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Where are the evolutionary "inbetweeners"?
The problem I've always had with evolution is the actual lack of variation between animals. More specifically, the lack of observable gradual change between species.
Take for example the hammerhead shark. It obviously has a strong connection with a normal shark, but where's the "half-hammerhead" shark? Where's the species that only has a SLIGHTLY wider head?
I really doubt that a single mutation on a normal shark resulted in a head shaped like that, it had to happen gradually. Right? As far as I understand, evolution works by random mutation in a child being somehow slightly beneficial to that animal so it get's to live longer and reproduce more, eventually resulting in it's genetic material in dominating the inferior ones before it. But if it was for whatever reason beneficial to have a slightly wider head, why don't all the sharks have slightly wider heads now? On the other hand, if it wasn't beneficial, how come the hammerhead still exists?
Furthermore, I feel like some characteristics of a certain animal can't really have gradual benefits. There's a lizard that shoots blood out of it's eyes. The original ancestor certainly didn't, and I'm sure that if it's child only bled slightly from it's eyes it wouldn't really help if much in life. So for it to actually become beneficial, it seems to me that there had to be a ton of lizards that had a disadvantage of bleeding slightly. In fact, there had to be so many that they evolved even further in the same direction and kept doing that until they bled so much it's an actual benefit (sorry for this turning so gross). So why did the inbetweeners survive long enough to evolve even more, and why did they THEN die out?

The fossil record in general contains transitional forms for some animals and not for others. Since geology and other factors enter into this, I think one has to choose a specific animal and ask why the fossil record might be deficient. Where would we find a transitional hammerhead shark, for example?

My question isn't about fossil evidence. It's about why those species aren't here TODAY. Or if they aren't because they're extinct due to their inferiority, then how did they live long enough for the superior species to evolve from them?

Have you studied the variety of hammerhead sharks? Do they all have precisely the same proportions? Even checking the Wiki entry, it indicates the winghead shark has the most pronounced cephalofoil. That would mean others are much less so. So there are gradations. It may not be a perfect spectrum but it may be that intermediates were poorly adapted.

Obviously not, but are you claiming there are species species of regular head to hammerheads and everything in between? I've also mentioned the lizard. Again, I don't know if all of those lizards perform the same. That's not what my question is saying.

Remi.b asked my next question for me. If there were only two grades of hammerhead would you insist on the two intermediates? And if there were four would you insist on eight, one between each gradation?

I am surprised to see that messy, unanswerable and very broad questions in evolutionary biology are often easily upvoted! I voted to close expecting the OP to ask his questions more clearly in two separate posts as it has been discussed below

I'm closing this according to our policy on creationist questions. If you're interesting in understanding evolution you're welcome to ask here. Questions that simply state the common creationist talking points will be closed.

The rostrum of a dolphin is control by the duration of promoter activity of a single gene. The gene is identical. But the longer the promoter is active, the longer the rostrum (and number of teeth in it). It is amazing that the length of such a complex structure is not even cause by genetic mutation to a gene but a mutation to the promoter sequence of that gene, which is not protein coding.

More specifically, the lack of observable gradual change between species.

Most significant phenotype differences occur over several thousand generations, which means several thousand years on up. While we certainly can create experiments where a controlled form of evolution occurs within a very small time-frame, I'm going to assume that you're not interested in closed laboratory experiments given the nature of your question.

It obviously has a strong connection with a normal shark, but where's the "half-hammerhead" shark? Where's the species that only has a SLIGHTLY wider head?

The data below does answer you question, but in reverse. Hammerheads are much older than most of their relatives; so their cousins have actually grown smaller heads... but there are certainly intermediates.
From Andrew Martin (1993 - mtDNA data) via Elasmo-research.org:
*The circles represent the head-width vs. body-length ratio.

Martin's conclusion: "...the hammer appeared rather suddenly and fully formed, and was later optimized along different lines to suit various selection pressures."

I really doubt that a single mutation on a normal shark resulted in a head shaped like that, it had to happen gradually. Right?

Not necessarily. Single Nucleotide Polymorphisms (a.k.a. - "SNPs" - a change in one nucleotide) can have pretty wide-ranging effects.
The vast majority of humans, for instance, are lactose intolerant in adulthood. However, lactose tolerance evolved twice from two different SNPs in two different human populations: One European and one African. One gene. One regulatory mechanism change. Massive benefits (essentially opening up a whole new resource in adulthood).
Significant differences in phenotypes (the physical appearance of something) can require more gene mutations, or not. It depends on where the mutation is in the genome and what the gene does.

But if it was for whatever reason beneficial to have a slightly wider head, why don't all the sharks have slightly wider heads now?

The simple answer is because either there wasn't enough selective pressure that the rest of the shark phenotypes succumbed to that the hammerhead avoided, or that the hammerhead design doesn't give enough of an advantage to completely dominate the gene pool. An alternate, but more abstract answer, is that there simply hasn't been enough time for the hammerhead design to dominate the shark phenotype. Remember, evolution works by generations - not years. It would take unknown thousands of generations for a weakly-advantageous design to dominate an entire niche - if it ever would.
Also, it is worth it to point out that evolution doesn't only select for advantageous mutations. Mutations that aren't very detrimental can still exist within a population as long as the detriment doesn't prevent resource exploitation and offspring production. Think Huntington's Disease which severely restricts a person's survivability, but only after their mid-30's (in general) - plenty of time for the person to have sex and raise a kid into semi-adulthood. It is a genetic defect which sticks around only because it allows humans to reproduce before it seriously affects them.

The original ancestor certainly didn't, and I'm sure that if it's child only bled slightly from it's eyes it wouldn't really help if much in life.

Maybe, maybe not. Maybe it shot something else before blood, and then a mutation caused it to shoot blood instead - but the overall effect (deterring predators) was the same so it doesn't really matter.
You're correct that some traits might appear very awkward if they had evolved gradually, but the question then becomes: Did they evolve gradually? Sometimes we simply do not know.

So why did the inbetweeners survive long enough to evolve even more, and why did they THEN die out?

