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Is the start codon regarded as part of the UTR (untranslated region)?
The Wikipedia entry for Gene contains the statement:

The transcribed pre-mRNA contains untranslated regions at both ends which contain a ribosome binding site, terminator and start and stop codons.

But the page on the Start codon says:

The start codon is often preceded by a 5' untranslated region (5' UTR)

So is the start codon a part of the UTR?

Because the start codon is translated into methionine, it clearly can not be part of the 5'-untranslated region, as @Johnny writes in his answer.
The more contentious question would be for the stop codons and the 3'-untranslated region. Then it really is a question of semantics. One might argue that as no amino acid is inserted in response to these codons, they are not translated. However if one considers the meaning of the word ‘translate’ and its application to the genetic code, a stop codon clearly is translated — it is read and translated into information which initiates the release of the nascent peptide from the ribosome.
And so in the Wikipedia entry on Untranslated Regions it (together with the start codon) is shown in the coding sequence, and not in the untranslated region. The annotations used by GenBank also include start and stop codons in the coding sequence (CDS in their annotations) — see, for example the annotation for this insulin precursor sequence.

The start codon both in prokaryotes and eukaryotes isn't a part of the 5'UTRs, it is present downstream the UTRs.
In prokaryotes the Ribosome binds to the Shine-Dalgarno sequence (AGGAGGU) of 5'UTR. This sequence is found 3-10 base pairs upstream from the initiation codon.
In eukaryotes the  initiator codon is usually the first 5'AUG3' present on kozak consensus sequence (GCCGCCRCCAUGG, where R is adenine or guanine). The ribosome does not bind to this sequence directly but browsing for it from the 5' end it starts synthesis once it reaches the consensus sequence.
This kozak sequence ranges from the terminal portion of 5'UTR to the first few (actually four) nucleotides of translating region.
Sources:

Principles of genetics by Snustard and Simmons
Berg's Biochemistry

That translation starts from the terminal part of the untranslated region seems unsemantic.

I've updated the answer.

This statement is incorrect.

The transcribed pre-mRNA contains untranslated regions at both ends which contain a ribosome binding site, terminator and start and stop codons.

The start codon always encodes for methionine (eukaryotes) or N-Formylmethionine (prokaryotes), thus, seeing that the start codon encodes an amino acid, it would be considered part of the translating region.


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What are housekeeping and constitutive genes?
I have come across two set of definitions which are not contradictory but different.
From wikipedia:

A constitutive gene is a gene that is transcribed continually as opposed to a facultative gene, which is only transcribed when needed.
A housekeeping gene is typically a constitutive gene that is transcribed at a relatively constant level. The housekeeping gene's products are typically needed for maintenance of the cell. It is generally assumed that their expression is unaffected by experimental conditions. Examples include actin, GAPDH and ubiquitin.

My question from these definitions: What does 'transcribed at a relatively constant level' mean? Does it mean that a constant level of gene product is maintained in a cell? I can't understand there meanings atal.
Again,according to Oxford dictionaries

Constitutive Genes are genes that are expressed following interaction between a promoter and RNA polymerase without additional regulation.
  (Oxford Dictionary of Biochemistry and Molecular Biology)
Housekeeping genes - Constitutive loci that are theoretically expressed in all cells in order to provide the maintenance activities required by all cells: e.g., genes coding for enzymes of glycolysis and the  and the citric acid cycle.(Dictionary of Genetics)

These definitions do not tell whether they are continually transcribed or the synthesised products are present in constant amount.
Which one best define them?

I don't really understand your question. What part of the quoted definitions confuses you?

I think you missing gene expression logic here. There are promoters that require transcription factors to start producing gene. In other words, housekeeping genes only require their DNA + RNApol to produce mRNA. Non-housekeeping genes require their DNA + RNApol + SomeOtherFactors (proteins)

@canadianer I've edited the content.

@BryanKrause You should post that as an answer. I would only add that transcription initiation is not the only level of gene regulation. Constitutive transcription need not imply that that protein levels will continually rise since that is also influenced by the rate translation and protein/mRNA degradation.

@canadianer Thanks, I'll include that important point in a brief answer and remove my earlier comment.

I think the best answer is both: they are continually transcribed at a rate that maintains the synthesized products at a (roughly) constant level. These terms are really just descriptive terms, there is no true biological dichotomy, it's just that some genes are expressed pretty much all the time and others are only produced when needed, for example genes for proteins needed at a particular stage of the cell cycle.
As @canadianer mentions in a comment, there are also other forms of post-transcriptional regulation, such that constitutive transcription doesn't necessarily mean constant production of protein at an equal rate.
Wikipedia has quite a list of different "housekeeping genes" and you will see the list is quite extensive. It certainly isn't true that all of these genes are expressed at exactly the same levels all the time, it is simply that their expression is consistent enough to be used as an approximate standard when comparing expression levels.
If I could produce a definition that reflects reality better than the ones you found, I would amend the Oxford definition to something like:

Constitutive Genes are genes that are expressed following interaction between a promoter and RNA polymerase at a level that doesn't seem to vary much across cells of the same type, doesn't require a very special transcription factor, and so far biologists haven't found an experimental condition that greatly impacts the expression level.

The questioner asks “What does ‘transcribed at a relatively constant level’ mean?” The answer is absolutely nothing!
A gene can be transcribed at a constant rate, or maintained at a constant level (in so far as ‘level’ — a word that should be avoided — is taken to mean ‘amount’). Perhaps it means ‘transcribed so as to maintain a relatively constant cellular concentration of the product’. It is unclear.
I’m afraid that it is a waste of time trying to find an authority for definitive meanings for terms that were coined in a period of incomplete scientific knowledge and have changed their meaning or importance as science has progressed and time has passed. Wikipedia is written by anyone who cares to contribute and its authority tends to vary with the amount of interest experts in the field have. For computing science you are on a winner, for molecular biology you may not be.
As far as the term housekeeping gene goes, a Google ngram shows that it appeared about 1980, at a time when little was known about the regulation of the expression of eukaryotic genes. The term expressed the simplistic idea of genes that were expressed continually (as in the examples quoted) as opposed to those induced by particular stimuli like sexual differentiation or perhaps change in diet. In fact little was known about inducable genes at the time, and the concept was very much based on an analogy with bacterial systems, which are different in many ways. It is still useful in a general sense, but no more.
PS
I've edited the Wikipedia entry. We'll see if anyone cares. (I can edit it, but anyone else can switch it back to the original. In that case it is best discussed.)

+1 for pointing out a key point that I glossed over in my answer: these terms are somewhat outdated, even if they are still in use. They really don't have a lot of useful relevance to our current understanding of biology. Sadly textbooks and curriculum are a bit behind the times, in part because its so hard to keep up with the pace of scientific discovery.

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How do S and L cone cells sense colors like deep blue and red beyond their peak?
So I found this diagram of retinal cone cells:

It looks like the S, M, and L cones peak at blue, chartreuse and orange, respectively. If so, how do we see colors past 575 nm and before 445 nm? If the cones really respond to purple, green, and red, (as I previously thought) why do they peak at colors closer to green, as shown in the image?

The answer is actually present in your chart: color perception depends on the ratios of activations of different photoreceptors. For example, as you go "more red" from 575, the responses of the Green photoreceptors are falling off more quickly than the Red ones. The same is true for any colors in between, and on the other end, where 400nm light would activate only the blue receptors, whereas at 445nm there would be some mix of activation of the green.
From the context of Fisher information it is actually interesting that photoreceptors don't actually provide much color discriminability at their peaks.
For example, around 575 nm, the "red" photoreceptors actually don't provide very good color discrimination: the response to 565 or 585 is going to be almost identical, for example. The way you can perceive a difference, though, is that the response from the green photoreceptors will be very different at those two wavelengths (just consult your chart!). In vision, as in all the other senses, the information is really held in the slopes!

The cones responsive to long wave lengths (L cones) are simplistically called 'red cones', those sensitive to intermediate wave lengths (M-cones) are often called 'green cones', and those sensitive to short wavelengths (S cones) are often referred to as 'blue cones'. Red, green and blue cones are hence terms reflecting simply their peak absorbance.  However, as your plot shows, there is a great amount of overlap in the absorption spectra of the red, green and blue pigments in the cones in the retina.
To your question: How can we perceive see light with wavelengths larger than 575 nm, and shorter than 445 nm
This is because the cones are sensitive to a whole range of wavelengths outside of their characteristic peak absorbance in the visual spectrum. However, the sensitivity does drop beyond the peak, so red light with wavelengths >445 nm will be perceived less and less clearly, up until the point it becomes undetectable (infrared). Likewise, shorter wavelengths than 445 will loose intensity and eventually become invisible (ultraviolet).
The green and red opsins are basically the same proteins with only a slightly shifted absorption spectrum - indeed, these opsins split late in evolution due to a tandem repeat and small point mutations.
Color vision is nonetheless very specific and millions of colors can be discerned by someone with normal trichromatic vision.
This is accomplished by color opponency:
The opponent color system has 2 channels, namely a red versus green and a blue versus yellow system. The input are the photoreceptors in the retina: red, green and blue cones. A third achromatic channel is used to code visual brightness (Fig.1.). The neurophysiological machinery is located in the retina and higher visual structures such as the lateral geniculate nucleus.

Fig. 1. Color opponency
This model is referred to as Hering's opponent color theory (Gouras, 2012). It states that the blue channel suppresses yellow (and vice versa) and red suppresses green (and vice versa). The advantage of this system sharpens color contrasts between opponent colors (Hurvich and Jameson, 1957). In other words, the broad flanks of the absorption spectra of the opsins are sharpened at their edges by opponent colors. This mechanism causes the fact that we cannot see yellowish blues or reddish greens etc. Instead we can only see mixed colors between channels, e.g., yellowish greens or reddish blues (purples).
References
- Gouras, Color Vision. In: Kolb et al., Webvision. The Organization of the retina and visual system, Utah University
- Hurvich & Jameson, Psychol Rev (1957); 64(6): 384-404

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What is the biochemistry of love?
How is love induced between humans? Say, between mother and child, couples, etc.
Does the phenomenon of love exist in other mammals, too?

