystoma macrodactylum predate on ceuthophilinaens like the one I observed?

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Bergmann's rule and Allen's rule: endotherms and ectotherms
Surface area to volume ratio (in terms of heat conservation) is not the only mechanism, but it is still an important mechanism for explaining Bergmann's rule and Allen's rule. Given that, I want to know why these rules are primarily applied to endotherms. I know there are some ectotherms that follow the rules, but here I am not asking for examples.

I guess, it is because these rules refer to how animal bodies are evolved to minimize heat loss, which is relevant only for endotherms (who have a different internal homeostatic temperature) and not for ectotherms, whose body temperature is equilibriated with that of the environment, making heat saving mechanisms redundant.


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A question about a succession study by Chapin et al. (1994)
The succession study in Glacier Bay, Alaska (Chapin et al., 1994) is an example that is used in almost all introductory texts on ecological succession. In the study, the effect of each succession stage on the germination and development of spruce seedling was examined, and complex results were found (see Figure 4b in here). For example, In Dryas stage (one of successional stages), spruce seedlings had weak germination and survival rates due to increase in seed predators. Likewise, the results show the effect of each successional stage on the various attributes of seedling germination and survival.
My question here is what is the control/reference of this study? For example, Dryas stage decreased the survival of seedlings compared to what condition? The results show "increase" and "decrease", but the reference is not clear. Is the control same for all successional stages?


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What were the first neural systems like?
I'm curious about the origin of the neural network.
I'm thinking perhaps once life evolved beyond the single cell organism, it needed a simple neural network to coordinate those cells, and cell functions.
What were the first neural systems like?
More specifically: What kind of cell did the first neurons evolve from and how did they work at first? (assuming there were few, if any, neural connections in the first organisms to develop neurons of some sort)
From what I understand about a neural system, it needs a few neurons linked together to keep firing.
Perhaps the first neurons had triggers other than dendrite connections?

I think this is too broad, since you are basically asking about the evolution of nervous systems (in any type of organism?), and there are multiple questions rolled into one. Also, why do you think that single neurons would be useless? They could still transfer information between cells (e.g. sensory/environmental input to motor action). Wikipedia: Evolution of nervous systems will also answer/hint at some of your questions.

@file I'll focus the question.

I think this question is unanswerable as neural tissue is not preserved in fossils. Looking at relatively 'simple' organisms may help to get an idea. For example the neural system in cephalopoda (various ganglions throughout the body each driving one tentacle etc) or in insects.

@ChrisStronks We know tons about evolution that isn't preserved at all in the fossil record. For instance, we can study evolutionary model organisms and do comparative genomics. In fact, fossils play a fairly minor role in the modern study of evolution.

@KonradRudolph : sure, that's what I say, perhaps use insects or other organisms. And if there's tons of info on the first neural systems I am curious to your answer!

In hydra it is like a net— no central organization. Developmentally neurons arise from the ectoderm (from where skin also arises). This may perhaps be a recapitulation of the evolutionary trajectory

This question can be answered by taking a look back evolutionary and see how other organisms have utilized neurology. The prime example, because it was one of the first real models of the neurological system, is the squid. It has neurons with singularly long axons to send electrical pulses long distance. This method of electric pulse transfer has been evolutionary updated, essentially, but we can get an idea of how these cells came to be. If we look back at squid predecessors, like the jellyfish, we see that it also developed electrical impulse cells to aide in defense and movement. Back further, we see the sponge has no neurons, but has something similar. This gives us potential insight into the development of the cell. It has protein clusters that act similar to post-synaptic signaling. So it is likely the electrical impulses were developed based on the function of these protein clusters, and bam! Electrical pulses became a must faster way to communicate to different regions of a system than simply trying to protein signal across cells.
Of course, looking at this question evolutionary is tricky since the question of divergent evolution comes into play, and we can't know if the sponge protein clusters offer a potential answer to neuronal development. But, is interesting evidence and makes an interesting debate!
Source= Sakarya O, Armstrong KA, Adamska M; et al. (2007). Vosshall, Leslie, ed. "A post-synaptic scaffold at the origin of the animal kingdom". PLoS ONE

I would really emphasize how limited our conclusion can be through looking at current organisms.
Yes we can say one organism may be "higher level" than the other, but knowing exactly what the primitive state was? That is most likely something we will never truly know.
Perhaps when we can finely simulate evolution through computers. An interesting new advancement has been the creation of circuit boards using algorithms for evolution. Essentially the circuits that are less efficient die out.

I agree!  New networking algorithms offer interesting new insight to these types of questions (and many others!). I actually am currently working on developing such algorithms for alternative toxicity testing methods! It's crazy the diversity of uses of different tools, right?

@FrankyG this ironic thing is, the use of algorithmic evolution of a brain was my purpose for asking this question to begin with. I've been experimenting with throwing out random configurations of tens of thousands of neurons of virtual neurons, which behave in a similar way to actual neurons, and let the ones die which arent capable of overcoming a pre-defined environment. This is a vague experiment at this point, and it hasnt gotten anywhere, because I think I need to start smaller, simulating an extremely primitive small group of neurons accomplishing a simple task.

But the issue with that is, our modern day neurons seem to be fairly useless in small groups. Theoretically, being able to figure out how the most primitive group of neurons worked would allow a good starting point for the evolutionary model.

I think starting smaller would be a good idea and then expanding off of that to see how evolutionary the different ways neuronal networking could have occurred. You could even throw in probability curves to estimate likelihood of evolutionary occurrence, but that would have to considered unknown environmental factors. Anyway, if you think the question is answered well don't forget to mark it as answered so other people can reference it!

The problem is that in smaller groups there isn't much pressure for neuron selection. What I suggest you do is simulate having many smaller groups of neurons all with connections to one another and allow it to start choosing the most effective way to send signals between the groups. We know primitive neurons worked much in the same way our own do using either chemical or electrical signaling. The problem isn't how they send signal but how they choose which signal pathway is the proper one to enhance and strengthen.

So if you create your simulation with small groups of neurons (say 100 per group, mess with the size) and have an algorithim that strengthens connections to groups around it based on what information needs to be sent and where. You can probably simulate it to have groups of neurons that do a particular mathmatical operation and give it (lets call it a "brain") problem sets to solve that require it to use either all/some/few of the small groups. Of course I have no clue where to start from a theoretical standpoint it sounds feasible.

You can further add variation to this by having the type of connections created be varied. You'll have to do some more research on specific neurology though as there are several different types of connections neurons can make to one another and it affects not only the speed of the signal but the strength when it arrives and how that signal propagates, reaches threshold, etc etc.


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Gradualism vs. Punctuationalism
TLDR? Just read the bold bits!
I started with Darwin's Origin of Species, and then read Dawkins's first three books The Selfish Gene, The Extended Phenotype, and The Blind watchmaker (I just started River out of Eden).
Dawkins talks of Gradualists and Punctuationalists as if their views are incompatible but my initial understanding of Darwin was that both of these are true. My understanding is that if you look at an individual line of heredity then you will see a very consistent and gradual change through the generations (at the mutation rate), but if you look at the population as a whole you will see "periods of rapid evolution".
To me this seems easy to reconcile. Imagine a gene for fur thickness in polar bears, if each nth generation has a 'random' mutation for thicker or thinner then for each line of heredity you'll see a random walk about the starting point. Most of them will go up a bit, then down a bit, and end up close to where they started, some will be a bit further away, and a small number will be far away (much thicker or thinner fur) in a Gaussian distribution. So any random sample from the population that happens to become a fossil is most likely to be in the middle (i.e. unchanged over many generations).
Now if there's a sudden environmental change, or a one-off freak event such as a very cold winter, say that only the 10% with the thickest fur survived this cold winter (and perhaps a very small number of others who got lucky). Now very quickly within a few generations, that thick fur gene will dominate and as the population grows back to whatever size the environment can sustain it will be present in much greater absolute numbers than before the selection event. When looking at random samples of the population throughout this period, you might conclude that there has been a "period of rapid evolution". If the change is more gradual than a single sudden event, for example it gets colder over 500 years, each year the ones with the thinnest fur die off and the thicker fur genes get more popular in the population. This would appear to be a very rapid period of evolution, but really all the evolving happened gradually, long before the selection event.
My question really is what's wrong with this view of things? Dawkins seemed to anticipate all my thoughts and objections while I read his books and provided explanations, except for this one. This kept nagging at me the whole time and he never mentions it at all. I can't imagine I'm the first person to think this way (especially since Darwin himself pretty much said this) so why doesn't Dawkins explain it (either as correct or as incorrect with the reasons why)? Can someone please explain it to me either way?