Like I said above, just because a trait is detrimental doesn't necessarily mean it will be eliminated. As long as the being can survive long enough to reproduce successfully with the trait, the trait might not be eliminated for a very, very long time- if ever.
As for in-betweeners dying out - it's difficult to think of it like that. You're talking bout LCAs ("Last Common Ancestors") of extant (currently-living) species. While some LCAs just die out for some reason or another, it's more common that the LCA simply continued to evolve and become a genetic relative due to some sort of isolation.
Think of it like the in-betweeners coming to a fork in the road. Some choose right, some choose left. There isn't anybody left behind - merely two populations that are changing over time that were once one group until they don't really mate between each other anymore (or can't). Heck, even Biologists have trouble deciding at what point a population is considered a different "species" because of discoveries in the last 50 years - so right now a firm answer like "It takes 15% of the genome to change for a new species to emerge" isn't possible as it doesn't really work like that.
We'll get to it eventually, but for the time-being, it might be easier to say that everything currently living on Earth is an in-betweener of something else in the future. Everything in its current iteration will eventually die off, but not before something else emerges from our offspring which may or may not be significantly different from us due to however many genetic mutations our offspring have from us. It could be one that opens up a whole new realm of possibilities (like lactose tolerance) or an accumulation due to selective pressures (like Phoemelanin production and pale skin in humans [Redheads] to produce more Vitamin D3 at higher latitudes).

Your shark head diagram sort of says it all.

This sounds like a very basic question in evolutionary biology that often ask for a very long answer. But I think that you may get the answer you're looking for just if we ask you back how many inbetweeners would you expect to exist between the hammerhead shark and whatever is the closest currently living species of the hammerhead shark? If you had one more inbetweener would you still be surprised to not have more inbetweeners?
Your question might actually be "Why are there species rather than individuals that show a long continuum of various traits?". If this is your question, then the answer would indeed need to be fairly long and explain about the process of speciation.
You might want to have a look at this related post as well.
Edit
Studying a bit further the question of the hammerhead sharks, I discovered that there are actually 10 species of hammerhead sharks! You can find them here on the french wikipedia page
Let us know whether this comment/answer helped.

This is a great question (in the first para.). I don't usually upvote comments but +1.

Actually, yes. I would ask the question. Why isn't there a continuum of species? Why are there species at all? If the answer is long I'd appreciate if you could point me to some useful links so I could read more about it.

But I'm still not sure if this answers my original question. How did the blood shooting lizard get to be if for it to exists there had to be lizards that just bled from there eyes slightly? Any intuition tells me that those species would die out in a generation, let alone thousands of generations required for evolution to make the bleeding even stronger.

So, basically your post can be decomposed into 2 questions. 1) Why are there species rather than a continuum? 2) How can a trait evolved while the intermediate trait seems to be deleterious (deleterious=negative effect on the reproductive success and survival of the carrier). Did I understand your post correctly? If yes, I'd suggest you to split your question into two new posts (vote to close the current post in parallel). Note: The second question being fairly common, there might already has a post on this site that answers it.

Yeah. That's exactly right. Thank you for organizing my thoughts.

I know how hard that is to ask good questions when entering in a new field of knowledge $\ddot \smile$. I vote to close and am looking forward your coming posts!

What about developing a standard answer for questions like this which are too broad? You have almost done this and I think this is the right approach. Otherwise someone tries to answer and others try to close. Better yet, a standard comment with a list of basic texts?

How would you create a standard answer that fit all these "kind of broad questions"? We may want to discuss that in MetaBiology.SE. I am leaving soon I may not answer quickly to this discussion! Cheers!

@Remi.b I have posted a new question here: http://biology.stackexchange.com/questions/19762/why-are-there-species-instead-of-a-continuum-of-various-animals
And could you point me to those other questions that ask about deleterious traits? Or at least, what to search for.

@Darwin, you should read about something called a ring species. ie A continuous gradient/chain of populations that freely allow gene flow between adjacent population. However if populations at the ends of the chains are brought together, they cannot breed. The ends of the chain are different species... yet so long as every population in the chain is alive we have a something that could be considered a single species as gene flow while slow, is possible between the population of two ends via the intermediate populations.

However once one or more population in the ring goes extinct, the ring fragments and you get two or more species.

If an inbetweener offers a slight advantage to survival, and if the full-fledged trait even more so, then once the full-fledged population becomes sufficiently large, they will have the advantage and the inbetweeners will die out.


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How did the horned lizard evolve?
It's a lizard that has the ability to burst blood vessels in it's eyes and shoot blood as self defense.
How can this behavior be explained evolutionary? Wouldn't it mean that there had to be some intermediate evolutionary step where the lizard could bleed from it's eyes only slightly? How did that not cause it's extinction?
To generalize more, how does a specific trait evolve when it seems the intermediate traits are detrimental to survival?

I like this question. Hope someone has a good, scientific answer.

each specific case is a separate question.

@user813801 I'm asking this about this specific case then.

The behavior can be explained evolutionarily just like any other trait. It came about either through adaptation, neutral evolution, or as a by-product of another adaptation.
An intermediate step, like the one you suggested, is not required. But if it did occur, there's no reason to believe that such a trait would cause extinction. Bloody eyes, whether they squirt or not, could be beneficial in some species. We know that blood-squirting eyes appears to be a defensive trait. Take away the ability to squirt and the blood could provide defense in some other unexpected way, or it may have had nothing to do with defense at all. Maybe the blood was just a lubricant before, or maybe the blood somehow enhanced vision during a stressful event. Or maybe it was just there and didn't do anything; nothing good, but nothing bad.
There's nothing special about this lizard. It does have a unique trait, but there's something novel in every species.

I'm speculating here, but it's likely that the taste of the blood has something to do with this. The blood of the horned lizard tastes foul to feline and canine predators. Therefore, a small amount of blood leaking out of the eye might put predators off immediately after the first attack, if that attack was aimed at the head.
Obviously, this is an advantage for the lizard, but since a large percentage of attacks to the head would result in debilitating injuries, there is a selective pressure to take this further so that the taste of the blood is "communicated" to the predator before the initial attack.

There isn't always an intermediate step like "oozing blood eyes", I suspect that this particular trait is pretty easily explained by having an area of weakness in a blood vessel that made the lizard bleed under high stress situations.
maybe in early version the lizard had to get some trauma or could intentionally hit its head on a rock or something... I don't know, but it doesn't really require any novel structure.