"Love" is a subjective phenomenon that can't really be applied to non-human animals because we can't ask them about their subjective experiences. However there is some clear evidence, especially in more social mammals, of caring behavior and social bonds for other conspecifics.
As far as biological basis, I suppose you could consider it biochemistry, the peptide hormone oxytocin is correlated with formation of social bonds between animals of many species (although Wikipedia isn't the greatest source, you will find this particular page is saturated with links to scientific literature). I would caution against the popular press treatment of oxytocin as "the love hormone" and caution against simplifying a complex set of behaviors to the action of one peptide, but certainly the evolutionary conservation and broad applicability suggest that this is indeed an important hormone in social relationships.

Till now, I only knew oxytocin as a birth hormone and milk let down hormone.Never heard about this love hormone concept.

@San If you search for something like "oxytocin love hormone" you will get a broad mix of crazy hyped pseudoscience as well as some fairly nice popular science press articles that are much more nuanced. There is good evidence that oxytocin can (moderately) change human behavior in certain situations, but it definitely isn't nearly as simple as put two people together, add oxytocin, stir 5 minutes, love! More like, "there is a modest statistically significant difference in trusting behavior versus controls."

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Trouble amplifying microsatellites using a 3 primer protocol, positives in negative controls
I'm trying to collect microsatellite data using primers developed on a related species but instead of having primers with fluorescent dye already on them, I'm trying to attach an M13-dye to the forward primer which also has an M13 tag on its 5' end. I am having some difficulties though because my negative control bands look identical to the positive bands, regardless of annealing temperature and MgCl2 concentration, and the bands seem too large for it to be primer-dimers, it seems like genomic DNA.. it's about 100-150bp.. so I'm not sure what is going on.
Before somebody suggests that it is contamination - I started over at a whole different lab bench, different pipettes, pipette tips, reagents, ordered new primers, thermocycler, everything, but the problem did not go away. Since I'm still optimizing the microsatellite primers I also ran a test using some invertebrate COI which I have positive results from in the past, and included a little bit of each reagent into each reaction instead of DNA, and I got a very strong band at the M13-dye. This was brand new, reordered after the last batch had this problem, suspended with TE and diluted with nuclease-free water. I am wondering if it has to do with the gel sybr-safe filter? Or the UV illumination for visualizing the gel? I am grasping at straws, please help or let me know if you have the same problem. The dye is just M13 labeled 6FAM: 5'-/56-FAM/TGTAAAACGACGGCCAGT-3' from IDT

I have no experience with this, but what is your negative control?


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Complementation cloning: what, why and how?
I get that you're cloning a whole cDNA library, but why does E. coli need a complementary gene to allow the gene expression?
Why is that complementary gene considered to be a mutant?
AND how does one detect the gene of interest after cloning?
What is this kind of cloning used for?

Your question is unclear, which is why there are four votes to close it. I have constructed cloned cDNA libraries and I have no idea what your question means. Please clarify it if you want an answer.

I thought your question was clear enough, but it may be closed as too broad since there are multiple questions on what is a rather large subject. Given that you apparently now understand the basics, perhaps you could    narrow your question to the specifics of what is still confusing you. Or start a new question.

PS You're not "too undergrad" (ha!) for the site. Most questions asked here are at an undergrad or popular science level.

@canadianer great that makes me feel much better because I really love this site! I will take you up on the advice to narrow the questions, thanks!

I figured it out. You're complementation cloning when you know the function of a mutant sequence but not it's sequence. For example, your organism (human) gets skin cancer from too much UV light exposure.
With complementation, two mutants can restore the wild type phenotype (well functioning UV repair).
We know E. coli has a well studied UV repair gene so you transform the cDNA library from your human into an E. coli which we know has the mutation, then grow them all under intense UV light. The  E. coli with the human mutant allele (the right cDNA fragment) will survive, so you can amplify that colony, sequence it, and then use it as a diagnostic tool in humans.
I'm wondering why that was vague. Is "complementation cloning" not a well used name for that technique? Was the question too broad or elementary? It's the first time I've used Stack and it seems I may be a little too undergrad for this crowd.

If my answer clarifies, please feel free to fill in gaps I left out because I'm still trying to understand some of the reasons this technique works and why we'd use it.


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How superficial an artery has to be for pulse to be measured manually?
Why arteries  pulse? How superficial an artery has to be for pulse to be measured manually?

They pulse because the blood flow follows the heart beat. I do not think there is a specific depth that they need to be to be measured, the ones from the wrist and neck are usually used.

The larger the artery, the deeper it can be and still be palpated, e.g. the descending aorta is palpable in the abdomen of the average person.


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How long do tiny spiders live?
I'm pretty sure there's a spider in my ear. I feel it move and hear the scratching (i blame my cat for playing with bugs in the bed). I've gone to the doctor, but all they do is flush my ear with water and it never works. I've decide to just wait for the damned thing to die.
How long will it live in my ear without coming out? How quickly will it die if i flush my ears with peroxide once a day?
any other advice for how to get the stupid thing out?

Unfortunately this is for all it's worth a personal medical question, which is not on scope for this site. Please don't do anything yourself without asking a doctor. If the last one did not help you, try to go to a specialist. Still, be open for the suggestion that it might be there is nothing alive in your ear.

Maybe lure it out of hiding with a fly? Scare it away with a big bird? Smoke it out? Play nasty music?

It's not a spider. It might be a paresthesia (more specifically, formication) that you're experiencing, though. Spiders don't survive flushing, or peroxide. I often used to see kids with insects in their ears in the ED. Never did any of them remain after flushing. Interestingly, my son once got a spider in his ear. I did get it out with flushing. There's another possibility: a bit of fluid in the middle ear.

I was asking how long it would take to die. The doc i did see DID say there was something moving in my ear. There are no other doctors who will take my insurance in my area, so he's the only one i can see. When nothing came out after the water attempts (and 5 hours of it mind you) he just said 'oh well, go home' essentially. Hence why i'm asking //how long it would take for a spider to die stuck in an ear./// I know the ear is self-cleaning and the wax will just push it out eventually. I need to know how long it'll take.

@anongoodnurse wow.... I removed that comment I really thought this was impossible...

If there's something stuck in your ear after five hours of flushing, you need to see a better doctor. Hardened ear wax is dark and can be hard to remove, and can mess with your hearing.

Did it die yet?


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Is Richard Dawkins's interpretation of the theory of evolution circularly?
I think we are all familiar with the basics of Dawkins's theory of evolution. In a nutshell: All creatures are nothing but vehicles of genes with the sole purpose of passing through these genes, and in the case of human beings besides genes also memes are involved.
Isn't this interpretation of evolution circularly:
"Why do all organisms exist? Because the purpose of organisms is to pass on genes which have the ability to develop new organisms, thereby creating new organisms under all kinds of environmental pressures". In short: "Life exists to produce new life", which is a circular expression because, in the reason we search for life, the term "life" (for which we try to find a reason) is used.
I think there are more "friendly" interpretations of evolution, of which I have no doubt that it took place.You can interpret evolution for example from a less egoistic perspective, and say evolution takes place to give new organisms a chance to live. Ande, in the case of human beings, create memes to let other people enjoy them (and not just to let your memes live further in other human beings).
If we follow Dawkins's interpretation then the scientific meme is self-undermining because the way we use science is damaging the earth to such an extent that it's the question if the earth will face a long-term future.

I'm voting to close this question as off-topic because it has nothing to do with science but with the philosophical question of what is the purpose of life.

I second that and fully support @Remi.b's claim.

descheleschilder you are confusing scientific questions with a pseudo philosophical one. "organisms exist becasue they are the most successful means by which genes make more genes" is a completely legitimate scientific answer. If you ignore this becasue you feel life needs deeper meaning you are no longer using science.

Why should they make more genes in the first place?

chemistry, Its one of the things certain sequences of RNA do becasue of the structure and the interaction of their charges, in the same way salts dissolve and phospholipids form micelles. Ones that are better at produce more thus increasing in number.

For the question Why should they make more genes in the first place?, you might want to have a look at How can the number of genes increase through evolution?.

You are definitely confused as you don't seem to be able to tell the boundary between science and philosophy. You should work out on that. You likely make a strong misrepresentation of what evolution theory is saying. You might want to have a look at a short and easy intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

Who says I am the one that is confused? I definitely believe in evolution, but my interpretation of it (like there are many interpretations of quantum mechanics or Christianity)  is radically different from the one of  Dawkins

I understand how evolution works and how genes and RNA can make copies of themselves, And I think this process started blindly, but I think that when evolution evolved the more complex creatures could steer in some way the direction the newly formed genes took, which is to say that it wasn't an evolution by accidental mutations in the genes.

@descheleschilder: You really need to stop believing in evolution.  It's not a religion, and doesn't need belief, any more than believing or not believing in gravity will keep you from falling.

You can ignore gravity and don't pay attention to it, or don't even invent the term gravity, but your keys will still fall on the floor. Likewise, you can ignore evolution and all flora and fauna will still be around and invent another story how all life came into being (to which your reply, of course, is that evolution isn't a story, but how it really is). But I think I'm gonna ask the same question in the philosophy department because we're drifting off.

If bodies are vehicles for genes, then "life exists to produce more life" should be understood to mean "genes, inherent replicators, within vehicles (bodies we call life or organisms), use vehicles to replicate further."

To make his writing more appealing and colorful, Dawkins quickly diverges into metaphoric terms. However, he often checks the reader to remember this and not lose sight of the point.

The following is more an extended comment than an answer...
Why the question is off-topic
Your question has actually nothing to do with biology. You are looking for a purpose behind the existence of organisms. Science does not care about purpose, nothing has a purpose, everything just happen mechanically. If the theory of evolution gives you a bad feeling, then I am sorry for you that it does but that point is not to be discussed on a science forum. I am voting to close for this reason.
Tautology
Please note that evolution is the science that has for goal to explain the change in allele frequency through time. The process studied is a continuous succession of reproduction and therefore in some respect a repetitive process but it does not make the explanation of how change in allele frequency occur a tautologic explanation. You will note by the way, that evolution does not explain the origin of life, this is the role of another of field of biology that we call abiogenesis.
Did you say Dawkins's theory of evolution?!
I often get a little mad when people write Darwin's theory of evolution thinking this is a modern concept. But writing Dawkins's theory of evolution is even worst. Dawkins is foremost a popular science communicator, so there is really no such thing as Dawkins's theory of evolution. Dawkins was also a researcher before and he brought some knowledge that allowed to grow our theory of evolution which we call the modern evolutionary synthesis (some argue that we should rename it Extended evolutionary synthesis in the light of recent discoveries).