Wlcome To Bio SE! It may help to bold-out the important parts, such as a specific question. It's a quite wordy question. Good luck!

If I understand your question correctly, you are essentially distinguishing between the timescale on which the variation in the character of interest is generated, and the timescale on which selection prunes the population based upon that variation. The argument is then that "all the evolving happened gradually, long before the selection event" because that is when the variation was generated.
To me, this seems to be a misuse of the term "evolution", which is usually defined as a change in trait or allele frequencies in a population over time. Under that definition, much of the evolution does occur via the selection event. Before, you have a wide range of trait values; after, only a narrow selected set of trait values. In such a model, selection indeed is the major cause of allele frequency or trait value change.
In practice, both processes are usually acting in concert; variation is being produced by mutation and recombination and eliminated by selection at comparable rates so that the net amount of variation in the population is at an approximate steady state. This is essentially the model Darwin espouses, though note that Darwin does not have our modern understanding of heredity and therefore is not able to explain how variation is generated or preserved.
Additional note: When thinking about models of the kind that you describe, it is also key to understand that if you have a large number of loci affecting your trait (e.g. coat thickness), then the Gaussian distribution prior to strong selection will not include the extreme phenotypic values. If there are 20 diploid loci interacting additively to determine coat thickness and the mean individual has 20 thickness alleles and 20 thinness alleles, no individuals in a reasonably sized population will initially have all 40 thickness alleles, or even 39 or 38 etc. Selection for thickness will change the mean, and will also result in individuals outside of the initial range of variation. If the mean is 30, you may well get an individual with 38 or 39 or even all 40 thickness alleles. So once selection occurs, new more extreme phenotypes will suddenly appear. Nothing strange has happened in terms of rates of generating new variation; in fact this is just a consequence of reassorting the current alleles under the new allele frequencies.

So why are they presented as incompatible and opposing factions? Was this previously the case but now it's widely recognised that they work together? Did I just misunderstand?

Regarding the multiple loci - doesn't this just narrow the distribution? Meaning that the same arguments hold true, even more so in fact.

Generation of variation and selection on variation involve a very different scale (microevolution) than do graduated versus punctuated evolution (macroevolution). In the microevolutionary context, generation of variation and selection on variation have always been seen as mutually compatible, and indeed both necessary for evolution by natural selection to proceed.

With regard to multiple loci, the idea is that multiple loci have a greater effect than any one locus could. If a single locus model and a multilocus model both spanned the same range of phenotypes, sure, you'd expect a narrower distribution for the multilocus case. But when each locus has an additive effect delta, we obviously have a broader ranger of effects and a larger variance in the multilocus case.


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Does the bending of a tree's trunk in the wind stimulate and strengthen root growth?
Recently Southern California experienced extreme wind velocities and afterwards the news reported over 300 trees had fallen in San Diego County. I had either heard or read somewhere that the action of the wind and bending of a tree assists to strengthen the roots ( I suppose as long as the wind is not strong enough to pull the tree out of the ground). And so that brings me to the point of my question.
Does some kind of mechanism exist within the tree that connects mechanical bending of the trunk with increased rate of root growth? I can imagine that bending might stimulate fluid movement through the phloem & xylem, and perhaps this might be the mechanism. Or does the bending cause a release of some type of growth hormone? Or perhaps the mechanism is epigenetic?
I suppose that if such a mechanism were to exist it would provide one means of evolutionary weeding; removing the weaker part of the gene pool. Perhaps that's what happened in San Diego this last week.

The response of trees to strong winds is an interesting question, but I'm not sure what you mean in your last paragraph. It seems pretty unrelated to the rest of the question.

In tree growth there is principle called The axiom of universal stress whereby the growth is in such a way as to equalise the stress across the whole of its structure. The roots, the stem and the branches are one continuous system and can not be thought of as separate.
On a simplistic level for a branch to grow, there must be a corresponding equal and opposite growth in the stem and roots. Of course it is not quite like this as the growth happens across the whole structure at the same time.
The trees on the edge of an even-age stand of trees will have grown to be more stable against wind. They are referred to as being a wind-firm edge to the stand. The trees that have grown up within a stand, with the shelter of their neighbours will not have the same stability in the face of wind, so that if the stand is opened up too quickly it can lead to wind-blow. In uneven-age woodlands, the same principle is true but the dynamics make it less pronounced.
The reason for mentioning this is just to illustrate that, absolutely the wind, and other external factors, gravity being the obvious one, will have an effect on the growth of the roots, as well as the rest of the tree. As the wind exerts a force on a tree that  force will travel through the structure and into the roots and into the ground.
To come back to the specific question then.

Does some kind of mechanism exist within the tree that connects mechanical bending of the trunk with increased rate of root growth?

Yes, and no. Because the increased rate of growth will be across the whole structure, but not equally. It will put on growth at the points where the stresses are, in order to self-optimise the loading including within the root system.
The next time you cut either the stem of a leaning tree, or a branch of a tree, take a look at the orientation, and thickness of the rings. You will see that in broadleaf trees (or more correctly angiosperms) the rings on the side under tension will be thicker. In conifers (or gymnosperms) it is the opposite. The thicker growth is found on the compression side.
Here is a great photo of compression wood in a conifer from http://www.copperman.co.uk/didgeridoo/how_to_make_a_wooden_didgeridoo/what_is_wood_2.php

The same principle will be happening in the roots also.
As to the actual physiological mechanism that causes this response I have not yet come across a definitive answer. The consenus, at least as far as I know, is that it is not fully understood.
The closest I have come across so far is from this phd in 1994. http://etheses.whiterose.ac.uk/2438/1/DX184141.pdf
I dare say there has been more work done on this in the last couple of decades.

Well organized and complete answer, after all this time. Thanks

I suspect that many of those trees were Eucalyptus. Eucalyptus trees have shallow roots. They are tall and rigid.
About 150 years ago, Eucalyptus trees were planted in San Diego with the hope of growing wood for railroad ties. The idea was that if they grow in the Australian desert, they can grow in San Diego. They do, and are now everywhere. Unfortunately, the wood isn't very strong. It isn't useful.
Usually San Diego is pretty dry. The soil is sandstone and clay. It is very hard when dry. A storm can soak the soil, making it loose and muddy.
Here is a picture of some Eucalyptus trees over 100 feet tall that blew down in San Diego (my parent's yard) in a storm about a year after your question was posted. One tree fell onto the next, knocking them over like dominoes. For reference, the pot is about 2 feet tall. As you can see, very little root was pulled up when they fell over.
Another common tree in San Diego is Oak. They have very deep roots, and are much less prone to blowing over.


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How far can we go in engineering our own evolution?
After recently seeing Christopher Nolan's Interstellar and reading Kip Thorne's The Science of Interstellar, I've seriously been reflecting on the challenges mankind faces in becoming space pioneers, which in my belief will be a necessity to survive as a species. Not just the technological challenges, but the biological ones as well.
Technology can only go so far to aid and protect an organism against the brutal environment of space travel. And so the day may come where we have to make a choice on engineering our own evolution to become a hardier species that can better cope with that environment. The two immediate attributes that come to mind are resistance to radiation and extended life spans.
And this brings me to my question. Putting aside for the time being the question Should we make this choice ?, my question is How far could we go towards engineering a space-durable human species?

How far could we go towards engineering a space-durable human species?