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Why are there species instead of a continuum of various animals?
As I understand it, various animal traits have to evolve gradually, but what happens to the species that are "neither here nor there"?
To put it differently, if a species evolved from another, it did so because it's somehow better, right? So why are there examples of the original species not being extinct?
What factors determine weather some species "stick"?

"if a species evolved from another, it did so because it's somehow better, right?" Evolution doesn't make species better. Evolution makes species.

There is a continuum occasionally, e.g. so called 'ring species'.

It's a fallacy to say evolution happens gradually.  Many forms of evolution involve the combining of two or more species together, which transforms their abilities.

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

Actually, the tree of life is a continuum of animals. Species is just a convenience for us to name and group those animals by their shared traits and whether they can or cannot interbreed.

Here is another post that may be of interest. Among other things, it talks about ring species

@BrianS I don't think that is quite true. If there is any selective pressure at all (and rarely there isn't) then the species will evolve to become better at proliferating in that environment. (of course, the environment may suddenly change and render all that specialization in vain)

Short answer

Why are there species rather than a long continuum?

Three important reasons I could think of are sex, non-uniform adaptive landscape and ancestry.
Long answer
I am not sure I'll answer your question so let me know if I miss your point or if I help!
To start with, you might want to read this answer on the semantic difficulties behind the concept of species

What factors determine whether some species "stick"?

Natural selection is nothing but differential fitness (fitness is a measure of both reproductive success and survival) among genotypes within a population. Individuals having greater fitness will leave more offsprings and therefore the genes of these individuals increase in frequency in the population. There are few generalities to be made about what phenotypic traits are beneficial in a given population. For example, "white fur" is a very good trait for a polar bear but would highly deleterious for a mealworm.
However, there is a thing called species selection wherein a given lineage at least, it is possible to identify specific traits that seem to either reduce the extinction rate or increase the speciation rate. This is, for example, the case for polyploidy in angiosperms (Whitton and Otto, 2000)

if a species evolved from another, it did so because it's somehow better, right?

If you observe different extant species you cannot say that any of these species evolve from any other one you can today observe. The correct way of looking at two species is that they share a common ancestor in a given past. Therefore, looking at a cat and a blue tit you cannot say that one species evolved from the other one but you can only say that these two species share a common ancestor (just like any other pair of species) that was neither a cat nor a blue tit. The example is obvious because cats and blue tits are "not so closely related" (everything is relative) but the same logic holds for any pair of species.

Why are there species rather than a long continuum?

Sex
The simplest and most obvious reason why there are species within which individuals are more similar compared to each than to individuals from other species is due to the definition (the most common definition because different definitions exist!) itself of a species. A species is a group of individuals that can interbreed. See this for more info on the concept of species.
Take two originally different groups of individuals and allow them to interbreed. Their traits will mix up and you won't be able to tell two different groups apart. All individuals within the new mixed group are a mixture of the individuals from the two previous groups (under some circumstances this process has been sometimes called "reverse speciation"). If now you take one single group of individuals. You split them into two groups in the sense that you don't allow individuals from group 1 to mate with individuals from group 2. You will see that after some evolutionary time, the individuals of group 1 will tend to resemble much more to individuals of group 1 (its own group) than to individuals of group 2. If you wait long enough so that these two groups of individuals become different enough so that they can't interbreed any more because they diverged too much, then you have what is called a reproductive isolation and under the common definition of species, you can say that a speciation (You may want to have a look to the wiki article for "speciation") occurred and therefore you have two new species instead of one ancestral species.
why the two groups tend to diverge through times?
You may wonder "But why the two groups tend to diverge through times?". There are several processes that explain that divergence:

Mutations

Different mutations occur in the different groups (just by chance)

Natural selection

The environment differs and the selection pressures differ selecting for different traits in the two species. Also, the accumulation of different mutations affects the selection pressure at other loci.

Genetic drift

Shortly speaking genetic drift is due to random events. Different random events occur between the two populations. For more info about genetic drift, see this post

If you are not very familiar with these concepts I recommend that you have a look at Understanding Evolution (UC Berkeley).
Adaptive landscape
Note also that there are other reasons for explaining this pattern. One other reason is "Because the adaptive landscape is not a flat function". What this means to the layman is that there are some combinations of traits that cannot really be beneficial.
Ancestry
Also, individual phenotypes are not independent of each other and not only for ecological reasons but also because of shared ancestry. If you consider two families, you will easily accept no to see a continuum of phenotypes but two distinct groups (maybe in one family curly hair is common while in the other they all have straight hair).

Mathematician/computer programmer's answer here:
There is a continuum of different animals — in fact it's pretty fair to say that every animal occupies a different place on this continuum. They're just not uniformly distributed over the continuum; they're clustered around forms that are most likely to survive and reproduce, and the lowest-energy paths between them.
This is because evolution is basically a stochastic optimization algorithm, one that finds the "best" set of parameters for maximizing some function by randomly perturbing an initial set of input values. In fact, some of the best optimization algorithms today are based on ideas drawn directly from evolution and called "evolutionary algorithms".
In mathematics, given enough time, these algorithms will all converge on one optimum solution and nothing else. Why isn't it like that in nature? Because in mathematics, the "fitness function" that we're optimizing for stays the same for a given problem for as long as the algorithm runs. It represents the specific problem we're trying to solve. In nature, there's no outside force imposing a fitness function; an organism's survival depends on millions of factors in its environment which change over time, many of which depend on the survival and properties of the other organisms in its environment (competition, symbiosis, predator/prey relationships, etc.) This is a chaotic system so complex that it could easily go for billions of years without reaching a steady state, and even if it did, external changes (like the odd asteroid impact, to use an extreme example) would still come around to shake things up.
Another reason for the clustering is because a lot of the "intermediate states" in the genetic space have a fitness of zero — these are the states between species that can't interbreed, or that have sterile offspring. The categorization of "species" is based on this, and although it's not exact, it's still generally true that the more different two creatures are, the less likely they can have viable offspring. This makes evolution more likely to explore the spaces near already-successful organisms, and less likely to produce radical new things by hybridization.

Genetic circuit design is a similar idea. The power of the nested loop gives a lot of insight into long processes. + 1

I like your last (5th) paragraph. I would however think that this very "selectionist" argument is weak compared to the consideration of random processes and spatial isolation.