Eh, I mostly agree with you (and definitely about the off-topicness), but I think if we reinterpret what the OP said as "Dawkin's ideas regarding evolution" (because that's what OP is referencing, not any of Dawkin's scientific contributions), which I think is what OP means rather than giving Dawkin's credit for the whole theory of evolution, the point that Dawkins emphasizes is essentially that there need not be a purpose. The existence of, and evolution of, organic life does not need to have a purpose to exist.

Thanks @Bryan. I read the selfish gene a while ago and I don't remember such saying but maybe he says that. Dawkins is known for mixing up philosophy, science and politics in its public speech. In which case, the question is of course still off-topic as the saying that 'there is no need for a purpose' is not a scientific claim but one that is to discussed in philosophy of knowledge (incl. philosophy of science).

I always get a little mad when people say that everything just happens mechanically. That means that everything they say also happens mechanically, so we can attach no meaning or purpose to the things they say. Which in turn means the evolutionary theory (which also developed mechanically) doesn't have a purpose or meaning. So what use is it discussing it? All the discussion develops mechanically too, depriving the discussion of purpose or meaning. I on the other hand can discuss the various interpretations of evolution, because I don't believe everything happens in a mechanical way.

I am sorry you don't like it but welcome to science anyway, where ones emotional response to an evidence should not alter the nature of this evidence. All of this is really a matter of philosophy of knowledge. Please consider having an intro course to philosophy of knowledge and consider asking your questions on philosophy.SE

I might be putting words in Dawkins mouth here, too, so maybe I should check that. @descheleschilder I think what someone like Dawkins would argue about purpose is that there is actually a lot of freedom in an approach to life that says there is no set purpose: it means that, as a human who has the fortune (and burden) of having a decent amount of intellect, you have an opportunity to choose your own purpose, to find your own meaning in your own life. It's a different "type" of purpose than some sort of guiding principle for the universe, but a purpose nonetheless.


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How to know what the expected value is?
I am confused as to how I was meant to know E for a X^2 test in the following question:

2.i and 2.ii give no more information.
Not knowing what to do I used E as 0 for the first row and 40 (3+37) for the second row, but that was just a guess. It was wrong and the correct answer for E is 20.
I suspect this has something to do with the 20 fields but I can't beleive that I'm just meant to know they expect one butterfly per field...
How was I meant to know E?

I'm voting to close this question as off-topic because it would be better suited for the statistics SE site, Cross Validated

The expected value is what the values would be if the tested conditions had no effect on the sample distribution. In your case, you are testing the effect of herbicides on butterfly populations. If the presence of herbicides wouldn't matter you would expect an equal number of butterflies on fields with herbicides as without.
So, the total number of butterflies being $37 + 3 = 40$, you would expect $\frac{40}{2} = 20$ butterflies on fields without and $\frac{40}{2} = 20$ on fields with herbicides.


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Classification of living organisms in kingdoms
What feature justifies the placing of prawns and grasshoppers in the same phylum

Is this a homework question?

Kingdoms represent phylogenetic relationship. As such there is no need for specific phenotypic features to group lineages together but only the recognition of their phylogenetic relationship. This being said, lineages from a certain kingdoms do share some phenotypic features.
As both the prawns and the grasshoppers belong to the kingdoms Animalia (aka. Metazoa), you can just look at the wikipedia article for animal and repeat the listed features. In short, they are both eukaryotic, multicellular, have motile cells and are heterotrophs.


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What is the maximum height of a tree?
I know there exists a huge variation in the height of trees. But what is the maximum height a tree can reach?
It must have something to do with the ability of the capillaries to transport life fluids all the way to the top. What is (are) the theor(y)(ies) about the maximum height, if there are any, and what do(es) it (they) predict?
Does it match reality?

You can refer to this link-http://www.livescience.com/14667-tall-trees-grow.html

The transport of water, and dissolved minerals, from the soil to the tops of trees is a combination of three factors. Root pressure pulls the water in due to factors related to osmosis. Capillary action helps draw it up the hydrophyllic vascular tissue. But the most important factor is due to evaporation in the leaves. This has some rather detailed aspects, search "transpiration" for details.
Although Coastal Redwoods are typically cited as being the tallest, some Douglass Firs are also in the competition. If you re seriously interested, here's a link to a Humbolt State University professor, Steve Sillett, who both studies and climbs these trees in search of the record. His book is a great read, also introducing you to the remarkable ecology near the tops of these trees. http://magazine.humboldt.edu/fall09/tallest-trees-unveiled/

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What unicellular eukaryotes reproduce sexually?
By sexual reproduction I am referring to, at least, gametogenesis or mating bridges. I was previously under the impression that unicellular organisms did not reproduce sexually at all.
So far the sexually reproducing unicellular eukaryotes I am aware of are yeast, diatoms, malaria-causing Plasmodium and some diplomonads.

Your definition of simplest is not exactly exclusive.

Huh! According to this article it is possible that sexual reproduction is the standard in eukaryotes: https://ittakes30.wordpress.com/2011/04/12/rewriting-the-history-of-sex/

This addresses your original question of "simplest" versus smallest. I'm not sure of sizes.
Investigate diplomonads: https://en.wikipedia.org/wiki/Diplomonad Most notable among them is Giardia: https://en.wikipedia.org/wiki/Giardia
These critters are primitive enough to lack Golgi and their version of "mitochondria" are substantially different enough (not synthesizing ATP) to be called by another name, mitosomes. Most have two nucleii and were not even thought to reproduce sexually  until relatively recently


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How to quantify the "stability" of a protein complex?
From experiment we've identified a subset of known mammalian protein complexes as interesting (approximately 50 CORUM complexes). We'd like to do an enrichment-style analysis to know more about them. One question I have is whether these complexes are particularly stable, since stable complexes should be biased towards detection. However, I don't have a chemistry or molecular biology background, so I don't know how to approach finding the stability of a protein complex.
Given a list of proteins in a complex, are there any conventional, in silico ways to estimate the stability of that protein complex? If not, have people published numbers for the stability of well-known complexes?
Edit: I'm okay being vague about the definition of "stability" since I'll be satisfied with an answer that uses any definition of it.
Edit: This question is answered on biostars.

Is this a homework question? If so, you should add the homework tag. Also, in general I would avoid using the word stability, because it is a vague concept. If you are talking about free energy you are talking about the structure of lowest free energy. Binding of ligands may involve quite different thermodynamic properties like binding energies. It's not my field. But my point is you should define precisely what it is you want to measure.

@David Thanks. I edited the question to be more precise, although I'm not sure how to define "stability" in this case. Really I'm asking if there are conventional ways to estimate the theoretical tendency for protein complexes to "stick together", whatever that means exactly.


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Heart failure and pleural effusion
Why does pleural effusion usually occurs in the right hemithorax in acute heart failure? Could someone explain the mechanism? Thank you.

where did you see/read that pulmonary edema usually occurs in the right hemithorax? as far as I typically see it's generally in both lung fields on a chest x-ray when it's present

Sorry i just realized i wrote it wrong. It should be pleural effusion, not pulmonary edema. I cannot say any reference textbook. Because it is written on a book for medical exams.

thanks for clarifying... I still have the same question... where have you seen that pleural effusions occur on the right instead of the left? can you cite that in your question?

@VanceLAlbaugh I am curious about this question though I don't know the answer. Searching for the source of this information I think OP might have it slightly wrong; bilateral pleural effusion is by far most common, but unilateral pleural effusion is typically in the right. This seems to be commonly reported, here's one example, here is another.

completely agree @BryanKrause


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Are there transposons which create homozygous genotypes in offspring?
Transposons copy or cut and paste gene sequences. Alleles are passed down from parents and offspring may be heterozygous or homozygous for an allele (assuming diploidy).
Are there any transposons which ensure the frequency of a given genotype in a population by converting heterozygous zygotes into homozygous zygotes?

I study transposons for my PhD; I am not aware of any that preferentially insert through an active mechanism to an un-inserted allele.
There are tranposons such as R1/R2 which have a 'favorite' insertion site and will insert/compete for that sequence. That's kind of similar to your question but not generalizable.
The predominant factor I can think of which would cause such a thing to arise would be gene conversion in which the insert allele is used as a repair template for an un-inserted allele. Gene conversion is rare but can explain how the TE insertion is found on multiple haplotypes.
It's very unlikely that the alternative hypothesis occurs in which the same type of TE inserts at the exact same position in two different haplotypes and that TE doesn't have a preferred insertion site.


text:
What is the lifespan of Skeletal Muscle Cells?
I have read that skeletal muscle cells cannot multiply and are generally not created after early development. However, I have also read that they have a "lifespan" of 10-15 years. Could this lifespan actually be referring to the turnover rate of the majority of material in the cell, and that the literal lifespan of the cell (if we count all of its components, including the nucleus) would be the same as that of the owner?

This is a huge debate and I'm guessing you read the lifespan numbers in one of the papers arguing that there is a certain degree of myocyte turnover.

Thanks for the comment, it's nice to know at least some context on the question. It was getting very confusing reading articles that would make arguments with absolute certainty but not qualifying those statements with much specification!


text:
Why and when did the misconception about the Panther being a species came to be?
People usually call Panther to any big black cat, I did so until I watched Apocalypto and saw they were calling the black cat Jaguar which confused me. (I have no biology knowledge)
It was kind of a shock to discover that Tigers and Lions, among other species, where Panthers too, and it surprises people when I tell them.
Does anybody know why and when this started to happen?
* I realize this might not be related to biology but actually to popular culture, but I couldn't find a stackexchange site about that.