I think this question is likely to get closed as off-topic. It is extremely hypothetical and would be a better fit on WorldBuilding.SE. But here is my messy attempt to answer this question.
Assumptions
So, I guess in your question, you assume that we know everything about how our genotype (≈the genes of an individual) make up the phenotype (≈how we look basically). So, I will try to give a short answer to this question by assuming that we were to know exactly what would happen if we were to add the sequence ATTTAG in the somewhere in the alpha-globulin gene or the sequence CCTATA somewhere in the regulatory sequence of the lactase gene. It is important to understand that today we are very far from having such knowledge. I also assume that we are able to recreate the environments we need to develop the new thing (human2.0 if you want) that we would have engineered. For example if we make up humans that need to grow in a different environment than the womb. By the end of the answer, I will pretty much assume that we know everything that can be known about organic chemistry and how chemicals process genetic information. Note that to the point we're doing the drastic modifications I will be talking about, it will be a philosophical issue to decide whether the new species we created is a human or not (it may even come to the discussion whether the new thing we created is a living thing or not).
Resistant to evolution as a species or only resistance as an individual?
Are talking about a species that would definitely be resistant to survive in these extreme environments or are you talking about a bunch of individuals surviving in this extreme environments. The difference is "evolution". Species evolve and not necessarily in the right way. High radiation may yield to high mutation rate and therefore to mutational meltdown (decrease in mean fecundity of the population through time yielding to extinction of the species).
General Limitation
With these very extreme assumptions, then we are only limited by physics. We could not add wings of the size of the wings of a warbler to a big animal like human and hope that it is going to fly.
Resistance to radiation
I know little about this subject but will try to say some things that may eventually help you. We cannot really make our DNA insensitive to radiation (although we may eventually make our DNA slightly more stable) because radiation will alter matter. It is a physical process that cannot be altered. We may create a lot more of tumour suppressor genes to protect ourselves from developing cancer. Eventually we could create a species that would be able to synthesize (and carry) a concrete shield around its body to protect itself from radiation. But it might eventually be easier to code genetic information with something else than DNA! Eventually made up of quartz because quartz is relatively insensitive to radiation. We could indeed create a whole new form of life.
High radiation yield to high mutation rate and high mutation rate may likely lead a species to extinction (mutational meltdown) but not necessary directly kill the first generations of this made-up species.
Extending lifespan
This sounds "easier". We may "just" target the alleles (=variant of a gene) that are known to diminish the human lifespan, to slightly (but probably considerably) increase human lifespan. Again, I assume that we can know these alleles and can replace them with better variants. However, evolutionary processes will just recreate those genes, just because there always has an equilibrium between the rate at which new deleterious mutations appear and selection purging the genome from these mutations. Moreover, at an age where reproduction has already occurred selection is less important and it allows for deleterious allele that are expressed late in the age of the individual to eventually spread in the population.

"What are you talking about?" - modifying our genetics to become less influenced by the space environment. To have  control over our genetics in getting into the space environment, and maintaining control once we are there. "Resistance to radiation" I guess something like emulating insect physiology. I once read something regarding how cockroaches have a high resistance to radiation.

I am not sure what you mean with your comment. I renamed the "What are you talking part?". Hope that makes more sense to you.

Well it is definitely not worth trying to answer bad questions if we receive downvotes for that!


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Examples of real biological applications of the Keller-Segel system
I am working on a model of aggregation behavior modeled with the Keller-Segel PDE system. I recently gave a talk on this and was asked what other examples there were of the Keller-Segel system. Since this is an obvious question, I was embarrassed to have no example other than my model and the aggregation of cellular slime molds (the application for which the Keller-Segel model was originally developed). So I did some googling and came up with bupkis. There are hundreds of papers about the system by mathematicians, but I failed to find any other biological examples.
What about it? Is the Keller-Segel model mostly just a mathematical curiosity, or is it a model with many real applications to biology?

This looks like a good starting place: Painter, K. J. “Mathematical Models for Chemotaxis and Their Applications in Self-Organisation Phenomena,” June 22, 2018. https://arxiv.org/abs/1806.08627v2 (published in Journal of Theoretical Biology, 2019). Lists examples from Dictyostelium (of course), bacterial aggregation, development, physiology and disease, ecology, social science.

In this review, I evaluate the use of PKS [Patlak-Keller-Segel] models in describing chemotaxis (and other taxes), particularly focussing on examples of pattern formation/self-organisation. I do not review the numerous excellent studies
that primarily concentrate on their mathematical analysis: a number of reviews already cover these aspects in depth [...] Next, the fundamental modelling that led to (1) is reviewed and an overview given regarding its patterning behaviour. I then proceed field-by-field, beginning with its motivations in microbiology and sweeping across areas including developmental biology, immunology, cancer, ecology and the social sciences. For each case, the historical justification for chemotaxis is described and models are discussed; a compendium
that contains many of these models is provided in the Appendix. Finally, I demonstrate how PKS models can continue to penetrate new areas, via a novel application to explain clique formation in research.

Here's a working link to the J Theoret Biol paper : https://doi.org/10.1016/j.jtbi.2018.06.019 .


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After how many generations descendant is not more related to ancestor, than to a random individual in an ancestral population?
Descendant of n generation has on average 1/2n DNA of ancestor. (For example children have 1/2 DNA of parents and 1/4 DNA of Grandparents, After 10 Generation 1/1024 DNA and after 100 Generations 1/2100 DNA).
Is there a point (value of n) when descendant is no more related to ancestor and is similarly related to random individual from an ancestral population.

Welcome to Biology.SE. Your question sounds like a Coalescent theory question. Do you assume that no mutations and no selection in your model? The answer will very likely depend on the population size.

Thank you. Answer will likely depend on effective population size. logically mutations will decrease value of n and selection will increase or decrease depending how it favors certain DNA.
I just did not thought about this and wanted to know if this is even possible, that descendant is no more related to ancestor than to random individual from an ancestral population.

There is an interesting way to look at this question. By definition, two individuals are related only if they have a common ancestor. (If you mean something else by it, please correct me. For completeness, I include the trivial case in this: that is, I regard you as one of your own ancestors.) So your question can be inverted: it is really asking after how many generations everyone in the ancestral population is your ancestor?
As indicated in the comments, the answer will depend on the specifics of the population structure, including its size. But a first stab can be taken in this way: you had 2 ancestors one generation back, 4 two generations back, ..., $2^n$ (not necessarily distinct) $n$ generations back. So you certainly cannot be descended from everyone in the ancestral population if less than $\log_2 N$ generations have passed. ($N$ = population size, which for simplicity I assume to be stable.) In a freely mixing population under the very simplest assumptions, you will eventually decay exponentially towards complete coverage with a half-time of one generation.
This is complicated by the fact that some lineages die out completely. For instance, some of the individuals in the ancestral population didn't have any children. Some had children, but no grandchildren, etc. Obviously none of them were your ancestors, so you will never be related to them (except through previous common ancestors), no matter how much time passes. In fact, as time passes, more lineages tend to die out. So, if you look back very far, you'll find that the entire current population has only a very small numbers of ancestors in the distant past. This is called coalescence, and is what people are talking about when they speak of "mitochondrial Eve", for instance.
So, in summary, it's complicated. It takes only a fairly small number of generations ($O(\log_2 N)$) before you're potentially related to most of the ancestral population. But over longer times ($O(N)$ generations) your relationship to the ancestral population actually goes down.

Thank you for answer, very interesting.
My question is slightly different, will make it more clear:
Is my DNA more similar to Mitochondrial Eve or Y Adam or it is not possible to distinguish from other individuals who live with Mitochondrial Eve or Y Adam.
I understand that Mitochondrial DNA and Y chromosome is not recombining, but they have higher mutation rates than autosomal DNA and also, they are just a small part from total DNA.

Your mitochondrial DNA is more similar to that of mitoEve than to her contemporaries. Your Y chromosome is more similar to Y Adam than to his contemporaries. Other regions of the genome will trace back to one of them, or to other humans living in the distant past. It's hard to say a lot more without making detailed assumptions about the genetic structure of the population.


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How does the molecular machinery choose where to cut a chromosome for recombination?
I'm wondering about a few technicalities of crossover in meiosis. The point of crossover is to create new chromosomes that don't have the same allele combinations as the original two chromosomes. Usually, the chromosomes are cut at the same place on both chromosomes, and each piece is then stitched to that place on the other. This is to avoid unequal recombination, a scenario in which one chromosome has several instances of a gene and the other no instance at all. I'm wondering how the molecular machinery knows where to cut.
So here's my question: How does the molecular machinery choose where to cut a chromosome for recombination?
This question has two parts: At what type of place does it occur (does the machinery choose a completely random place, regardless of where genes start and end, does it just cut at the start of genes, or does it do something else)? Given that it happens at this type of place (e.g. start of a gene), how does it decide that it will cut here (the start of this gene) and not there (the start of that gene)?

Presumably you added a bounty to this question because you're not satisfied with the answers already given. If that's the case, could you explain what else you're looking for?

The question is very broad and complicated, since the situation may differ in prokaryotes and eukaryotes. Nevertheless, I'm citing a good paper that is closely related to your question:

Studies in yeast show that initiation of recombination, which occurs by the formation of DNA double-strand breaks, determines the distribution of gene conversion and crossover events that take place in nearby intervals. Recent data in humans and mice also indicate the presence of highly localized initiation sites that promote crossovers clustered around the region of initiation and seem to share common features with sites in yeast. On a larger scale, chromosomal domains with various recombination rates have been identified from yeast to mammals. This indicates a higher level of regulation of recombination in the genome with potential consequences on genome structure...
  ...DSBs (Double Strand Breaks) occur in highly localized regions and spread over 70–250 bp. DNA sequence analysis reveals no unique conserved consensus sequences, although a degenerate 50-bp motif partly correlates with DSB sites. However, one common feature is that DSBs are located in accessible regions of the chromatin next to either promoters or binding sites for transcription factors. Based on two studies, DSB activity does not correlate with local transcriptional activity, but depends on transcription-factor binding (HIS4 in S. cerevisiae and ade6-M26 in S. pombe).