I am not sure I totally get how your 4th paragraph really addresses the question "Why aren't individuals distributed uniformly along the axes?". Seems to me that you mostly answer why not all populations may not reach an optimum. And I am not sure whether it is really wise to say "there's no outside force imposing a fitness function". Sounds a bit wrong to me (although I agree that we should include the social environment in the fitness function).

hobbs's answer I think best answers the question of discontinuity. The species landscape is directly shaped by the environmental landscape (natural selection). And the niches comprising an environmental landscape are discrete. The shape of the interface between these two landscapes is always changing. Biology would rarely (if ever) speciate in an unchanging and uniform environment. Species diversity increases with the number of features in the environmental landscape. However, some species (e.g. people) can adapt to dominate multiple niches, reducing diversity.

I disagree that "given enough time, these algorithms will all converge on one optimum solution". It's easy to imagine that there is an evolutionary algorithm that never converges to the optimum solution.

Could you support the statement "some of the best optimization algorithms today are based on ideas drawn directly from evolution" with an example of a problem where an evolutionary algorithm is better than any other currently known algorithm? (I think it's hard to find one.)

Re "these algorithms will all converge on one optimum solution and nothing else", that's not exactly the case.  Rather, they will tend to converge on various local optima, so you try (with e.g. simulated annealing) to inject a degree of randomness that can kick the convergence out of those minima.  Which is really like evolution: a group of species converges around some optimum, and can persist for a long while before some random event - say an asteroid impact in the Gulf of Mexico - jolts the system out of that optimum and eventually into a new solution.

@jamesqf I agree entirely. Better to say that we hope to find a global optimum in the mathematical setting. There are other bits of this answer that I'm not entirely happy about either. But I'm not sure how to make it more accurate without making it distractingly wordy :)

Nothing happens to them. Organisms exist.  They breed with other organisms who are genetically compatible.  We humans might try to categorize them according to certain traits, but our labels are just labels, biology isn't governed by them.
Over time, we might see that a population used to have one trait, and its descendants no longer have it, they look different. Nothing earth shattering happened, no bright line was crossed, there was just a change in allele frequencies.

if a species evolved from another, it did so because it's somehow
  better, right?

No.  This is just plain wrong on your part.
It's just different.  Maybe it changed so that its traits better match the current environment, or maybe the change was random drift.  You can't easily categorize one species as "better" than another.

I like "better" put in context to "different". It may occur that "better" is in the inside of anything different. If a one species not different to the other specializes on worms only in their barn yard, it's "no better", but it will. It shall be forced with it, with how to fork that worms.

Typically when both new and old species still exist it is because evolution pushed the new one into a different habitat or role.
As a hypothetical example reef fish vs. deep water fish and their relative size.  Let's say deep water fish evolved into reef fish, but we still have deep water fish.  So there were deep water fish that were a little smaller than the rest of the deep water fish, and this gave them access to a new place to hide from sharks, shallow waters near reefs.  As time goes on this puts evolutionary pressure on the fish to shrink so as to better hide in the reef, those "neither here nor there" fish may have gotten some benefit from being near the reef but the smaller fish got even more benefit and eventually outcompeted the middle species.  Vice versa for the deep water fish vs this middle species. It was not as good in deep water so it was outcompeted there as well.  This continues until evolution has separated them into two new species.
edit:

What factors determine whether some species "stick"?

Evolution optimizes for the current environment, as long as that environment is stable and the species is a good fit for it then there is little pressure to change. If the environment changes then a species will adapt to it. Here environment is everything relevant to the species: predators, food availability, weather, everything that impacts their life.

Organisms on Earth did not evolve in a homogenous environment. A critical part of speciation (when you go from a single species into two or more) is a reproductive barrier.
This can be a literal, physical barrier - mountain range appears between two populations, valley in the middle of habitat floods and isolates the two halves of the population, a small group is thrown by some catastrophe on a remote island and cannot escape, etc.
It can also be a genetic barrier: Imagine a bird species where males compete for mates with their bright blue crests, and rare mutations occasionally lead to red-crested males which cannot mate at all. If some female birds happen to mate with undesirable red-crested males for a few generations, two parallel sub-populations may develop: Birds which prefer red crests and bird which prefer blue crests. These populations may be very unlikely to interbreed.
There may be more complicated ways of erecting a barrier. For instance, a population of flowering plants that could previously interbreed arbitrarily may find that the ecosystem has experienced some crisis, and now the pollinating insects have become fastidious and only visit certain flowers and not others. Another example: While humans are currently a single species, because of culture (eg. language) certain human subpopulations (such as European nations) are much more likely to breed within themselves than between themselves.
Regardless of how the barrier comes to be, once a barrier can separate a species into sub-populations, the machinery of speciation is set in motion. All species evolve over time in different ways, especially if their environment does not have a very long history of unusual stability. As populations evolve, they try to stay somewhat coherent - the changes tend to be such that they still permit everyone in the population to mate with each other; otherwise they would impose a fitness cost.
However, if two subpopulations are not in contact, there is nothing enforcing compatibility between them. Therefore, as evolution does its work, these are free to wildly diverge from each other. Recall the example of the bird species in which males with blue crests enjoy reproductive success. The color itself is not particularly important, but it is important that the males all have the same color crest and the females prefer the same color. So as these birds evolve, the crest color can slowly drift in hue.
Now let's say you took these birds, and set a few of them free in one continent, and another group free on another continent. Again, over time, the crest color will shift. However, there is nothing stopping from the color in continent A from shifting to red while the color in continent B shifts to green. There is, after all, no advantage to being compatible with a population you are not in contact with.
The example above is largely behavioral, but non-behavioral examples are also possible. A very fundamental process is fertilization: Eggs have an ECM made up of proteins unique to that species, while sperm have enzymes to digest the coat of their own species. Because of this, cross-species fertilization is very difficult. Again, once you erect some kind of barrier between two populations, the systems of coat proteins and enzymes in the gametes of either population may evolve in divergent ways - they evolve in small steps, so that the interaction partner protein can always keep up, but compatibility with the isolated population is not selected for, and if the isolated groups are reunited after a very long time their gametes may end up becoming unable to fertilize each other.

Yeah, to me it's diploidity that saveguards that what is good becomes only better, not different.