Tigers, lions, jaguars and leopards are all different species. Panthera is a genus, a broader classification than a species. Tigers are Panthera tigris, lions are Panthera leo, and jaguars are Panthera pardus. In each cases the formal species name is the genus followed by the species identifier. Common usage rarely gives a hoot about the subtleties of biological classification.
Your initial impression was correct: any member of the Panthera genus that has a black coat is called a black panther. In South America they are jaguars, in Africa and Asia they are leopards.

Now I am somehow wondering if there could be black tigers.

@skymningen Yes, (sort of): https://en.wikipedia.org/wiki/Black_tiger_(animal)

@KoenvdH Is it just me, or is there something strange about black tiger and her cub? The face/head seems a bit unusual.

@HarrisWeinstein the small head/big nose might mean they are south chinese tigers from what little looking around I did.

Oh I see, I was using Panther and Panthera interchangeably. Mainly because both sound the same in spanish (Pantera and Panthera) my native tongue.


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How do communities relate to food webs?
I am a biology student who has just completed drawing a food web for class. As I was making it, I learned that a food web is the sum of all feeding interactions. My teacher associated food webs with communities, but I do not understand what the communities of a food web are.
How are communities related to food webs?

Tim can you add some information about your drawing? Also, where have you looked for this information already?

The Details
Ecological communities are groups of multiple (2+) species of either plants, animals and/or other organisms that interact in a unique habitat. More accurately (from Wikipedia and corroborated by Begon et al. (2006)), we can define an ecological community as an:

assemblage or association of populations of two or more different species occupying the same geographical area and in a particular time.

These organisms could be interacting in a number of ways:

As you can see, one or both species can be effected either positively, negatively or neutrally (not at all) in these various types of interspecific interactions.
I should note that a community doesn't have to contain all organisms within a certain habitat.

Sometimes we might limit our discussion of a community to a single guild or single trophic level. Other times we might use the terminology simply to describe two interacting species (either within or between guilds/trophic levels).

Really, "communities" are more conceptual "units" used to describe two or more interacting species. More accurately, it's an interaction between populations of 2+ species. In this way, community ecology is an extension of population ecology.

Food webs (i.e., a system of interlocking and interdependent food chains) are essentially summaries of the feeding relationships within an ecological community (Molles, 2010). In other words, they are focused strictly on trophic interactions. These trophic interactions are primarily concentrated within the (+,-) interactions between species. This means that the interactions that dictate a food web are going to consist mainly of consumption (predation/herbivory).

From University of Michigan (my emphasis):

Food webs are graphical depictions of the interconnections among species based on energy flow. Energy enters this biological web of life at the bottom of the [web], through the photosynthetic fixation of carbon by green plants.
Energy moves from lower to higher trophic (feeding) levels by consumption.

Example
An example of a community that does not qualify as a food web:

A community of plants includes just the plants that are competing in the same space and as a result make up (i.e., are classified as) some sort of vegetation type. These species are competing at the same trophic level and do not consume one another. This is classic ecological competition.

If we examine the trophic interaction between each of these plants with each of their sources of energy, each of their consumers, each of their consumers' consumers, etc. then we are talking about a food web.

Final Thoughts
So the term "community" is used generally to describe interacting species of organisms in a given habitat, while "food webs" describe a more specific aspect of a community -- the trophic interactions of the members of that community.

Of course, it could be the case that all species in a given community are represented in a food web, but this is not necessarily the case.

It could also be the case that not all species represented in a food web be part of the same community...

One could also consider food webs to be broader than a community because they can describe the trophic interactions of species/populations across communities. From this perspective, food webs "lie at the interface of community and ecosystem ecology" (Begon et al. 2006).

Citations:

Begon, M., C.R. Townsend & J.L. Harper. 2006. Ecology: From individuals to ecosystems. Fourth edition. Blackwell Publishing Ltd. Malden, MA. pp 469 - 601.

Molles, M.C. 2010. Ecology: Concepts and Applications. Fifth edition.  McGraw-Hill. New York, NY. p. 544.

I give up :-) +1

A food web is a representation of who eats whom.

A qualitative food web provides for every pair of vertices just the information whether or not one feeds on the other.
This can be represented e.g. by some directed graph with a set of vertices $V$ and a set of arrows $A$ between the vertices. An arrow has the form
$$a: v_1\rightarrow v_2$$
for some vertices $v_1$ and $v_2 \in V$ meaning $v_1$ feeds on $v_2$.

A quantitative food web provides for every pair of vertices a quantity (e.g. in form of a postive real number) defining how much one feeds on the other.
This can be represented e.g. by some weighted directed graph with a set of vertices $V$, a set of arrows $A$  between the vertices and additionally a set of weights $\mathbb{R}^{\geq0}$ providing one weight for each arrow. An arrow has the form
$$a: v_1\rightarrow_x v_2$$
for some vertices $v_1$ and $v_2 \in V$ and a positive real number $x\in\mathbb{R}^{\geq0}$ meaning $v_1$ feeds on $v_2$ to an extend of $x$.
The specification of the weights $x$ can vary (bio mass, energy, ...).

The arrows in a graph representation of a food web represent a feeding relationship - the exact specification can be versatile: qualitative, quantitative (diverse units).
The vertices in a graph representation of a food web can be species (i.e. grouping according to genetics), traits (i.e. grouping according to certain properties or combinations of properties).

Community. In ecology, a community is a group or association of populations of two or more different species occupying the same geographical area and in a particular time.

See
Wikipedia: Community
Thereby a species based food web (i.e. a representation of the feeding relationship between species) that is e.g. represented as a graph with a set of vertices $V$ and arrows $A$ thereby implicitely also represents a community by forgetting the representation of the feeding relations $A$ and regarding just the set of the included species $V$.
A trait based food web can also be regarded as a community in the above sense. E.g. assume the food web is represented as a graph with a set of vertices $V$ (not being species) and arrows $A$. Assume the traits are about individuals (respectively species). Then translating $V$ in the case of species based traits to the set of involved species:
$$S(V):= \{s|s \text{ is a species for which some trait }v\in V \text{ is true}\}$$
or in the case of individual based traits:
$$S(V):= \{s|s \text{ is the species of some individual for which some trait }v\in V \text{ is true}\}$$
yields again a community.

Summarized. You should always be able to yield a community from a food web by forgetting the feeding relationship and taking all involved species.


text:
Do lower animals have instinctive behaviors?
Can an organism such as C. elegans, with only 302 neurons, exhibit "instinctive or innate behavior"? If not, then at what basic minimal structure is instinct manifest?

Pretty much anything that such a simple organisms would do with its neurones would be called instinct behaviour, wouldn't it?

Short answer
'Lower' organisms like C. elegans exhibit innate behaviors. In fact, unicellular organisms [without any nerve cells at all] can exhibit instinctive behaviors.

Background
Let's start by defining the central terms here, namely Behavior and Instinct:
Merriam-Webster has a general definition of Behavior:

[A]nything that an organism does involving action and response to stimulation

And according to the Cambridge dictionary, Instinct is:

[T]he way people or animals naturally react or behave, without having to think or learn about it.

And Merriam-Webster defines Instinct more elaborately:

Largely inheritable and unalterable tendency of an organism to make a complex and specific response to environmental stimuli without involving reason
Behavior that is mediated by reactions below the conscious level

Hence, C. elegans' actions are indeed instinctive behaviors.
An interesting distinction here is whether behaviors in simple organisms should be indeed called behavior, or rather be classified as [lower-order] reflexes.
According to Merriam-Webster, a Reflex is:

[A]n automatic, often inborn response to a stimulus that typically involves a nerve impulse passing inward from a receptor to the spinal cord and then passing outward from the spinal cord to an effector (such as a muscle or gland) without reaching the level of consciousness and often without passing to the brain, such as the pain-withdrawal reflex, or the knee-jerk reflex.

This is a typical schoolbook approach-based definition of a reflex. Strictly spoken C. elegans' behaviors would not classify as reflexes according to this definition, because invertebrates do not have a spinal cord.
Nonetheless, sea anemones show protective withdrawal responses by retracting their tentacles and oral disc. Some may even detach from the substrate in response to a variety of aversive mechanical, electrical, or chemical stimuli. And earthworms show rapid withdrawal responses mediated by giant nerve fibers when subjected to unfavorable stimuli, that are in fact classified as reflexes (Smith, 1991).
Indeed, Wikipedia defines a Reflex as

...[A]n involuntary and
  nearly instantaneous movement in response to a stimulus. Scientific
  use of the term "reflex" refers to a behavior that is mediated via the
  reflex arc.

Thus the question then becomes what is a reflex arc? The Medical dictionary defines a Reflex arc as:

Route followed by nerve impulses in production of a reflex act, from peripheral receptor organ through afferent nerve to central nervous system synapse and then through efferent nerve to effector organ.

Hence, in all, instinctive behavior is appropriate general terminology. When in simple organisms the behavior can be directly linked to a responseive action to a sensory stimulus, the term reflexive behavior may be a more appropriate term than instinctive behavior as far as I can see.
To push the definition of instinctive behavior even further, we can conclude from all this that single-celled organism exhibit it too, as they can show simple instinctive behaviors, such as phototaxis and chemotaxis, where they change their direction of movement in response to light and chemicals, respectively (source: Khan Academy).
Reference
- Smith, ILAR J (1991); 33(1-2): 25-31

I would like to poke at this a bit more. I believe instinct does require a nervous system, and in fact requires a higher CNS organ or brain.  I agree it does not require learning, but would preclude simple reflexes. I think instinct also involves memory, and an inheritable, yet "conscious  behavior". Reflex action can be studied in the unconscious or even transected CNS. But instinctive behavior I think requires a conscious, awake animal with a fully intact brain.   I realized these statements are at a minimum debatable, and possibly just incorrect, but might keep the topic alive.