Bernard de Massy, Distribution of meiotic recombination sites. TRENDS in Genetics Vol.19 No.9 September 2003
I'll sum that up into a more answer-like form. Seems like the process is not random, because the double strand breaking events are clearly not evenly distributed across a genome. As the paper says there are no specific consensus motifs found as of yet, though there clearly is something special before promoters and TF binding sites, which makes them more likely to be a breaking site. How the machinery choses the place? Once again, as the paper says the breaking event depends on TF binding. But that is for S. cerevisiae. There are 17 hot spots found in human and mice genomes some of which are intergenic (they occupy introns or 5'/ 3' flanking regions).
Here is the distribution of recombination frequencies across one chromosome (the figure is taken from the paper).

Here is a list of recombination sites in humans and mice

Great! I gave you the bounty for pointing out where recombination occurs with respect to the gene (intragenic or in intron/exon), even though Ankur pointed out how the molecular machinery chooses which hotspot it will cut this time.

In humans and mice anyway ,a lot of it boils down to the recognition of a specific sequence that marks recombination hotspots by PRDM9.
http://www.sciencemag.org/content/327/5967/836
Edit - I'm expanding in response to the comment below...
Meiotic recombination occurs at vastly greater frequencies in some locations in the genome than others and these are called Recombination Hotspots. For example, the figure here, sourced from http://www.sciencemag.org/content/327/5967/876/F1.large.jpg

shows the recombination rate at the hotspot and further away from it for Chimps and Humans.
These hotspots are recognised by the cutting machinery thanks to the binding of PRDM9, a zinc finger protein, to a DNA sequence that it specifically recognises and is present at hotspots. The DNA sequence varies from species to species (as does the sequence and the function of PRDM9) but in humans is a well-characterised motif 13 base pairs long and of the sequence CCNCCNTNNCCNC (where N is any one of the 4 bases in DNA) , and accounts for the activity of nearly 40% of known hotspots.
The first link I posted has evidence to suggest that variation in composition of PRDM9 is a determinant of which hotspots get used. PRDM9, it appears, stimulates the formation of a specific histone modification - H3k4me3 (DNA is wrapped around histones, there are five histones - H1, H2A, H2B, H3, H4, and each of them has a tail that can be chemically modified, and eight of these (2 of H2A, 2 of H2B, 2 of H3 and 2 of H4) form a nucleosome - in this case the fourth lysine residue of the tail of Histone H3 is trimethylated as regulated by PRDM9, and facilitates crossing over and recombination initiation.
Edit Summary

I've now updated the answer with an extended explanation, cheers Chris.

Thanks Ankur! It was hard for me to choose to whom to give the bounty. You suggested how the machinery chooses which hotspot to use. But GrayFall9 showed at what type of place hotspots exist in the genome, which was an important part of my question.

In meiosis, homologous recombination occurs. Two Spo11 proteins utilize tyrosines to induce a double-stranded break in the DNA. Spo11 has no specific cleavage site. However, cleavage by Spo11 lead to the discovery of Spo11-Oligonucleotide (Spo11 w/ attached oligonucleotide post-cleavage) complexes which could be mapped to 'hotspots' which the linked study finds a number of discriminating factors to Spo11 cleavage in meiosis:

From the precise locations of the 2.2 million Spo11-oligonucleotide sequences, Pan et al. [1] showed that local DNA composition also influences Spo11 cleavage sites. As expected from previous studies, Spo11 does not have a specific recognition or cleavage site. However, sequence biases were detected: the 10 to 12 bp surrounding the cleavage site and predicted to be bound directly by Spo11 is relatively AT rich, predicting relatively narrow and deep helix grooves facing the bound Spo11 dimer. Cleavage favors sites immediately 3' of a C and disfavors G in the same position. Also, within a 32-bp core surrounding the Spo11 cleavage sites, a twofold rotational symmetry for complementary dinucleotide composition can be discerned, suggesting separate contributions of the flanking 'half sites' to Spo11 binding and/or cleavage. In addition, cleavage sites are negatively correlated with positioned nucleosomes. Similarly, Spo11 is generally occluded from cleaving sites where transcription factors are bound, even though the binding sites of several different transcription factors positively correlate with hotspot sites.

While all the answers above are correct and insightful for the process of DSBs formation, recombination has another layer of complexity.
 Mediating proper chromosomal segregation is more likely the real point of crossovers since crossovers still happen in inbred genomes, which do not result in novel haplotypes.
 CO create a heteroduplex structure between DNA strands, Holliday junctions. This structure creates tensions forces which are needed to pass the spindle assembly checkpoint before the meiotic cell can progress into anaphase (see papers by Nicklas work on grasshopper chromosomes and Hirose et al 2011).
In most* organisms, at least one CO is needed per chromosome arm to pass the spindle assembly checkpoint and mediate proper disjunction. Lacking COs or misplaced COs can result in non-disjunction and increased risk for aneuploidy  (Hassold, Hall, Hunt 2007).
(*an exception are male Drosophila melanogaster, which have a CO independant chromosome segregation pathway).
Additionally it should be noted that DSB =/= COs that is, not all DSBs are converted into COs. In all organisms, DSB outnumber the resulting COs. The majority of DSBs are resolved into non-crossovers (NCOs). There is new evidence (in mice at least) that these numbers are not proportional. That is, if total DSBs in the genome are reduced, the total CO number is unaffected. (Cole et al 2012).
I think a more interesting phrasing of your question would be, How does the genome choose which DSBs to resolve into COs vs NCO?


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How many NOD like receptors in Human?
This is pretty specific question maybe. Anybody have an estimate? For Toll Like Receptors there are something like 10...
http://www.jbc.org/content/276/4/2551.long
I'm only finding NOD1 and NOD2 => only 2?

The following wikipedia article has an aggregation of some of the different members of the NOD-like receptor family, and the following journal article goes over the nomenclature for the NLR family, and I believe will assist you.

This review 22 proteins in the NOD like human repetoire. It was published in 2013...
The families are broken down into 9 general groups according to their domain composition in Figure 1 from that review.  Most of them are not named "NOD".


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How to build a trimeric protein structure from monomeric PDB file?
Problem: I have a PDB file, with a monomer, but I would like to show the entire structure - which is trimeric - but I don't understand how to merge/build or combine the monomeric units to its full structure in COOT, SWISS-PDBviewer or pymol?
Here is a link to the protein complex I am looking at
I would appreciate: Guidelines on how to do this (preferably in coot, pymol or Swiss-PDBviewer), or referral to a tutorial that actually goes through this would be great!
For reference: I found some descriptions on how to "build/merge" with Swiss PDB viewer here. And in threads from this discussion I found descriptions of how to do it with other molecular graphic tools as well (although I don't completely understand it)
What I have tried: In the tutorial for the SWISS-PDBviewer ( link ), I am able to follow some of the instructions, but I can't follow them for long:

I upload three of the same PDB file in SWISS PDBviwerer (they are layered on top of each other)
I can access/see the layers in the "layers info"
I am told to open the "text icon" to see the PDB text file, and look for "mtrix" rows - which should come right before the "atom" rows. As cited from the instructions:

" Scroll down the pdb file until you find MTRIX lines (they are just
  before the ATOM lines). You can see 9 lines MTRIX. They represent
  three transformation matrices, and allow you to build the
  non-crystallographic symmetries of the protein"

I cannot find the "mtrix" rows in the PDB-text file, and am very unsure of how to follow the next instructions (link) after this as well. I am not able to click anywhere in the text file, then I get the error: "sorry can't recognize any clickable information under this pointer..
This is what I see above the "atom" row:

I also found that the trimeric state can be downloaded as "biological assembly", however, I would still like to know how to do this on my own.