I shall introduce you to the phenomena called ring species
Examples include gulls, Ensatina salamanders, house mouse, etc
A ring species is a series of adjacent populations that can interbreed with each other.
Say population A, B, C, D, E.
A can interbreed with B
B can interbreed with A and C
C can interbreed with B an D
D can interbreed with E

All very good. Sounds like a regular species. But here is the weird part. The populations furthest from each other cannot interbreed. ie Population A cannot interbreed with Population E.
A and E are by definition different species.
And yet, population A and E are linked, genes can flow between A and E via adjacent populations.
What is most likely happening is that there is a gradual change in gene variation between populations, so that there is gradually increasing barrier between successful hybridization. This barrier increases until the terminal ends of the ring cannot hybridize.
Furthermore, if any intermediate population within the ring were to go extinct, and break the ring, the two ends of the ring would become two separate species.
A ring species is a snapshot of one species that is one local extinction event away from becoming two species.

An even better example is where A and E CAN interbreed, thus closing the ring.

But that this not the definition of a ring species.

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How are new chromosomes replicated into the next generation via sexual reproduction?
If an individual has a new chromosome, which is very unlikely to happen, he will not have any luck in finding a sexual partner with this same trait. How will the offspring inherit this trait. And given that extra/fewer chromosomes are often undesirable traits (e.g. Turner Syndrome) how can it propagate?
I assume that humans and rats have different number of chromosomes, so a common ancestor must give a lineage where some individuals had a different number of chromosomes than their parents.

You are right that a person with an abnormal number of chromosomes will be unlikely to find an "equal" partner to mate with. This does not prevent a chromosome aberration from spreading though, and it is not necessary that the mutation is initially beneficial for it to spread. While it is true that many chromosomal aberrations may be detrimental and cause various syndromes, a chromosome split or multiplication may also be netural except for the matter of reproduction. A change in chromsome number will not be inherited deterministically, but can give rise to various new permutations in the offspring due to the mechanics of chromosome segregation during meiosis.
You can find a good explanation at Scienceblogs.com: http://scienceblogs.com/pharyngula/2008/04/21/basics-how-can-chromosome-numb/ :

The net result [of a chromosome split] is that although this
  individual is fine and healthy, a significant number of his or her
  gametes may carry serious chromosomal errors, which means they may
  have reduced fertility. They aren’t sterile, though; some of their
  gametes will have the full complement of genes, and can similarly
  produce new healthy individuals who will probably have fertility
  problems. (...)
  So our two chromosome individual will have a reduced fertility as long
  as he or she is breeding with the normal one chromosome organisms, but
  those split chromosomes can continue to spread through the population.
  They are not certain to spread — they’re more likely to eventually go
  extinct — but by chance alone there can be continued propagation of
  the two chromosome variant. Which leads to another misconception in
  the question: something doesn’t have to provide a benefit to spread
  through a population! Chance alone can do it. We don’t have to argue
  for a benefit of chromosome fission at all in order for it to happen.


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Why such strange enzyme kinetics?
I measured some enzyme kinetics in a practical course using a substrate-based FRET assay. Unfortunately some of my plots show weird effects. There was always a decrease in signal after 35 minutes. But the curve always regained.
During the whole measurement the plate was placed in the reader, and was heated to 37°C.

My question is: Does someone know how/why this effect occurs?
Thanks for your help!

Those points are within the error bars of the previous measurements, so perhaps they aren't statistically significant. How many replicates did you do?

Worth considering whether it is an effect of the instrument or the system. What would happen if you preincubated your plate for 10 minutes? Would you have the "dip" after 25 minutes or again 35 minutes?
I know our plate reader will want to calibrate its detector at some intervals, perhaps that coincidences with 35 minutes for your combination of variables?

In addition to these suggestions, running the samples on a different instrument could be informative.

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


text:
Difference between LIGR-seq and PARIS methods
I would like to reuse a dataset produced by LIGR-seq for ncRNA secondary structure prediction in the style of PARIS method.
At first glance, the methods appears to me to be very similar: use AMT for cross-linking, ligation of chimeric reads, sequencing.
Can anyone point-out the crucial differences between those methods?
Relevant papers I've found:
LIGR-seq - https://www.sciencedirect.com/science/article/pii/S109727651630106X
PARIS - https://www.cell.com/fulltext/S0092867416304226
Originally posted on Biostars (https://www.biostars.org/p/9507932/)

LIGR-seq

LIGR-seq (Figure 1A) employs in vivo crosslinking of RNA duplexes using the modified psoralen derivative 4′-aminomethyltrioxalen (AMT), which intercalates into RNA duplexes and, upon 365 nm UV irradiation, generates inter-strand adducts between juxtaposed pyrimidine bases (Calvet and Pederson, 1979). Following cell lysis and a limited single-strand S1 endonuclease digest, free RNA overhangs adjacent to duplexes are ligated using circRNA ligase. This ligase catalyzes the ATP-dependent ligation of proximal RNA ends and has optimal activity at elevated temperatures that reduce RNA hybridization. RNase R, a 3′→5′ exoribonuclease that digests linear and structured RNAs (Vincent and Deutscher, 2006), is then used to digest uncrosslinked RNA, thereby enriching AMT-crosslinked duplexes (Figures 1A and S1). Following reversal of crosslinks using 254 nm irradiation, the RNA samples are subjected to high-throughput sequencing to detect chimeras formed by ligation. To assess background ligation artifacts, uncrosslinked ("–AMT") samples are prepared in parallel, and unligated samples are used to determine the relative expression of transcripts forming chimeras for downstream normalization and analysis.

Summarized
AMT crosslinking ⟶ cell lysis ⟶ S1 endonuclease digestion ⟶ RNA-RNA ligation with circRNA ligase ⟶ RNase R digestion of uncrosslinked RNA ⟶ crosslink reversal ⟶ sequencing library preparation (adapter ligation, reverse transcription, etc.)

PARIS

HeLa, HEK293T, and mES cells were treated with or without AMT and crosslinked with 365 nm UV. Cell lysates were digested with S1 nuclease and RNA purified using TRIzol. Purified RNA was further digested with ShortCut RNase III to smaller fragments. RNA was separated by 12% native polyacrylamide gel and then the first dimension gel slices were further electrophoresed in a second dimension 20% urea-denatured gel. Crosslinked RNA above the main diagonal was eluted, proximity ligated with T4 RNA ligase I and photo-reversed with 254 nm UV. The proximity-ligated RNA molecules were then ligated to barcoded adapters and converted to libraries for Illumina sequencing.