I just surveyed eight definitions of instinct, some of them "biological". None of them indicate a nervous system is necessary. For example: "a largely inheritable and unalterable tendency of an organism to make a complex and specific response to environmental stimuli without involving reason" https://www.merriam-webster.com/dictionary/instinct#medicalDictionary
The protist Euglena gracilis, for one "lower animal" example, shows an innate photatatic response to light. http://www.nature.com/nature/journal/v216/n5119/abs/2161042a0.html Euglena's response to light includes the "complexity" that some definitions include.


text:
Determining net charge of amino acid at given pH
I am trying to calculate the net charge on an amino acid, but I seem to be doing it wrong. The question I am trying to answer is "In a pH 7.0 buffer, what will be the charge of Methionine?" We are referred to a table that gives us the following information:
$$\pu{p}K{_\pu{a\mathrm{1},\ce{COO-}}}=2.28$$
$$\pu{p}K{_\pu{a\mathrm{2},\ce{NH3+}}} = 9.21$$
$$\pu{pI = 5.74}$$
From what I understand, if pH > pI, (which it is here), the amino acid should have a negative charge because even though the pH is high enough to deprotonate all the carboxyl ends and not enough to deprotonate all the amino ends, since it is higher than the pI some of the amino ends have been deprotonated (in addition to all the carboxyl ends).
Yet my answer book says that the net charge would be zero! Are 5.74 and 7.0 "close enough" that we can consider net charge to be zero still? If so, what is the standard permissible 'fuzzy' range? If not, then what is going on here?

You are right in your reasoning: at any pH for any titratable group, there is a distribution between the protonated and deprotonated species. We can calculate this distribution and therefore the average charge of the species with the Henderson-Hasselbalch equation:
$$\mathrm{pH = pKa + log\left(\frac{[B]}{[A]}\right)}$$
Or, rearranged:
$$\mathrm{\frac{[B]}{[A]} = 10^{pH - pKa}}$$
Where A is the conjugate acid and B is the conjugate base. For carboxyls and primary amines, this can also be written as $\ce{\frac{[COO-]}{[COOH]}}$ and $\ce{\frac{[NH2]}{[NH3+]}}$, respectively. As a simple example, if the pH was 2.28, the ratio between the protonated and deprotonated form of the carboxyl group (pKa = 2.28) would be $\ce{\frac{COO-}{COOH} = 10^0 = 1}$. This means $\ce{[COO-] = [COOH]}$ and the average charge of the carboxyl is thus -0.5.
Now, for cases where $\mathrm{pH \neq pKa}$, we need to determine the mole fraction, $\chi$, for each charged species. Given that $\mathrm{\frac{[B]}{[A]} = \frac{\chi_B}{\chi_A}}$ and $\ce{\chi_A + \chi_B = 1}$, we can derive these equations:
$$\mathrm{\chi_{COO^-} = \frac{1}{1 + 10^{pKa - pH}}}$$
$$\mathrm{\chi_{NH_3^+} = \frac{1}{1 + 10^{pH - pKa}}}$$
Plugging in the numbers, we get:
$$\mathrm{\chi_{COO^-} \approx 0.999981}$$
$$\mathrm{\chi_{NH_3^+} \approx 0.993872}$$
To state it another way, ~99.9981% of the carboxyl groups are in the deprotonated (negative) state and ~99.3872% of the amino groups are in the protonated (positive) state. The average charge of methionine at pH 7 is simply the sum of these mole fractions, accounting for the charge of each species, and is approximately equal to -0.006109. I assume your textbook is rounding.

You can plot these functions to see how charge varies with pH:

Your answer is very detailed and interesting. However, I thinks it raises an additionnal question: if the amino acid's charge is around 0 for a wide range of pH (approx. between 4 et 8 here), why bother defining a pHi?

@Flo The pI will tell you where the transition from net negative to net positive charge occurs. Depending on your application, that information may or may not be useful. I work with proteins, and the pI of a single amino acid has never been crucial information for me. However, knowing the pI (usually estimated) of an entire protein is important for applications such as gel electrophoresis and chromatography. Because proteins contain many titratable side chains, their charge can vary more significantly around the pI.

Thanks for this great answer! Are there any guiding rules by which to determine/estimate when it could be rounded, or would I need to use these equations to see how close to each other the values are?

@Jo.P For your case, the rules would be dictated by the instructor and you should ask them for clarification. A rule of thumb that I've heard is that when the pH is >2 units away from the pKa, you can treat the species as either protonated or deprotonated. At |pH-pkA|=2, the ratio of acid to base will be 100:1 (or vice versa).

Oh the horrors of Schiff bases and pHs..... +1

IMO the inclusion of a chart like the one you provided turns a good answer into a great one. +1 and more if I had them.

@BryanKrause I always appreciate pictures in answers. Thank you and AliceD

@canadianer-Tnx!


text:
Biological replicates
We are currently doing an screening where supernatans from a bacteria genus are tested againts a pathogenic bacteria cell culture in a 96-well plate where OD is measured each 2 hours.
Each supernatant from a strain has 3  replicates  and the control phatogenic bacteria cell culture has about 11 replicates inside the plate.
Once each experiment is finished cell growth curves are modelated and 3 growth parameters are determined (mu, lambda and max absorbance) from each supernatant tested and from the control. Then a Mann-withney U test is performed for each growth parameter from each strain againts corresponding control parameter to check if there's some kind of possible inhibition.
The strains which has some inhibition efect againts this pathogenic bacteria will be tested again in further experiments to confirm the possible positive.
I  have a doubt about if performing statistical test to compare supernatants from each plate againts its corresponding control is correct considering that the possible candidates will be again tested in further experiments to confirm its inhibition. Since there's loads of strains to test, repeating each single experiment more than 3 times would take too long.
What it is your oipinion? Is it correct to do statistics for single plate (technical replicates) to gather possible positive for a later confirmation (biological replicates)?
Thank you
Are biological replicates strictly needed in this case?

You might have better luck with this question on https://stats.stackexchange.com.

These might be interesting to you: http://www.nature.com/nature/journal/v492/n7428/full/492180a.html https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321166/


text:
What is an example of a plant species that is a halophyte with seeds that germinate quickly?
I’m doing an experiment on the effect of salt concentration on the germination of seeds from halophyte plants. What would be an example of a species that is suitable for such an experiment? I would prefer a species the seeds of which germinate relatively quickly under not very difficult conditions.

where have you tried looking for the answer to this question?

It turns out that your research question about halophytes has been asked many times before. You should learn from your predecessors...
Seed germination in halophytes displays a high degree of inter- and intra-specific variability. However, Khan & Gul (2006) report that germination patterns respond to a number of environmental factors (including temperature, NaCl concentration, and presence of different regulating chemicals).

Their paper has over 100 citations, many of which cite germination studies of numerous halophyte species. I'd recommend you start your search there.

You'd also probably benefit by perusing the sources in Ungar (1978) and Panuccio et al. (2014).

Citations

Khan, M.A. & B. Gul. 2006. Halophyte Seed Germination. In Halophyte Utilization and Regional Sustainable Development of Agriculture. pp.11-30
Panuccio, M.R., S.E. Jacobsen, S.S. Akhtar and  A. Muscolo. 2014. Effect of saline water on seed germination and early seedling growth of the halophyte quinoa. AoB PLANTS 6: plu047
Ungar, I.A. 1978. Halophyte Seed Germination. Botanical Review 44(2): 233-264

Thank you for your helpful post, it was exactly what I was looking for.


text:
Gestation period of African savanna elephants?
I found out it is 22 months for African bush elephants, but is this also true for African savanna elephants?

The African bush elephant and the African savannah elephant are the same species (i.e., they are just different names for Loxodonta africana).
According to here and here, the African savanna/bush elephant (Loxodonta africana) has a gestation period of 22 months.
The only other African species of elephant, the African forest elephant (*Loxodonta cyclotis), has a gestation period of 20 - 22 months (see here). Both Wikipedia and this source corroborate this higher expected range of 22 months, but with the latter source adding:

from zoo data a gestation length averaging 660 days has been determined while the average in one wild population (Amboseli) was 656 days.

And for fun, click below for a video of an elephant fetus!

Pink elephants - I must be on acid; comes close to a blue dart frog :D +1 for the well illustrated answer


text:
can a point mutation cause a frameshift?
During translation initiation, a tRNA loaded with Methonine binds to the small ribosomal subunit. Subsequently, a mRNA molecule, recognized by the 5 cap, binds to the small subunit, and the tRNA scans the mRNA molecule for the presence of AUG which is the start codon. A point mutation could result in the the sequence AUG to be present after the ribosome binding site, but upstream of the "true" start codon.
Question 1:Will translation start at the mutated site?
Question 2: Could the mutation result in a frameshift, with a truncated protein as a consequence?
I have not found much information about this. I did find one homepage, with lecture notes from a genetics course at University of New Mexico referring to this type of mutation as a start-gain mutation.
http://www.discoveryandinnovation.com/BIOL202/notes/lecture14.html
"Start gain. A start-gain mutation is a point mutation creating a new ATG start codon upstream of the original start translation site. If the new ATG is close enough to the original one (so that it is within the processed transcript and downstream of a ribosome-binding site) and in frame, it will be used to initiate translation, adding amino acids to the amino terminus of the original protein. It is also possible for a start-gain mutation to be out of frame, which will not affect translation of the original protein. In general, start-gain mutations have a low impact on gene function."
I have not come across the term start-gain mutation before, but it sounds like what I am describing.
Question 3: If the start-gain mutation is out of frame, why will it not affect translation of the original protein?
Question 4: It is my understanding that the start codon sets the reading frame, and not the bases prior to the start codon. If the bases prior to the start codon are also "read" in triples, which position in the mRNA transcript sets the reading frame?
Thanks

where have you looked for this answer?

Welcome to Biology.SE. Homework questions are off-topic here unless you have shown your attempt at an answer. For more information see our homework policy.