The PDB-file only contains the asymmetric unit, and no information on a potential biological relevant multimer. So you will need to get information about the state in solution experimentally.
That being said, one can often deduce from the size of the contact surface whether you have a potential quarternary structure. You can do this by hand, but the PISA-server is quite helpful there, and it will also output the multimer PDB-file:
http://www.ebi.ac.uk/pdbe/pisa/
If you just want to apply symmetry operators to your asymmetric unit in order to create symmetry mates, you can do so in
Pymol:
- click Action/generate/symmetry mates/within X Å
- from the command line:
        symexp prefix, selection, cutoff
        , e.g. symexp sym,1GVF,(1GVF),5
   see also http://pymolwiki.org/index.php/Symexp

Coot:
- if you just want to look at the symmetry mates, activate View/Cell&Symmetry with an appropriate radius and/or select "Symmetry by molecule"
- if you would like to actually create the symmetry mates, try Extensions/Modelling/New Molecule from Symmetry Op  - however you will have to specify the SymOp manually.

You will need to have the CRYST1-record in your PDB-file with the correct space group.

Remark 350 can be used to describe the biological unit.

There are no MTRIX cards for that molecule. This seems like the easiest path:
http://www.rcsb.org/pdb/explore.do?structureId=4G3Y
Download Files -> Biological Assembly 1
i.e.:
http://www.rcsb.org/pdb/files/4G3Y.pdb1.gz
And read that file into Coot (should you wish)

Thanks for the link, but as i commented on my own post - I do understand that I can get the biological assembly (whole structure). But what is an mtrix card? and why is it not possible to combine the monomers (due to lack of mtrix) ?  I am more interested in how I would do this on my own, regardless of that the whole PDB structure exists. Are you saying it is not possible with this file?


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Optimal pH of protein buffer? Basic principles to adjust buffers according method and analysis
Protein buffers such as PBST, which is used in western blotting, are normally adjusted to pH 7.4. When I try to find why, I find some information about optimal pKa for protein stability. Im not sure I really understand this, because it seems as through regardless of protein - most laboratories just use PBST with a pH of 7.4.
I am a bit curious about this, and have a few questions

Why is pH 7.4 set as the standard for western blotting?
For an optimal western blots, should the pH always be above the pI of the protein?(since 7.4 seems a bit high)
Should the pH of a buffer be at the pI of a protein for extractions before SDS-pAGE, and while washing NC-membranes after blotting?
How should one calculate the optimal pH, or evaluate/think about this when working with a protein?

That's the average pH of extracellular fluid and cytoplasm but it can vary. Compartments such as lysosome and mitochondrial matrix would have a different pH. Functional studies with native proteins should employ pH buffers with right pH. During western blots, proteins are denatured and so their isoelectric points/functional pH do not matter. The pH in SDS-PAGE is adjusted according to isoelectric point of glycine which helps in stacking of the proteins.

Thanks! So basically all you would care about is the pI of glycine, which is why pH 7.4 is the optimal pH for western blotting.

Well.. it matters for SDS-PAGE.. Not for the blotting step. A specific pH may have differential effect. I have not really thought about that. Good question. I'll look up.

Thanks again, this is interesting and I think its important to get the basic understanding of how things work. I will add this reflection as a point in my question above!

The correct pH depends on the properties of the proteins that you are trying to exploit. These are a good deal different between extracting proteins from tissue and performing Western blots.
Extracting proteins means keeping them soluble in aqueous solution. Working at the pI of the protein might be the worst choice as the protein then has no net charge, typically reducing its water solubility. An extreme case would be the highly basic histone proteins with very high pI values but best extracted at low pH.
After proteins have been run on a denaturing gel and transferred to a membrane for Western blotting, they are already denatured and bound strongly to the membrane through hydrophobic interactions little affected by pH except perhaps at extremes. For the blotting, you want to exploit the interaction of epitopes on the protein with the antibodies against them. During antibody production, the interactions between the epitopes and the antibody-specific receptors on the antibody-producing cells occur at normal extracellular body pH, 7.4. Using that pH for the blotting best recapitulates the charge state of both the epitopes and of the antibodies as they existed when cells producing the best antibodies were selected.


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metabolism in kangaroo rats
Many documents (e.g., this, this, and this) state kangaroo rats are special because they can use water produced by metabolism. Is the metabolism of kangaroo rats more efficient in producing water than that of other organisms?
Or the metabolism mechanism of kangaroo rats is the same as other organisms, but kangaroo rats can subsist with little water produced by metabolism because they conserve water from various mechanisms?

Various adaptations help desert animals survive in dry and hot environments. These adaptations are not specific to Kangeroo rats in particular.
From Wikipedia :

Metabolic water refers to water created inside a living organism through their metabolism, by oxidizing energy-containing substances in their food. Animal metabolism produces about 100 grams of water per 100 grams of fat, 42 grams of water per 100 g of protein and 60 grams of water per 100 g of carbohydrate.
Some organisms, especially xerocoles, animals living in the desert, rely exclusively on metabolic water. Migratory birds must rely exclusively on metabolic water production while making non-stop flights. Humans, by contrast, obtain only about 8-10% of their water needs through metabolic water production.
In mammals, the water produced from metabolism of protein roughly equals the amount needed to excrete the urea which is a byproduct of the metabolism of protein. Birds, however, excrete uric acid and can have a net gain of water from the metabolism of protein.

Also see Xerocoles - Water Conservation


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the effect of aquatic photoautotrophs on CO2 concentration in the air
The CO2 concentration in the air is more strongly influenced by the northern hemisphere than the southern hemisphere. A given explanation is that the northern hemisphere contains more terrestrial photoautotrophs. Does that mean that the effect of aquatic photoautotrophs on the CO2 concentration is much weaker than that of terrestrial photoautotrophs? If so, how is it so?

the obvious guess would be that it's because the terrestrial autotrophs affect the atmosphere directly while aquatic ones can only directly affect CO2 in the ocean; and mixing between the ocean and atmosphere is much slower than mixing within the atmosphere itself

@timeskull i guess guessing is the least usefull thing one can do on a science site.


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Coniferous trees in temperare rain forests
In temperate rainforest, the dominant plant form is often coniferous trees (source). However, coniferous trees are also the dominant plant form in a very different climate and form a different biome (boreal forest). Why are broad leaved evergreen trees not so adapted in temperate rain forests as in tropical rainforests? What is the advantage of needle-shaped leaves in the climate with temperate rainforest?

The Wikipedia article you link to notes that temperate rainforests may be either broadleaf or coniferous.

Yes, some parts are dominated by broadleaved evergreen trees, and some parts are dominated by coniferous trees.

The largest area of temperate rain forest in the world is on the west coast of North America, which has a summer dry season. In other words, at precisely what would be the best time for plants to grow (based on temperature), there's a shortage of water. (Summer vacation visitors to the rain forests on the Olympic Peninsula are often wondering "where's the rain?")
Conifers have small, waxy, and (generally, with a few exceptions) evergreen leaves. All the conifers in the rain forests of western North America are evergreen; that allows them to grow in the cooler months of the year, when there can occasionally be hard frosts (and when deciduous trees are dormant). The waxy, small leaves help them conserve water in the dry summers. A double advantage.
North of about central BC, there's no longer the summer dry season, but by that point the growing season is getting short enough that conifers have an advantage despite the perhumid climate (Prince Rupert, BC is further north than Edmonton, Alberta).
I'll add that this is not the only non-boreal climate where conifers are abundant: consider for example the piñon-juniper woodlands of the American Southwest or the Piney Woods of the Deep South.


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Can plants directly use sulfuric acid?
In the explanation of the sulfur cycle, it is often said that sulfur moves from the atmosphere to the ground by acid rain in the form of sulfuric acid. Can plants directly use sulfuric acid to assimilate sulfur?

Plants have sulfate transporters which they use to assimilate sulfur. Since sulfate is the conjugate base of sulfuric acid, this could be construed as a "yes" for your question. Sulfuric acid would be present in its conjugate base form at physiological pH values.
However, it would be unwise to water your plants with sulfuric acid, as many plants have an optimal pH range which will quickly cause death when sulfuric acid lowers the pH of the soil below that range. As a result, areas afflicted by acid rain may require treatment with alkaline limestone to resolve this issue.

Not just the pH. Sulphuric acid is also a strong dehydrant

I would presume that since the question is talking about acid rain, we don't mean concentrated sulfuric acid.

Yes.. Didn't notice that..


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Do plants have preference for the form of nitrogen as nutrient?
In the nitrogen cycle (ecology), it is usually described that plants can use nitrogen in the form of ammonium (NH4+) and nitrate (NO3-). Do plants prefer one form of nitrogen over the other?