Summarized
AMT crosslinking ⟶ cell lysis ⟶ S1 endonuclease digestion ⟶ TRIzol purificaiton ⟶ ShortCut RNase III digestion ⟶ 2D gel purification ⟶ RNA-RNA ligation with T4 RNA Ligase 1 ⟶ crosslink reversal ⟶ sequencing library preparation (adapter ligation, reverse transcription, etc.)

Concerning the capture of RNA-RNA interactions, these methods are essentially the same. Given that both papers were published in Cell Press journals in the same week, they were likely developed concurrently in competing labs. It may be the case that the editors coordinated publication so that neither group would feel they "got scooped".
From what I can tell, the major difference is in how the methods distinguish in vivo RNA interactors from transient RNA-RNA hybridization events that occur during the course of the protocols. In LIGR-seq, they include an uncrosslinked ("–AMT") control so that they can differentiate true interactions from background noise by looking for ligation chimeras that are enriched in the +AMT samples relative to –AMT. In PARIS, the second dimension of the 2D gel is 20% urea, which would serve to denature any non-crosslinked dsRNA molecules prior to ligation; see the full methods for more details:

Gel slices of each lane were embedded and polymerized into the top of the second dimension 20% urea-TBE denatured polyacrylamide gel ... The second dimension gel has higher temperature due to the high power, and the high temperature facilitates denaturation of the dsRNA fragments.

There may also be a difference in the length distributions of the chimeric RNA molecules obtained at the end each method, since LIGR-seq and PARIS use different RNase enzymes with different digestion parameters.


text:
What can be used for DNA preservation?
I am neither a student nor really advanced in biology, I am just writing a tabletop role-playing game scenario that I want as realistic as possible. In the story, the players find an old laboratory where genetic mutations were studied, but as the electricity is off since 40 years, most of the embryos are "rotten". I still need to have some embryos still "fresh" so someone could get DNA from it and continue the experiment.
Problem is, I thought about formol (the experiment is supposed to have taken place in the 1980's, so the health problem is not one right now), but I've read that formol alters and destroys the DNA. I've seen older ways with alcohol, but the process doesn't seem as efficient.
What liquid (or technic) could have been used in the 80's to preserve embryos and their DNA so we could still exploit it 40 years later, and with not electricity?

70% alcohol preserves DNA well.

Hi Lyzvaleska, and welcome to Biology.SE! You mention you've read that formol destroys DNA, and that alcohol preservation seems less efficient.  Can you link to sources for these claims?

dry/lyophilized DNAs are also rather stable. https://www.idtdna.com/pages/support/faqs/are-lyophilized-oligos-stable-when-stored-frozen-

@acvill For the formol destroying DNA, I've seen it in a french source (but can't seem to put my hand on it right now anymore) that it could alter the DNA. For the alcohol, I saw claims about being less efficient, but apparently it was more of a visual problem and the evaporation. But it looks like that alcohol fits my needs perfectly :)

There are a few plausible ways:
As someone mentioned in the comments; Alcohol works well for this. We have samples from a hundred years ago (e.g. Thylacine), which have been stored at room temperature in a museum for that period of time and have had DNA easily extracted from them.
Unfortunately for many species, alcohol preservation fell out of favour due to it shrinking (by dehydration) specimens, so that they no longer look "realistic" in terms of morphology (something that is very important for classical identification methods). In addition, ethanol and other alcohols tend to evaporate fairly fast if not sealed properly. For these reasons aldehyde based solutions came into favour about 100 years ago. The downside to this is that formaldehyde and other aldehydes cross-link the genetic material, making it more or less impossible to extract and use.
Another possible method is dehydration - mummification. Small samples like embryos or tissues can be dehydrated quite fast. In the absence of water, these samples should last more or less forever - we can extract DNA from mummies in many places around the world, but these ones might interest you in particular.
There are also specialist chemical solutions such as RNAlater that are routinely used in labs for preservation of precious genetic material.
Given that we knew these sorts of things in the 1980's and that the lab was staffed with competent scientists, and that they knew that the lab was going to shut down but would re-start at some time in the future, then it is entirely plausible that they would have used alcohol or something like RNAlater.
In the absence of this knowledge, but still competent scientists, it is much more likely that they would have used some sort of cold (frozen) storage method;  whether this was cryopreservation (liquid nitrogen), such as is used for storage of cells or a specialist -80 $^\circ$C freezer or a -20 $^\circ$C freezer like you might find at your house. Some samples may have been still stored in chemical preservation in the interests of space-saving in freezers though.


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How old is the Pogona genus?
What it says on the title, how old is the genus Pogona, which includes all bearded dragons? I tried looking online, and all I got was the useless answer of “bearded dragons are descended from their parents, who are descended from their parents… etc.”

Welcome to the site. What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

Another way to ask this question:

How old is the most recent common ancestor of Pogona lizards and their closest relatives?

Diporiphora is a sister clade of Pogona, as stated in Hugall et al. 2008.1 Figure 4 of the same paper suggests that Diporiphora and Pogona diverged around 12 million years ago (see star in red box -- annotations mine):

An ultrametric chronogram generated from the Bayesian combined data phylogeny (Fig. 2C), under penalized likelihood rate smoothing (PLRS; optimal smoothing factor 80). The Riversleigh Physignathus calibration discussed in the text is used (indicated on figure as equal to 21 Mya). Tree pruned to show Australasian group only. Markov chain Monte Carlo (MCMC) sampling 95% confidence interval shown for selected nodes.

So, a reasonable estimate for the age of the Pogona genus is 12 million years.

References

Hugall AF, Foster R, Hutchinson M, Lee MSY. Phylogeny of Australasian agamid lizards based on nuclear and mitochondrial genes: implications for morphological evolution and biogeography, Biological Journal of the Linnean Society, Volume 93, Issue 2, February 2008, Pages 343–358.


text:
Can CNVs have a phenotypic effect unrelated to the direct modification of transcriptional units?
I'd like to know how (or if) copy number variations can have a phenotypic effect unrelated to the direct disruption/movement/duplication of sequences for coding regions, promoters, enhancers etc.
I ask this question with the premise that CNV duplications or deletions may change the organisation and shape of chromosomes in the nucleus, and that this may then affect the phenotype, perhaps indirectly affecting transcription or methylation.
However, I'm interested in any way that isn't just direct modification of sequences composing transcriptional units.