I saw the OP edited it's question quite a lot.. This answer answers the questions before the edit, I will not delete this because it will maybe help other people
I'm not sure if you fully understand the terms you used so I will start with clarifying these.
Missense mutation

a point mutation in which a single nucleotide change results in a
  codon that codes for a different amino acid (wiki)

Example
    DNA: 5' - AAC AGC CTG CGT ACG GCT CTC - 3'
         3' - TTG TCG GAC GCA TGC CGA GAG - 5'
   mRNA: 5' - AAC AGC CUG CGU ACG GCU CUC - 3'
Protein:      Asn Ser Leu Arg Thr Ala Leu

-------------------------↓↓↓↓↓↓↓--------------------------
    DNA: 5' - AAC AGC CTG CTT ACG GCT CTC - 3'
         3' - TTG TCG GAC GAA TGC CGA GAG - 5'
   mRNA: 5' - AAC AGC CUG CUU ACG GCU CUC - 3'
Protein:      Asn Ser Leu Leu Thr Ala Leu

The 4th codon which was CGT (and GCA on the other strand) is changed because of a subtitution of the G for a T. Because of this change the codon will not code for Arg anymore but instead it will code for Leu. So a missense mutation causes the sequence to be in the same frame as before however a codon is changed and subsequently an other amino acid is added to the polypeptide chain during translation (this is not always the case see wobble)

Frameshift mutation

A frameshift mutation (also called a framing error or a reading frame
  shift) is a genetic mutation caused by indels (insertions or
  deletions) of a number of nucleotides in a DNA sequence that is not
  divisible by three. (wiki)
  Example

    DNA: 5' - AAC AGC CTG CGT ACG GCT CTC - 3'
         3' - TTG TCG GAC GCA TGC CGA GAG - 5'
   mRNA: 5' - AAC AGC CUG CGU ACG GCU CUC - 3'
Protein:      Asn Ser Leu Arg Thr Ala Leu

-------------------------↓↓↓↓↓↓↓--------------------------
    DNA: 5' - AAC AGC CTG CTT ACG CT C    TC - 3'
         3' - TTG TCG GAC GAA TGC GA G    AG - 5'
   mRNA: 5' - AAC AGC CUG CUU ACG CU C    UC - 3'
Protein:      Asn Ser Leu Leu Thr Leu ..........

In this case the nucleotide T is removed and thus causing a framehift because we need tree bases to form a codon. by removing a nucleotide we just read further till we find a third base and this will be our "new" codon. This new codon does not code for Ala anymore but will code for Leu. (I added the dots because of the fact that the stop codon will/can be shifted and the transcript can be either shorter or longer (the previous stop codon will no longer exist).

Could a missense mutation cause a frameshift

In the case of a missense mutation the DNA sequence will be in the same frame (no nucleotide is added or removed) and in the case of a frameshift a nucleotide needs to be added or removed and therefore a missense can't cause a frameshift.

such that a mutation results in the sequence AUG?

Both a missense and a frameshift could result in a start codon.
Example (frameshift)
mRNA 5'     AAC AUU GAC 3'
Protein:    Asp Ile Asp
    -------------------------↓↓↓↓↓↓↓--------------------------
mRNA 5'     AAC AU G  AC.... 3'
Protein:    Asp Met   ........

Example (missense)
mRNA 5'     AAC AUU GAC 3'
Protein:    Asp Ile Asp
    -------------------------↓↓↓↓↓↓↓--------------------------
mRNA 5'     AAC AUG  GAC 3'
Protein:    Asp Met  Asp

So both a frameshift mutation and a missense mutation can introduce a Met --> a start codon.

a mutation results in the sequence AUG to be present in the transcript
  but upstream the start codon?

A gene is only transcribed if this gene is preceeded by the appropriate sequences:

The start codon will be present in the first exon so the only way to put a start codon before the "old" start codon while remaining all other sequences(UTR,promtor, enhancers etc.) in tact is to "create" one just behind the 5' UTR and before the "old"  start codon in the first exon. This can be done by just inserting AUG in there, HOWEVER we are talking about point mutations:

A point mutation, or single base modification, is a type of mutation
  that causes a single nucleotide base substitution, insertion, or
  deletion of the genetic material, DNA or RNA

The start codon we are talking about is positioned AFTER the 5' UTR (as said above):

By inspecting the "general" 5'UTR sequence we can see that there are already "start codons" (not really start codons because they are not translated") present before the start codon. We could probably add one using a frameshift or a missense mutation as described above and in your edited question:

If the new ATG is close enough to the original one (so that it is
  within the processed transcript and downstream of a ribosome-binding
  site) and in frame, it will be used to initiate translation, adding
  amino acids to the amino terminus of the original protein

As far as I can reason is the only way to create a start codon BEFORE the old one is to change the UTR. As stated in your queation this can only "work" if the UTR parts which have an important function are not affected. Further to get this working the 5'UTR should contain a (not "important" )sequence which can be mutated tot form an AUG (see my explanation above)


text:
Bacteria trapped in crystal inclusions found 'alive' after 50,000 years - what were they eating all that time?
The phys.org article Biologists find weird cave life that may be 50,000 years old describes the announcement by NASA Astrobiology Institute director Penelope Boston at the 2017 AAAS meeting$^{(1)}$ of micro-organisms found in small inclusions within crystals of hydrated [Calcium Sulphate][] (Gypsum) that had grown while underwater in a cave in Naica, Mexico. It is estimated that some of these organisms have been isolated within inclusions for as long as 50,000 years, and yet can grow and reproduce when carefully extracted and provided with fresh chemosynthetic nutrients.
(BBC Radio interview with Penelope Boston)
This particular discovery has just been formally announced so there is no peer-reviewed material to read yet, but it's possible someone here in Biology SE attended the meeting or has read further about the announcement.
50,000 years is a long time (for a bacteria, not a crystal), and if I understand correctly the energy source for these organisms is chemosynthesis. Put simply, wouldn't they have eventually used up all their food and died? I'm thinking the crystal is a good electrical insulator and the cave was dark, so there couldn't be external energy sources to replenish the oxidation state of the iron or sulphur or whatever they were eating.
The elevated temperature and ubiquitous radiation would have presented a relentless, potential source for DNA damage mechanisms, and repair would require a constant supply of energy. So I'm guessing there had to be some minimal source of energy to keep them viable, if not actually 'alive' for 50,000 years.
Is this thinking roughly correct? If so, what might that source of energy have been?

Below: Giant gypsum crystals in a cave in Naica, Mexico, from here. Note the person for scale at lower right.

(1) Currently 2017 AAAS meeting links are all re-directing to the 2018 meeting, so I can't find a link to the particular talk or session.

There is no chemosynthesis tag.

now there is one!

The question is interesting, but I must say it is too early to say anything. But let me tell you what I can.
Dormancy, first of all, is a state in which all metabolic activities of an organism temporarily stop or slow down, and when saying all, I literally mean it. Dormancy can be considered, in layman's terms, as molecular level of hibernation. Any organism, in dormant state, does perform all kinds of activities, but in super slow motion. Again, we don't know anything about those microbes, so I can just tell the currently known mechanisms by which those microbes could have survived. Gypsum i.e. $CaSO_4.2H_2O$ contains sulfate ($SO_4^{2-}$), so those microbes (let me call them X from now) must be sulfur metabolizing ones to survive. Now, known mechanisms of sulfur metabolism include:

sulfur oxidation
sulfate reduction
sulfite reduction

which are summarized as:
source
Now, with sulfate already available from gypsum (considering dissociation) as:
$CaSO_4.2H_2O \rightarrow Ca^{2+} + SO_4^{2-} + 2\hspace{1mm}H_2O$
The reactions it can perform are sulfate reduction and sulfite reduction. Some of the mechanisms are:
source
In the presence of $CO_2$, glucose can also be formed as:
$12\hspace{1mm}H_2S + 6\hspace{1mm}CO_2\hspace{1mm}\rightarrow\hspace{1mm}C_6H_{12}O_6 + 6\hspace{1mm}H_2O + 12\hspace{1mm}S$
The required $CO_2$ might come from respiration. During dormancy, this process is highly slowed down, so that X may have survived such a long time by just this process.
Again, this is just the known mechanism, X may have evolved other, possibly even more efficient, mechanism. The above example was just to suggest how X could have survived in gypsum crystals for as long as 50K years. We don't know anything about X yet. From the article you cite:

If confirmed, the find is yet another example of how microbes can survive in extremely punishing conditions on Earth.

meaning we don't even know yet whether they are really viable or not.

The life forms—40 different strains of microbes and even some viruses—are so weird that their nearest relatives are still 10 percent different genetically. That makes their closest relative still pretty far away, about as far away as humans are from mushrooms, Boston said.

Now, viruses ain't alive. And 90% similarity means a lot of difference, which means they almost certainly have different mechanisms for survival. At last, I would again remind that it is too early to say anything unless some scientific studies are performed and published.
P.S. talking about energy source, even the heat and radiation from environment could be used as a source of energy. Obviously, harnessing energy directly from external heat is pretty difficult, but when one finds fungi using radiation for growth, then you never know!

This is exactly the answer I was hoping for. Background to put the question in perspective, the possibility of constituents from the crystal itself participating, and a whole lot of caution not to draw any conclusions until the normal business of science takes its course. Thanks! (rad-munching fungi was an eye-opener, I hadn't heard of that before.)

From the radio interview I had the impression that some things were in fact viable, but they may not simultaneously be the 50Ky old things. I'll listen again at some point, and wait for more to be written, and published in the future.

I've just asked this question.

keep in mind the cave in question is so hot humans can only enter it is special cooling suits, and even then only for short periods of time.

@john thats a nice point, but I can't understand how it relates to the question... :/

Under high heat you have a wider array of reactions to work with. Such as Iron sulfur reactions.

@john talking about wider array, it just comes out as a bonus that iron sulfur reactions are also the ones we already know, who knows what kind of reactions could those microbes perform! ;)

Thanks for the great answer! I have a hunch I that shouldn't hold my breath for any conclusions/consensus to be announced soon.

@uhoh yeah, research takes quite a long time, so a better answer might take years or so :)

...and even an answer with new information may not be a "better answer" in terms of being helpful or thorough. These "nonstandard ecosystems" (ones that look different than the rabbit eating the plant and returning nitrogen that I remember from school) are fascinationg!