Quoting verbatim from this site. The reference is not really a scientific article but you can check the references it cites. Some were not in English so I did not check. However these points are fairly logical

Nitrates are the preferred nitrogen source:

Non-volatile: unlike ammonium, nitrate is non-volatile, so there is    no need to incorporate it in the soil when applied by top- or side dressing, which makes it a convenient source for application.
Mobile in the soil - direct uptake by the plant, highest efficiency.
Nitrates synergistically promote the uptake of cations, such as K, Ca    and Mg, while ammonium competes for the uptake with these cations.
Nitrates can be readily absorbed by the plant and do not need to    undergo any further conversion, as is the case with urea and ammonium, before plant uptake.
No acidification of the soil if all the nitrogen is applied as    nitrate-nitrogen.
Nitrates limit the uptake of harmful elements, such as chloride, into    large quantities.
The conversion of nitrates to amino acids occurs in the leaf. This    process is fuelled by solar energy, which makes it an energy-efficient process. Ammonium has to be converted into organic N compounds in the roots. This process is fuelled by carbohydrates, which are at the expense of other plant life processes, such as plant
  growth and fruit fill.

Many plants can carry out nitrification but this is not universal. From this article:

Nitrification is sometimes considered so universal and rapid that
  applications of NH4-N are considered equivalent to
  NO3-N. This is not true in many forest, orchard, and
  grassland soils.

However, nitrate being more soluble is susceptible to leaching and wash off, care has to be taken when using nitrate based fertilizers. From the previously mentioned paper:

Unlike the positively charged ammonium ion, which is relatively
  stationary because of its adsorption to organic matter or clay
  particles, the negatively charged nitrate ion is freely mobile in the
  soil solution (166). Thus, leaching and denitrification primarily
  involve a loss of NO3-N (171). Inhibition or retardation of
  nitrification of applied NH4-N can reduce nitrogen losses,
  increase efficiency of applied N, and establish a predominantly
  ammoniacal form of nitrogen available for plant uptake (105, 171,222,
  232).

@quibble Ammonium can at high concentrations even be toxic to plant (roots). This is not uncommon in aquatic peat vegetation.

authors: أحمد المرادي


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Non-ribosomal peptide synthesis: why Glutathione cannot be produced by the ribosome?
Case: I am writing a summary for a class in protein structure and function, and was asked to describe some different ways that peptides are synthesized (that does not involve the ribosome). I understand that glutathione is a tri-peptide consisting of L-cystine with a "gamma" bond to L-glycine which is then bound to glutamic acid.
Problem: Why is it that the ribosome cannot produce this peptide? What is special about the peptide-gamma-bond?
My reasoning: The peptide is too short, meaning that the large ribosome complex cannot bind to mRNA of this length as it need many different binding spots in order for the large and small subunit to come together. Also, the "gamma" bond is very special, and the ribosome can only produce peptides with the "Standard" peptide bonds.

Is this correct, and is there something else I am missing?
Does the "gamma" bond relate to the fact the glutathione is not that easily degraded by peptidases in the cytosol?

It's definitely not the length. Although ribosomes can't make really really small peptides because they need something to hold onto and in any case proteins start with methionine(usually), there are workarounds. There's no reason why a tripeptide couldn't be coded for by a gene directly.
The 'traditional' method of producing very short peptides is producing a longer protein and cleaving off a chunk of it, which works great for signal peptides and a number of other systems. Very small peptides are more efficiently made by enzymes like this but in principle there's no reason to besides efficiency and complexity. (You need a special protease for each small peptide etc etc etc)
However, this gamma bond is a different beast entirely, and no ribosome could ever produce it, even in the middle of a longer protein. Amino acids 'snap' together in a very specific way. The amino group bonds to the carboxyl group of the previous amino acid, making a chain. The side groups of an amino acid aren't involved. Like Legos that snap together only one way and can be any color or have any designs on the side. The difference here is glutamate has a carboxyl group as part of its side chain. It's like a Lego with holes on two sides. The NRPS here connects the cysteine to the side chain of the glutamate instead of the 'bottom' where it would go if a ribosome-synthesized glutamate-cysteine bond.
This gamma bond also explains the increased longevity of the product. Proteases aren't designed for things that look like this. The gamma bond doesn't 'fit right' in the protease active sites and therefore activity is slower.

From I've read about glutathione, I think the answer to your question is :
"Because there is no glutathione gene ", and hence, no glutathione mRNA.
Concerning the gamma bond, this wikipedia article quotes :

This peptide coupling is unique in that it occurs between the amino
  moiety of the cysteine and the terminal carboxylic acid of the
  glutamate side chain (hence the name gamma-glutamyl cysteine)

citing this paper as a reference.
Also, it seems like the gamma bound is indeed the reason why is not degraded in the cytosol.
I don't know how you perceive wikipedia, but to me the english version is a good way to gather general informations about an unknown subject, before going more deeply in details with scientific litterature.

Yes, it makes sense that there is no mRNA and thus is has to be produced with other methods. But, is there a general reasons why the ribosome has problems with short peptides? It would be good if someone has a reference of why that is - or is it just as simple as I stated "ribosome is too large". Also, is the gamma-bond just a concertino between the "gamma" carbon and the amide group?.. what is the regular binding patters "beta" carbon to amide group?..

I am not sure that the ribosom could have a problem with short peptides, because the size of the mRNA that code for a peptide is not exactly 3*(number of amino acids of the peptide) : there is the ribosome binding site in 5' of AUG, that can be a part, or the whole, 5'-UTR. But it's an interessting question, and I wonder what's the shortest mRNA known.
The gamma bond is an unusual link between the two amino-acids. The classical bound is between the carboxyl group bound to the alpha carbon of the first amino acid and the amino group bound the the alpha carbon of the second amino acid.


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Protein purification: Linear elutions or stepwise elution, using imidazole or pH gradient?
I now work in a lab with a protein and a pre-made purification protocol, were they purify a His-tagged protein using linear elution which then gives a steady increase in the imidazole concentration. However, I am curious to as if you plainly have to test which elution scheme you want to use, or if there are some "rule-of thumb" on what is a more standard way to elute protein, and what in general is more common?
Also, say for instance (just as an example) that I use a protocol which in the end loses about 80% of the protein before it's pure, is one of the first things you could do is to change the elution schemes to increase the yield? Are there other very basic things one can do to optimize a purification protocol which has not been so thoroughly optimized?
So basically:

Is linear "usually" better/more common than stepwise?
Is imidazole gradient "usually" better/more common than pH gradient?

Linear is better typically. The flow rate combined with fraction size and length of time gives you better resolution for which proteins are coming off the column at what point.
Once you've narrowed down the imidazole concentration at which your protein comes off the column, you can in future just stick to concentrations around that area, though it's still advisable to use gradients either side of that concentration as your preps are never likely to be completely consistent.

How do you know you're losing 80% of your protein before achieving purity? If your protein isn't separating from other contaminants during IMAC, you can try switching to an IMAC optimised strain (I use NEB BL21(DE3) NiCo21's).
Usually you'll have to do some downstream purification in any event. Gel filtration is common. You could also consider a different column chemistry such as anion exchange.
EDIT
Typically I wouldn't expect that you would need to mess with pH very much when performing IMAC. I certainly have never had to. You are likely to need physiological pH to ensure native folding of your protein.
You can however use other additives if your protein is recalcitrant. For example, I often add 1mM DTT and 2M urea to my samples and then heat them slightly as my protein binds things easily and is extremely stable. GE Provide a whole booklet of supported additives for their columns, you may have the same thing for yours too.

thanks for the input, the optimization is just because I'm curios in general what steps could easily be altered a bit and most likely give you metter protein yield. I just stated 80% as an example, but that might be a bit extreme. Although I am working on a protocol that i know they really just went with without really trying to optimize it.

You can't say categorically that linear is better. There are cases where increasing the imidazole concentration step-wise results in cleaner, more concentrated fractions, and other cases where steadily increasing its concentration via a gradient over a period of time works better. It all depends on the protein and the starting material.

For the purposes of calibration and optimisation linear is typically better so I stand by my point. Stepwise doesn't give you the same resolution. Once you've established your ballpark elution concentration then sure.

This does answer what I'm wondering about (thanks), however what about pH vs. imidazole concentration?

Edited my answer


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How genetically similar are worker ants from the same colony?
I've been reading https://en.wikipedia.org/wiki/Ant and it says

If the egg is fertilised, the progeny will be female diploid; if not, it will be male haploid.

Since the males have only one set of chromosomes to pass on to the queen, all of their direct offspring (which can only be female) will contain all of their DNA. How similar is the DNA that the queen provides? Is there a high likelihood that there will be genetically identical individuals within a single colony, even if they were hatched at different times?