If I understand your question correctly, you want to know if gene copy number can have an indirect effect on transcription, i.e. an effect that does not arise from the dosage effects of the copied sequence or the direct disruption of proximal genes?
I think the answer is yes, insomuch that CNVs can change chromatin architecture.
In many eukaryotes, the genome is spatially organized into topologically associated domains (TADs). Though their necessity in all contexts is contested, there is research that suggests TADs delineate meaningful associations between distal regulatory elements like enhancers and promoters.1 Duplications can be pathogenic if they occur within a TAD or across a TAD boundary.2 Deletions at a single CNV locus have been implicated in causing genome-wide transcriptional changes at loci important for human brain development via ablation of TAD boundaries.3
Note that chromatin conformation capture experiments (i.e. Hi-C) are often confounded by CNVs due to the effect of copy number on library prevalence and, consequently, contact frequency calculations, making the inference of CNV effect on genome organization inherently problematic. However, new computational tools have been implemented to account for such biases.4,5

References

Beagan JA, Phillips-Cremins JE. On the existence and functionality of topologically associating domains. Nat Genet. 2020 Jan;52(1):8-16.
Franke M, Ibrahim DM, Andrey G, Schwarzer W, Heinrich V, Schöpflin R, Kraft K, Kempfer R, Jerković I, Chan WL, Spielmann M, Timmermann B, Wittler L, Kurth I, Cambiaso P, Zuffardi O, Houge G, Lambie L, Brancati F, Pombo A, Vingron M, Spitz F, Mundlos S. Formation of new chromatin domains determines pathogenicity of genomic duplications. Nature. 2016 Oct 13;538(7624):265-269.
Zhang X, Zhang Y, Zhu X, Purmann C, Haney MS, Ward T, Khechaduri A, Yao J, Weissman SM, Urban AE. Local and global chromatin interactions are altered by large genomic deletions associated with human brain development. Nat Commun. 2018 Dec 17;9(1):5356.
Servant N, Varoquaux N, Heard E, Barillot E, Vert JP. Effective normalization for copy number variation in Hi-C data. BMC Bioinformatics. 2018 Sep 6;19(1):313.
Wang X, Xu J, Zhang B, Hou Y, Song F, Lyu H, Yue F. Genome-wide detection of enhancer-hijacking events from chromatin interaction data in rearranged genomes. Nat Methods. 2021 Jun;18(6):661-668.


text:
What is accumulation and release centre of neurohormones?
What is accumulation and release centre of neurohormones?
Is it hypothalamus?

Have you tried googling it ?

Incidentally yes.
I just want to be sure whether it is hypothalamus.

The neurohormones in most mammals include oxytocin and vasopressin, both of which are produced in the hypothalamic region of the brain and secreted into the blood by the neurohypophysis (part of the pituitary gland).
A second group of neurohormones, called releasing hormones, also originates in the hypothalamus. The members of this group, however, are transmitted within the neural cells to a second locus in the brain, from which they pass in the bloodstream to the adenohypophysis, which also is a part of the pituitary gland. There they either stimulate or inhibit the release of the various adenohypophysial hormones.
A third group of neurohormones includes the enkephalins and other endorphins. The endorphins are effective in relieving pain, a property apparently related to their function as neurotransmitters, passing nerve impulses from one neuron to another. Their neurohormonal activity is manifested by their stimulation of the secretion of somatotropin and vasopressin by an indirect process involving a site (other than the secretory neuron) in the central nervous system.


text:
Question regarding 2 constructs of tobacco plant
Six independent transformation experiments of tobacco leaf explants were carried out using
two different constructs - (1) construct I containing only a Hygromycin-resistance gene
$(HYG^R)$ as a selection marker and (2) construct II with the $(HYG^R)$ gene as a selection
marker and a passenger gene encoding a dephosphorylase enzyme $(DEP)$ that inhibits
phosphorylation in cells in which it is expressed. The marker as well as passenger genes
were placed under transcriptional control of a constitutive promoter $(CaMV35S)$, which
expresses in all cells/tissues. The results obtained are tabulated below.

Explain how The $HYG^R$ gene used in construct II lost its functionality probably due to
mutation(s) either in the gene or in the promoter.
My approach: There is a probability that Expression of the $DEP$ gene is lethal to the transformed cells.

Having a toxic product for the cell in an expression vector is a not uncommon problem when overexpressing proteins.
The other possibility is that the selection marker itself is the problem. Here you can have mutations either in the promoter of the gene as well as in the gene itself resulting in a protein which is not capable of protecting the cells from the selection. Both possibilities (no expression and mutated protein) leave to the death of the transfected cells, since there is no protection of them by the resistance protein.


text:
Image formation
I have learnt that the brain provides a perception of image due to previous memory and experience. Then how does a blind person attain vision after cornea replacement?

Note: Questions of neuroscience are not off-topic on biology.SE but they are also on topic on CognitiveScience.SE. If you don't get a satisfying answer here, you may want to give a try later on on this other site.


text:
Majority of transcripts are from sense strand?
I am wondering whether majority of transcripts are transcribed from the 5'->3' strand? Because I encounter a lot of expressions like "anti-sense transcripts". Could anybody help clarify this? Thanks.

Could you elaborate on your question?  Anti-sense transcripts are also transcribed in the 5'->3' direction.  What type of data are you looking at?

Thanks, GWW. Maybe I was wrong, i thought the "anti-sense strand" as the 3'->5' strand. So you mean, for example, the DNA is "AAAAATTTTT", some transcript could be "AATTT" and some could be "TTTAA"? Could you please further clarify it?

do you have questions after reading http://en.wikipedia.org/wiki/Sense_%28molecular_biology%29 ?

These terms depend on circumstances.
If I give you a sequence .AAATTTGGG
You would say AAATTTGGGis sense strand while TTTAAACCC antisense. So far it's regarding sense and antisense.
And there is no transcript transcribed from 3'-5'.
RNA polymerases work only in 5'-3' direction.