Why do you presuppose bacteria needed to "eat" something all the time to survive. Let me give you an example-if I take a batch of a billion bacteria, throw it on a meteorite and let it bathe on the "sunshine" in space for a million years, then took it back to Earth, put it in a culture where the bacteria can grow again and out of those billion bacteria a single one was able to restart its metabolism and grow a new colony of billions of bacteria, would you consider it alive all those years it was in space? Especially, when it comes to bacteria, because they are so small they can easily go to huge numbers and if just a tiny fracture of those manage to survive you have Life Immortal.
The matter of Life is it can look quite, for the lack of a better word, "dead" for a very long time and despite not having the "need" to eat anything it can(when given the right conditions)flourish back to its full potential. Life can be pretty resilient and biomolecules remain unscanted for very long periods of time, so the question-"What it feeds on?" can be surmised as-"Can it survive unscented for so long?". And be sometime the answer is-Yes!
You may be interested to read this here and see the original paper here

Please read the question again and note that I've mentioned the molecular mechanism of DNA repair. Unless I'm mistaken these are hydrated - bacteria or some organisms floating around fully constituted in water. Under those conditions, over 50,000 years, I am suggesting at least a minimal amount of energy is needed for repair against inevitable DNA damage. If you can cite a specific known example of hydrated, single cell organisms remaining for 50,000 years with absolutely no source of energy, please provide a link. I write with careful constraints to this specific situation.

As it stands now, your answer wanders all over the place, and isn't helpful. You start out by mis-stating my question and then literally go into outer space from there.

I don't think the space analogy is out of context here but let us not waste any more space with this but will not go further on the topic.

The question is then "Do really the bacteria need an energy source to prevent them from decay, right? Is this your specific question?"

Please try to address the question as written, thanks!

The question is then "Do really the bacteria need an energy source to prevent them from decay, right?" If it is then there are two possible answers-the first is the number of bacteria is big enough and their mutation slow enough to leave survivors after 50,000 years. The other is the possibility of sulfur metabolism discussed in the previous answer. I would also suggest the possibility that these microbes might be able to make spores or synthesize special protectors to prolong their dormancy but as the article goes-we don't know enough about them yet. How about that answer?

@YordanYordanov you've written a nice answer, but you missed a crucial point: situation! The OP wants to know about the specific case of recently discovered bacteria, not a general case. So please try to be as specific about this case as possible, and a +1 from me is then guaranteed ;)

Thank you another "Homo sapiens" but I think the information provided in the source material is too little for now to jump to conclusions. If we can know more about the metabolism or the relationship of these bacteria to other genera I think we can make better suggestions. But the way I see it first we should wait for the formal paper or at least NASA to give us something more about their genetics and taxonomy. How about this answer?


text:
Can translocation occur within a gene?
I know genes can be translocated between chromosomes but can nucleotide sequences be moved around within an individual gene?
Could the following gene:
MEN SAW OLD HEN
Become:
MSA WOL DHE NEN
By moving the EN at the beginning to the end?


text:
Isolating the vasculature of an organ?
Is there a chemical or process that would dissolve or remove all other tissues in an organ and leave all the vasculature intact? I am planning to make a shelf display of the blood vessels in the heart of a pig for use as a shelf display.

Plastination, corrosion casting, and paraffin embedding can be used for this process, though each with different methods and results.  Body Worlds uses primarily plastination, and they create awesome "models" such as this

@theforestecologist Although Body Worlds is famous for their use of plastination, the picture you linked is a corrosion cast.

The typical name for this technique is "corrosion casting" - if you search for literature on corrosion casting you will find many many papers detailing the technique. Another answer mentions "plastination" but I don't think this is really what you are looking for; plastination is a technique for preserving the tissues themselves (though the "Body Worlds" exhibit that post references also uses corrosion casts extensively).
Briefly, in corrosion casting, you gravity or pressure-fill the vasculature with a plastic, typically acrylic. It is best if the vessels are flushed free of blood before injecting the plastic, with saline/PBS, for example. (Organs from a butcher will work fine but you will get better results if you can administer heparin premortem to prevent clotting, which of course is not possible for a meat animal.) The acrylic cures, and then the tissues that remain are digested with a basic solution, ranging from 0.5 M NaOH to 6M KOH depending on the protocol (lower concentrations or NaOH will digest more slowly, higher concentrations or KOH will digest more quickly), often at elevated temperature (~37C). Note that this solution technically digests all of the vasculature as well, but you have already filled the vascular lumens with plastic, so that is what you are left with.

I think that you are looking for plastination. Its developer, Gunther von Hagens, uses it to preserve whole bodies as well as selected tissues, such as muscles, nerves and vessels, for teaching uses and the exhibition BODY WORLDS.
I think this is the best method, but I'm not sure about its feasibility without a dedicated laboratory. Other methods, such as paraffin embedding, would leave you with the problem of removing the rest of the tissues without using high temperatures.


text:
What amount of protein comprises the feces of a domestic cat?
I've heard it said that the fecal excrement of cats, Felis catus, contains adequate amounts of protein so as to attract the interest of other animals e.g. dogs (Canis familiaris).
However, I am unable to locate any studies which reported the composition of a cat's feces as compared to those of any other animal with regards to a controlled quantity of proteins in the diet.  I do see a lot of people on the internet making claims one way or the other, but never a citation to be seen.
Would anyone be interested in citing some references here so as to provide a more reputable resolution to this oft–repeated “fact”?
Unlikely as that would be, I'll post an answer here next time I check the university library.


text:
Why does the refractory period of neurons only allow signals to pass in one direction?
My textbook states that the advantages of the refractory period is that it means that action potentials are discrete and also that it results in signals only being able to pass one way,  but provides no explanation. Could anyone explain why this is?

The axon is an uniformly excitable structure; if you would stimulate an axon electrically somewhere in the middle, an action potential would be generated in both directions. Hence, an axon in itself does not have directionality.
Nonetheless, under normal physiological conditions, an axon  conveys action potentials from the dendritic region to the axon terminal, called anterograde signaling. The reverse direction, retrograde action potentials,  normally do not occur because signals arising in the dendritic region travel unidirectionally to the terminal. The reason why an action potential travels unidirectionally is because of the refractory period. Because the refractory period will cause the part of the axon that just generated an action potential to become unresponsive, the traveling action potential cannot generate another action potential in the retrograde  direction, because the only excitable region available is in the anterograde direction to the terminal (Fig. 1).

Fig. 1. Refractoriness. source: University of British Columbia
As an analogy, it's like a car driving across a road and throwing a temporary road block behind it that first has to be taken away before the road can be used again. This means that when a car leaves the parking lot and enters the road, it can never go back,  because it throws up road blocks that prevent it to return the way it came.


text:
FPLC based separation of serum proteins
I am working on a project which involves bio-marker discovery in neuro-developmental disorders. I have an akta-prime FPLC instrument in my lab but I do not know how to use it.
According to theory, plasma, or serum, normally contains numerous proteins of high molecular weight — which might mask the concentration of small-molecular-weight proteins that could be relevant to my study.
I am looking for the abnormal expression, if any, of such protein molecules.
But I am concerned that if I run the serum sample directly, I will get too many bands to allow me to identify my desired molecule.
Which column should be used to separate such masking proteins from serum — or, alternatively, what previous separations should be done?
Also, what reagent concentrations should I use (particularly re: binding buffer and elution buffer)?

Firstly, may I suggest 2D electrophoresis as a technique for identifying differences in protein/marker expression levels. This technique will give you greater resolution and ease of comparing your sample in basically one step/experiment. Added bonus once you determine your protein of interest you can easily excise it and send for mass spec analysis to identify your protein. In short, 2D electrophoresis separates protein based on their pI(isoelectric point) in 1st Dimension and then by their size in the 2nd Dimension. Once you identify the protein of interest you can purify it using the below steps.

Image Source
Now onto tackling the problem of separating your proteins for analysis. The general outline you can follow to separate a protein, is a follows:

Ion Exchange Column
Hydrophobic Interaction column (HIC)
Size-exclusion Chromatography (SEC)

Ion Exchange first because you elute the protein off the column using increasing concentration of salt (0 --> 1M of NaCl). Whereas you need a high concentration of salt to load the protein onto HIC column. So, the elute from setup 1 can be easily spiked with a 5M (Nh4)2SO4 and loaded onto HIC column (No dialysis). Also, Ion-exchange and HIC are high capacity columns whose resolution can be improved with shallow salt gradients.Hence my recommendation to be used first. However, if you are certain your marker/protein of interest is small you can directly use SEC column
Ion exchange column, as the name suggests, separates protein on the basis of their charge (Least ---> Most Ionic, also note charge +/- of the protein at that pH matters). The buffer to use for Ion exchange would be:
 1. Binding Buffer
    10-50mM Phosphate Buffer pH7.4 (plasma pH)
    0-25mM NaCl
 2. Elution Buffer
    10-50mM Phosphate Buffer pH7.4
    1M NaCl

Use low salt as possible to get the most efficient binding to the column.
Elution is done with a gradient of NACL from 0% of elution buffer to 100% Elution over about ~20 column Volumes.
HIC column separates the protein on the hydrophobicity of the protein. The order of the elution from the column is least --> most hydrophobic.
1. Binding buffer
    10-50mM Phosphate Buffer
    1M (Nh4)2SO4
 2. Elution Buffer
    10-50mM Phosphate Buffer
    (No Salt)

You can find a good protocol for HIC here. The elution is also done over ~20 CV with a gradient of 0-100% elution buffer, similar to Ion exchange elution.
Finally, size Exclusion or SEC separates proteins based on their sizes. The elution order is biggest ---> smallest size. The column is run in an isocratic mode i.e only one buffer used.
Buffer composition:
1. 50-100 mM Phosphate Buffer
2. 150mM NaCL

The salt in buffer is to prevent non-specific interaction of the protein with column, which might result in protein eluting later than necessary. This might result in poor resolution.
The most important thing to realize is each of the above column have their own sets of cavets. 1) Ion exchange columns are specific to the charge of protein, so you will end up having a lot of protein not binding to the column at all based on type (anion/cation) of column used. 2) Similarly, HIC column might not bind well to your protein as well. Also, adding 1M (Nh4)2SO4 will precipitate proteins which might include your protein of interest. 3) SEC columns have an upper limit on protein size they can accept, above which all the protein elute together at the void volume decreasing the resolution(However, this shouldn't be a problem in your case as you trying to separate out the lower molecular weight protein from the higher weight ones.)
Finally, all the above step work great considering you know the protein you are looking to purify(separate). Since that is not the case you will have to collect and run SDS-gel Electrophoresis of the fractions at each column purification stage. Also, run a side by side comparison of control and sample plasma to figure out which protein is being expressed differently.
In closing, I would like to point out that 2D electrophoresis gives you a gel to compare, as shown in the pic, anyway. So it might be a better solution to your problem. However, I do admit you might have to setup purification to confirm your findings.
Hope that helps, good Luck!


text:
Are Nilaparvata nymphs winged?