Relatedness of ants within a colony vary from species to species (as different species may use different mating systems) and from colony to colony. I will consider a basic (simplified) model of a honeybee colony and describe it a little bit to try to address your question.
Simplified Model of an ant colony
There is quite a lot of diversity in mating systems among ant lineages. See for example the amazing case described in Fournier et al. 2005 (which is quickly summarized at the end of this answer). I will assume a general and simplified model below.
In general, a queen can have several mates. The queen is storing the sperm of these males in her spermatheca. As you noted, the queen is diploid while the males are haploids. The queen will use the stored sperm for all of her life. Each egg that is fertilized will give rise to a worker. Although, a worker does not reproduce (in our simplified model), a worker is still considered a female for morphological reasons. At some point in the life of the colony, some larvea that could have become workers are fed with royal jelly and they will then develop into queen. These queens will fly away to mate with multiple males and make up a new colony. The queen also produce males. The males are haploids. The queen only uses her own gametes to make up a male.
Relatedness
In our simplified colony, a male has no father and has the same mother than any other male and any other worker. Two workers may or may not have the same father. Let's imagine to simplify the story that the queen mated with a single male so that all the workers have the same parents (they are sisters).

queen-worker: 1/2
worker-worker: 1/2

This relatedness decreases with the number of father. At the extreme when there are an infinite number of fathers, the relatedness between two workers drops down to 1/4.

queen-male: 1/2
male-male: 1
male-worker: 1/4

The calculation of relatedness is a little bit problematic when comparing individuals that differ in ploidy (queen - male comparison for example).
Consequences of these relatedness
The fact that the workers are more closely related to their sisters than to their brothers have been suggested to cause a queen-worker conflict for the sex-ratio. Indeed if workers are more closely related to their sisters than to their brothers we might think that they would tend to bias the sex-ratio of the colony toward more sisters to a degree that would not be optimal for the queen. The degree of relatedness between workers depends on the number of fathers. There more fathers there are, the lower is the relatedness among workers and the lower is the incentive to bias the sex-ratio. As a consequence, while the queen would wish a sex-ratio of 0.5, the workers will deviate this sex-ratio toward more workers with a strength that is decreasing with the number of father.
Personally, I have some trouble with these predictions (that I won't express here) but empirical evidences (Chapuisat et al. 1997; Passera et al. 2001) support that the sex-ratio differ depending on the number of fathers (and therefore on the worker - worker relatedness).

"At some point in the life of the colony, some larvea that could have become workers are fed with royal jelly and they will then develop into queen." Are you confusing this with bees, or do some or all ants use a specific foodstuff to make queens? All the sources I've found refer to differences in nutrition but make it sound like it can just be a matter of how much food the larvae get, not what kind.

Also, with one father shouldn't worker-worker relatedness be 3/4, because the males are haploid so workers share 100% of the genes they get from their father instead of 50%? And similarly male-male should be 1/2 because their mother is diploid; they all have half of her genetic material but don't all have the same half.


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How exactly are nucleoli made of NORs?
I read that nucleoli are made of DNA, RNA, and nucleolus organizer regions. I don't quite understand how that happens with NORs. Isn't there an envelope delimiting the nucleolus from the rest of the nucleus content? Do NORs from different chromosomes come together? I mean, they are not detaching from the rest of the chromosome and aggregating freely...

No there is no membrane that separates the nucleolus from the rest of the nucleus. The nucleolus is an aggregate of all kinds of molecules involved with ribosome assembly like: precursor and mature rRNA, Small nucleolar RNAs, rRNA-processing enzymes, ribosomal proteins and partly assembled ribosomes (but no fully functional ribosomes)
Aside from all these protein and RNA there are indeed regions of the chromosome called Nucleolus organizer regions (NORs) present in the nucleolus. These NORs are located near the tips of the short p region of chromosome 13, 14, 15, 21, and 22. During interphase these regions decondensate due to proteins like nucleolin and are thus open for transcription. Many of the protein I mentioned are needed to form or present in the aggregation that is the nucleolus.


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How is a thickening of grey matter possible?
There are plenty of studies that document grey matter thickening in certain brain areas as a result of meditation or exercise. However, it's often said that the extent of neurogenesis outside of the hippocampus is negligible. So can certain activities promote significant neurogenesis in the adult brain or can grey matter thickening be explained through other mechanisms (e.g. cell migration)?
An excerpt from Wikipedia article on grey matter:

Grey matter (or gray matter) is a major component of the central nervous system, consisting of neuronal cell bodies, neuropil (dendrites and unmyelinated axons), glial cells (astrocytes and oligodendrocytes), synapses, and capillaries. Grey matter is distinguished from white matter in that it contains numerous cell bodies and relatively few myelinated axons, while white matter contains relatively few cell bodies and is composed chiefly of long-range myelinated axons.

Sources:
Meditation-related increase in grey matter:

https://pubmed.ncbi.nlm.nih.gov/27983555/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004979/

Grey matter increase in response to exercise:

https://academic.oup.com/biomedgerontology/article/61/11/1166/630432

Except in three specific areas (olfactory bulb, dentate gyrus, SVZ) where neurogenesis continues to occur in adult organisms, it is virtually absent from everywhere else, including the cortex. However, there have been many reports that the grey matter of the cortex, i.e. the zone where cell bodies and their processes reside, can enlarge. Cortical expansion has been linked with changes in dendritic branching, neuronal soma size, synapse size, the number of dendritic spines, and the number of glial cells.
References
- Diamond MC, Krech D, Rosenzweig MR. The effects of an enriched environment on the histology of the rat cerebral cortex. J Comp Neurol. 1964;123(1):111 119.
- Diamond MC, Law F, Rhodes H, et al. Increases in cortical depth and glia numbers in rats subjected to enriched environment. J Comp Neurol. 1966;128(1):117 126.
- Diamond MC, Lindner B, Raymond A. Extensive cortical depth measurements and neuron size increases in the cortex of environmentally enriched rats. J Comp Neurol. 1967;131(3):357 364.
- Holloway RL. Dendritic branching: some preliminary results of training and complexity in rat visual cortex.
Brain Res. 1966;2(4):393 396.
- Volkmar FR, Greenough WT. Rearing complexity affects branching of dendrites in the visual cortex of the rat.
Science. 1972;176(4042):1445 1447.
- Greenough WT, Volkmar FR. Pattern of dendritic branching in occipital cortex of rats reared in complex environments. Exp Neurol. 1973;40(2):491 504.
- Uylings HB, Kuypers K, Diamond MC, Veltman WA. Effects of differential environments on plasticity of dendrites of cortical pyramidal neurons in adult rats. Exp Neurol. 1978;62(3):658 677.
- Mollgaard K, Diamond MC, Bennett EL, Rosenzweig MR, Lindner B. Quantitative synaptic changes with differential experience in rat brain. Int J Neurosci. 1971;2(3):113 127.
- West RW, Greenough WT. Effect of environmental complexity on cortical synapses of rats: preliminary results. Behav Biol. 1972;7(2):279 284.
- Altman J, Das GD. Autoradiographic examination of the effects of enriched environment on the rate of glial multiplication in the adult rat brain. Nature. 1964;204(4964):1161 1163.

So, do you think that neuronal migration from the SVZ is unlikely?

I think you could adapt this answer slightly to make it more directly answer the OP's question about gray matter volume. That is, 1) cortical gray matter is not only cell bodies, a Ramon y Cajal drawing would be a good starting point, and  2) that no migration or new cell birth is necessary for gray matter to thicken.


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What is a Mitochondrial Eve and Y-chromosomal Adam
I've read this question:
What kind of event would cause the current Mitochondrial Eve to be replaced by a new one?
And the values in Wikipedia about Mitochondrial Eve and Y-chromosomal Adam and I am not sure I understand the concept behind them.
When talking about a maternal unbroken linage and a paternal unbroken linage, is the meaning that Mitochondrial Eve had a linage of only women reaching every person today, and the same with Y-chromosomal Adam and men? So that other humans that lived in their age, didn't have an unbroken line of linage consisting of only same sex descendants?
How is the specific "identity" or time period of those persons is known, assuming that researchers didn't check the Mitochondrial DNA or Y-chromosome of every single living human being today, how can they know for sure that there aren't some tribes in the Amazons, which have a direct female linage to Mitochondrial Eve's sister?

I'd note that if they have a direct female lineage to Mitochondrial Eve's sister then that would make their mother the true Mitochondrial Eve. Whilst the estimate may be inexact, there must be a mitochondrial eve at some point in our ancestry.

When talking about a maternal unbroken linage and a paternal unbroken linage, is the meaning that Mitochondrial Eve had a linage of only women reaching every person today, and the same with Y-chromosomal Adam and men?