Source: nbair.res.in
I'm wondering if the first individual on the left is a nymph. Even if not do Nilaparvata sp have wings in nymphal stage?
I'd appreciate any authentic source for reference.

The family-level identification I had given I now see was unnecessary; the Wikipedia site for an economically important member of the genus (there called the Brown planthopper) is here: https://en.wikipedia.org/wiki/Brown_planthopper.  The species covered there has long- and short-winged forms; other members of the genus are probably similar.  All of the individuals in the photograph above are adult.  A late-instar nymph will have wing pads (not yet wings) which are fused to the thoracic segment to which they're attached (a life-cycle diagram with drawings of two nymphal instars -- there are probably more -- is found here: http://www.cpsskerala.in/OPC/pages/ricePestbrownplant.jsp [the eighth slide]).
 So nymphs and short-winged adults won't be flying out of danger -- they'll be hopping away.

So the one on the left's a pre-adult (may be? of short winged form)? Comparing with the wings of short-winged Nilaparvata sp (Photograph-6) it's wings look different, too much gap between them.

The different colors of the animal's body and the wing makes me think that if the left-hand example is still a nymph (I'd have to test that idea on a local species--we're on opposite hemisheres) it reached adulthood within a day or two of the photo being taken (either wing-length form would still be possible).


text:
Is nucleosomal DNA ever degraded?
A hallmark of apoptotic DNA fragmentation is the digestion of DNA into individual nucleosomes. In addition, in the following experiment that tried to isolate the components of the nucleosome, the micrococcal nuclease only cleaved the linker DNA and not the nucleosomal DNA.

I've tried searching the internet but I couldn't find a clear answer to my question. Is nucleosomal DNA ever degraded? Are there nucleases that degrade it, and if there are, are they common? If nucleosomal DNA is not degraded, what protects it? The histone proteins?

Are you specifically looking for a nuclease that cleaves DNA wrapped around the histone octamer or is your question why does such DNA not normally get degraded? Or both? Generally the histones proved a stearic barrier to nuclease digestion and so protected DNA is not degraded, but I seem to recall that both DNase I and MNase are capable to nicking such DNA at a low rate.

Heat the sample which will denature the histones then add excess nuclease and it will be degraded. Even if you add a large excess of micrococcal nuclease it will degrade nucleosome-associated DNA. For DNase assays, the amount of DNase has to be carefully titered to get just linker DNA degraded

@canadianer More of the latter, but both if possible.

Nice question! Nucleosome is quite a stable structure because of electrostatic attractions between the phosphate group of DNA and Lysine or Arginine of histone octamer1. In fact, both histone and DNA are known to protect each other from degradation: histone protects DNA from some kinds of damage2 and DNA protects histone protein from proteolysis3. Also, the histone protein gets modified whenever there is damage to nucleosomal DNA, so that DNA repair machinery can be activated4. Thus, nucleosome is not only structurally stable, but also tries to maintain its stability by its constituents protecting each other.
source
This stability has also been taken to a whole new level. In a research paper, scientists predicted that the reason for discovery of thousands of years old DNA, in intact form, is due to the stability of nucleosome5. They have even predicted that nucleosomal DNA can remain readable for even millions of years, because the time when histones start degrading is also the time when proteases and nucleases degrade, leaving very few chances for DNA to degrade.
But, nucleosomal degradation is not impossible. In a research, scientists concluded that the enzymes Caspase Activated DNase (CAD) or DNA Fragmentation Factor 40 (DFF40), together called CAD/DFF40, are indirectly required for degradation of nucleosome6. See this paragraph (I only pasted the main points):

We report here that in response to apoptotic signals from a death receptor (CD95 and tumor necrosis factor-$\alpha$) or mitochondrial (staurosporine) apoptotic stimulus, the core nucleosomal histones H2A, H2B, H3, and H4 become separated from DNA during apoptosis in Jurkat and HeLa cells and are consequently detectable in the cell lysate prepared using a non-ionic detergent. The timing of this histone release from DNA correlates well with the progression of apoptosis...Taken together, these data demonstrate that CAD/DFF40 functions indirectly in mediating nucleosomal destruction during apoptosis...In this study, we have found that core nucleosomal histones separate from chromatin in apoptotic cells, but that this is not simply a by-product of DNA fragmentation. This event is indirectly related to CAD/DFF40 in the sense that CAD/DFF40 is required but is insufficient for the apoptotic histone release.

Thus, though it was the only paper I could find, nucleosomal DNA can also degrade in the same way as linker DNA if larger amount of CAD/DFF40 is present to degrade it.
References:

Histone structure and nucleosome stability; Leonardo Mariño-Ramírez, Maricel G Kann, Benjamin A Shoemaker, and David Landsman
Nucleosomal histone protein protects DNA from iron mediated
damage; Helen U.Enright, Wesley J.Miller and Robert P.Hebbel
Actin and DNA Protect Histones from Degradation by Bacterial Proteases but Inhibit Their Antimicrobial Activity; Asaf Sol, Yaniv Skvirsky, Edna Blotnick, Gilad Bachrach, and Andras Muhlrad
Histone - Wikipedia
Degradation of ancient DNA; Zvi Kelman, Lori Moran
Apoptotic Release of Histones from Nucleosomes; Dongcheng Wu, Alistair Ingram, Jill H. Lahti, Brie Mazza, Jose Grenet, Anil Kapoor, Lieqi Liu, Vincent J. Kidd and Damu Tang


text:
How does salt concentration affect chromatin compaction?
I've read that the primary obstacle to the compaction of chromatin is the negative charge on the DNA phosphate-sugar backbone. This negative charge is slightly stabilized by the positive charges on histone proteins. In solutions with high salt concentrations, chromatin adopts a more condensed state, whereas in solutions of low salt concentration, chromatin is less condensed. The explanation I found was that cations from the salt help provide additional stabilization to the negative charges on the DNA molecules—thus, solutions with higher cation concentration promote greater condensation of chromatin.
But what about the anions in the solution? A solution must be electrically neutral; when salt concentration increases, the concentrations of both cations and anions increase. Even if the salt cations stabilize the DNA's negative charge, won't this be perfectly offset by electrostatic repulsions between the DNA and the salt anions?

I think the 'whereas' part is excessive and misleading - I'd say "Higher concentration results to more condensed state".
So charge of DNA + solution will be the same but it will be distributed differently:
$$ D^{-} + nK^{+} + nA^{-} \rightarrow (D^{-}+mK^{+}) + (n-m)K^{+} +nA^{-} $$

Could you explain what the symbols in your formula mean?

D - DNA, K - cation, A - anion, n - number of water molecules, m - number of attached to DNA cations.


text:
What is the cell matrix?
What is the matrix in the cell, and how does it connect cells together?
I read about this in my textbook. I know that a matrix is the material (or tissue) that connects other cells together. My book says:

In biology, matrix (plural: matrices) is the material (or tissue) in animal or plant cells, in which more specialized structures are embedded, and a specific part of the mitochondrion that is the site of oxidation of organic molecules.

This wording feels very complex, and I'm having trouble picturing what it's trying to describe.

Where is the quote from?

Maybe the full sentence would help. Anyways, the quote seems to refer to organells and not to the extracellular matrix

Maybe the OP is referring to the matrix of mitochondria

The text passage you quote refers to the mitochondrial matrix (https://en.wikipedia.org/wiki/Mitochondrial_matrix). The thought you describe before is about the extracellular matrix (https://en.wikipedia.org/wiki/Extracellular_matrix). Besides being called "matrix" the two don't have much in common. Be aware that "matrix" also describes very different things, e.g. an embedding matrix used to prepare samples for SIMS (secondary ion mass spectrometry).

Cell matrix is the matrix of the cell

The quote (which you more likely got from Wikipedia) discusses multiple types of matrices.
Let's break down the quoted definition:
The general definition of a matrix would be "an environment or material in which something develops; a surrounding medium or structure." In biology, we think of a matrix as a material, tissue or area in which more specialized structures (molecules, cells, organisms, etc.) are embedded.

In animals or plants, the matrix is often describing a material or tissue.

The nail matrix is the layer of cells that your fingernail or toenail sits on that actually produces the nail.
The extracellular matrix (or ECM) consists of a collection of extracellular molecules secreted by cells that provides structural and biochemical support to the surrounding [more specialized] cells. One very familiar example of "matrix" tissue is connective tissue.

Here's a video from Khan  Academy's Youtube channel to walk you through this a bit.  And here's a more graphical walk-through explaining extra-cellular matrices.

The cytoplasmic matrix (aka cytosol) is the liquid found within cells in which organelles reside. It constitutes most of the intracellular fluid (ICF)

The mitochondrial matrix, a type of cytoplasmic matrix, is the fluid within the inner membrane of a cell's mitochondria that splits it into numerous compartments. This viscous "space" contains the mitochondria's DNA, ribosomes, soluble enzymes, small organic molecules, nucleotide cofactors, and inorganic ions; it is also the site in which oxidation of organic molecules occurs.

So whats this look like under a microscope? Here's an image of a mitochondria and surrounding cellular cytosol under an electron microscope:

In ecology, a matrix is the general area in which your population, community, or habitat "patch" exists within. In other words, Matrix is the "background ecological system" of a landscape with a high degree of connectivity.

Is this how actually the matrix and cells look like when we put our skin on a microscope?

@OkamaKsakas I've added an image of these cellular matrices as seen under an electron microscope.