Kind of, yes. The concept behind Mitochondrial Eve and Y-Chromosomal Adam has to due with cell replication and basic genetics.
The Mitochondria ("Power Generators" of the cell) are directly inherited from mother to daughter cell. That is, new cells do not start with 0 and are forced to make them de novo. Some Mitochondria are replicated before division and some are 'given' to the daughter cell to start with.
Because of the unique way that Mitochondria are inherited, when it comes to creating new humans it means that only the Mother's Mitochondria are given to any children she gives birth to regardless of the sex of the child. So I, being male, have my Mother's Mitochondria - which the same as my Grandmother's - and the same as my Great-Grandmother's - etc. etc. etc. until you can trace that line back to "Mitochondrial Evel" whose Mitochondria are the origin for all humans on the planet and are inherited Maternally.
In that sense it is an unbroken lineage of genetic information as inherited from mothers, though not exclusive to women.
"Y-Chromosomal Adam" is a similar concept - Women do not have a "Y"-Chromosome, so every Y-Chromosome men have today had to originate from somewhere. It's trickier to do than tracing Mitochondrial DNA because while Mitochondria are inherited exclusively from mother to child, there could have been multiple Fathers to Mitochondrial Eve's children and other similar complications that muck things up.

How is the specific "identity" or time period of those persons is known, assuming that researchers didn't check the Mitochondrial DNA or Y-chromosome of every single living human being today?

For "Y-Chromosome Adam" it's still more or less in the data-gathering phase as far as I was last aware. It's not as concrete as "Mitochondrial Eve", which has a very solid body of work supporting her.
The "identity" is known because the more in common a person's genes have with the genes of another, the more closely they are related. The researchers took a lot of genes from very divergent populations, and compared them. The researchers were then able to tell which portions were common among all of the Mitochondrial DNA, which had changed the most, and which had changed the least from each other. Using that data, you can construct a rough image of what the originator (or LCA - Last Common Ancestor) had for their own genetic makeup.
You can construe a time period because portions of your DNA (either Mitochondrial or Nuclear) acquire/tolerate mutations at an expected rate - say 1 mutation every 1.5 Million Years. So as long as you have a rough idea of what your LCA's genes looked like (see above), then a modern day sample with 5 mutations is 7.5 M.Y. away from the LCA.

how can they know for sure that there aren't some tribes in the Amazons, which have a direct female linage to Mitochondrial Eve's sister?

They didn't when they started testing. That's part of the fun of the project.
The "Out of Africa Hypothesis" rose in prominence partially due to the findings of the research. It basically posits that the ancestors of humans evolved once in Africa, and then spread from Africa to the rest of the world. Because the Mitochondrial Eve research concludes that "Eve" was around before we spread throughout the rest of the world, it implies that every ancestor already had Eve's legacy when they started migrating into Europe, Asia, the Philippines, etc. Thus every human on Earth, no matter where they are today, shares traits with Mitochondrial Eve.
For the Amazonian tribes, they would have inherited it from their ancestors in North America, which were ancestors of tribes in Asia who crossed an ice bridge into North America, and the tribes in Asia came out of Africa.

Just to note that you don't always get the mitochondria from the mother, sometimes you get some from the father too (but this is very rare.) This doesn't really change anything other than the "unbroken line of mothers" aspect.


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What happens to the holes in the skull where teeth were developing?
In Skeptics.SE, a question regarding the skulls of children arose. Depicting a scary skull where the permenent teeth are "hidden" inside the jaws and the milk teeth are in the their place.
After all milk teeth fall out, and the permanent teeth "rise", do the holes left by them filled up, or do we go around with holes in our jaws?
The question on Skeptics
The picture:

Permanent teeth have much larger and stronger cemented roots.

Jaw development is very prominent during the growth of a child. There are no holes that remain in the jaw after the emergence of all the permanent teeth. Permanent teeth are not fully formed and hidden. They develop while milk teeth, meanwhile do the temporary job.

When the tooth falls out you can see a little adult teeth behind it after a couple of weeks the adult teeth will grow and move to the front and the adult teeth will not fall out so look after your teeth for your life

Bone growth continues in the human body for quite awhile after permanent teeth come in. Generally, the complete closure of all growth plates doesn't occur until the mid 20s.
As the top and bottom primary teeth come in, the empty space left behind is gradually filled by growth of the maxilla and mandible, respectively. During the time period when teeth are actively coming in, teeth can displace into the empty space left by other permanent teeth that are no longer there, resulting in crooked teeth.

This is a skull of a child of around 5 plus years; based on the eruption status and is an example of  classic development and eruption pattern of of the teeth at that age. everyone goes through it. It probably looks scary to persons unfamiliar with normal anatomy and because the outer cortical plate has been removed to show the developing tooth germs. This is out of a anatomy museum meant for medical or dental students.
At no point of time during the eruption is a cavity left behind. As the tooth erupts the base of the crypt (cavity) gets filled up.


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Does your iris color have an effect on your vision?
I've always wondered if having different iris colors, (eye colors) may have any advantages or disadvantages on ones vision. Specifically regarding the effects of light.
Personally, I have troubles being out in the bright sun without sunglasses. My girlfriend on the other hand does not share this issue. Coincedentally my eyes are a light blue and hers are brown. After realizing this, I began to notice a trend when it comes to blue eyed people having this same issue.
So, on a bright day, does a person with blue eyes have a higher sensitivity to the light than their darker counterparts?  Thank you.

I don't have time to do proper research and give a nice answer, but here is an answer from an unverified source. By unverified I mean I didn't check the credentials. It seems like a pretty good answer though.

@SolarLunix "when melanin develops, it creates a protective filter that reflects the light back out of the eye"??? REFLECTS?

@Ilan it's the same principle that makes the sky look blue from what I understand.

Firstly, note that "eye color" is actually iris color.
The person with a lighter iris will have more straylight compared to person with brown iris:

The graph represents Intraocular straylight of the age-matched groups. Participants with light-blue-colored iris showed significantly higher values for intraocular straylight than those of the other groups.

Persons with light-blue-colored eyes have significant higher IOSL
  (intraocular straylight)
  values than persons with darker-colored irises (blue-grey,
  green-hazel, and brown). Light-blue-colored eyes had 0.07 to 0.08 log
  units higher IOSL values, which is an increase by a factor of 1.2. In
  regard to CS (contrast sensitivity), subjects with light-blue iris color showed also lower CS
  values than subjects with other iris color.

Edit: The study concluded that in people with blue irises, IOSL was significantly higher. Although IOSL did not affect best-corrected visual acuity (e.g. visual function based on a standard letter chart test at the optometrist), it did affect contrast acuity, meaning that folks with blue eyes had more difficulty assessing contrast differences (e.g., telling apart two grays with a slightly different brightness).
Christian Nischler & al. Iris color and visual functions. Graefes Arch Clin Exp Ophthalmol (2013) 251:195–202.

Thanks for the answer!  Seems like a fair study aswell. All european participants but other than that I would say pretty unbiased. Also, appreciate the iris tip aswell, not always on my "A" game when it comes to adding proper jargon.

Too bad though... kinda wish the study would have come to a more neutral conclusion. Guess light blue eyes aren't so great after all...

I added the functional consequence of straylight. +1


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Clownfishes and Sea anemones
Relation between clownfishes and sea anemones is a classic example of mutualism. I wanted to list the species of sea anemones that are involved in this mutualism but I got lost.. Could you help me with that?
How many species of sea anemones which host clownfishes are there? Could you list them?

I only found this two references, but these are only secondary sources at the moment.
Look here "Clown Fish Anemone" and here "Choosing Clownfish and Anemones for Your Aquarium". It seems that there are only around two handful of anemones capable of supporting clownfish.
Here are some primary sources which confirm the 10 anemone species: "The anemonefish symbiosis: What is known and what is not." and "Field guide to anemonefishes and their host sea anemones". The last two links point to PDFs which contain a lot more references.


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Identify insect found in cupboard
Opening the cupboard I am shocked to find it full of these insects inside. Haven't found them anywhere else. At first, I thought it was ticks, but not so sure. Plan on cleaning out the cupboard and using Bifen I/T to hopefully kill them.
I live in the Caribbean and would like to identify and find out how to get rid of them.

You should add tag species-identification. It can help other people to help you.

Looks like some sort of weevil to me.

@GerardoFurtado I agree. Is there any reason you're posting that as a comment rather than an answer?

I wouldn't have been offended if I had commented "weevil" and you had made your more detailed response an answer. I see a big difference between a quick first impression and a reference to a specific species. :)