From my understanding sense and anti sense is contextual. If you are looking at a gene from 5'->3'(which is convention) that strand is the sense strand and the complement to the gene is the anti sense strand.
However further along the DNA there could be a gene on the 'original' anti sense strand, if you are discussing this new gene, there is a new context and it is now on the sense strand (oriented 5'->3'), and it's complement on the anti sense strand.
I hope that's clear.

Thanks, @Ben. I found this on Wiki: "The only real biological information that is important for labeling strands is the location of the 5' phosphate group and the 3' hydroxyl group because these ends determine the direction of transcription and translation." May I have this conclusion: the cell is going to read the DNAs ONLY from 5' end to 3' end, regardless whether it is reading the 5'->3' strand or 3'->5' strand? And whichever strand is used as a template to produce the transcript, it is called "antisense" strand? Moreover, when aligning, result "+" means aligned to sense strand?

You are indeed correct, as the antisense strand is used as the template to make the mRNA translation of the DNA sense strand.

Can you link the web page into your answer? Answers should be accompanied by useful resources. Thanks.


text:
Are there examples of PTMs that add different chemical groups (and mass) to different amino acids?
I'm talking about this type of post-translational modifications. What I'm interested in is not whether some modifications can only occur on specific amino acids (that's clear), but if the nomenclature has examples of addition of slightly different chemical groups to different amino acids known under the same name.
Thanks.

Not clear about what you're asking. Are you asking if there is a class of PTM that describes the addition of a variety of chemical groups to a variety of amino acids?

Well, yes. Of course I don't expect this variety of groups to be diverse; maybe just a single deviation for a single amino acid.

The term "methylation" may be what you're looking for, if I understand your question correctly. A CH3 group can be added to one, two, or all three nitrogens on arginine's side chain, for example, potentially resulting in slightly different chiral conformations.


text:
Can tardigrades survive being eaten?
Compared to a tardigrade, the cockroach seems fragile.
But can tardigrades survive the acidic environment of being eaten by most animals?

In there natural state no, tartigrade have absolutely no way to survive the acidic content of stomachs and are fragile.
In their cryptobiosed form (extremely resilient form) there has been no research to determine if they could survive extremely acid environnements. The things that we know they can survive is:

Temperature
Pressure
Dehydration
Radiation
The outer space environnement
Toxins

However, very few organisms possess mechanisms to tolerate highly acid environnement since acid affect cell membranes by "attacking" mainly the proteins and lipids. These organisms have evolved these traits because they live in acidic environnements, tartigrades on the other side don't.
Another point to add is, entering cryptobiosed form takes time, if the tartigrade would be eaten in it's natural form, it wouldn't have the time to cryptobiose and thus it would die.
Tartigrades
I hope this gives you some useful information

That depends on how long it takes for the tardigrade to get from point A, your mouth, to point B, your rectum. Provided you aren't extremely allergic to tardigrades or eat something poisonous or die while digesting the tardigrade. Also provided you had unlimited time with the tardigrade in an area of your digestive system that does digest things, not point A or B, eventually the tardigrade will succumb to your body's attempts to kill/digest it.

Hi welcome to BIO.SE. Please provide support for your answer. We want to ensure that people are answering with reputable, supported facts, and answers that fail to provide reputable support will be downvoted or deleted. Thanks.


text:
Which surfaces contain no epithelial tissues and which epithelial tissues are vascular?
Epithelial tissues are found on all the surfaces of the body; including external surfaces and surfaces of organs etc.
Are there any surfaces which do not have epithelial? I have read in my book that almost all the surfaces has epithelial tissues but there are some exceptions. What are the exceptions?
Similarly, almost all the epithelial tissues are avascular. But there are some exceptions which are vascular? Which epithelial tissues are vascuar?
*I'm talking about a human body.

no, epithelial tissues are avascular @Skippy-psI'mawoman. A few exceptions are vascular. I want to know what are these exceptions.

read the 4th line.
http://en.wikipedia.org/wiki/Epithelium

Most of the epithelial cells do not have vascular supply because they are exposed to the external environment. They can easily be damaged and severe bleeding can occur.

vascular wall cells are called endothelial cells.

@Skippy-psI'mawoman Epithelial tissues get all their nutrients from the blood vessels in the basal membrane. All( almost ) epithelial tissues have a basal membrane.

Most people wouldn't consider osteoblasts as epithelial cells, thus many surfaces of bones could be said to be without epithelium.  Your going to get objections to that, however, on the idea that the periosteum is still a "connective tissue."

I think you're talking about two different things.  I assume Rafique is referring to vascularized epithelium, but user4693 is referring to vascular epithelium.  Although the terminology is very similar, the difference is important.
vascular epithelium = endothelium of a blood or lymphatic vessel.
vascularized epithelium = epithelium with a blood supply, meaning that small vessels invade the epithelium (pass between epithelial cells) rather than simply occurring in the underlying basement membrane or connective tissue.
Most epithelia are avascular (lack blood vessels).  As far as I know the only vascularized epithelium in humans is found in the inner ear (1).  I've been told that the lips have vascularized epithelium (which is why they appear reddish), but I don't completely trust that source and I cannot find anything online to support it.
Also, some pathological conditions can cause vascularization of certain epithelia, like the cornea (2).

I suppose "vascular eipthelium" could be a correct term, but I've always seen endothelium (or endothelial as adj as @wysiwyg pointed out). Perhaps this helps prevent the confusion.

I've always used endothelium.  However, I noticed that some online sources (notably wikipedia) use the term "vascular epithelium".  I thought that may be why earlier comments disagreed, so I was trying to, hopefully, provide some clarification.


text:
When life first formed in earth's ocean, was it salty yet?
Do we have any tangible proof, e.g. by studying fossils of primitive life forms, that during their time the ocean was already salty, and at roughly similar levels to today's, or on the contrary, that water has no or very low salinity?
Did life had to adapt to dramatic changes in sea water salinity, as it has (I believe) for changes in air composition?

I've answered your first question.  I suggest you post the second part (concerning adaptation to changing salinity) as a standalone question.

Current estimates suggest that last universal common ancestor of life on earth lived in hydrothermal vents 3.8–3.5 billion years ago.1 Petrologic examination of quartz formed near these vents during that time suggests that seawater had a higher salinity compared to current oceans 2 --

Our data are in agreement with six other data sets—from the 3.75 Ga Isua Greenstone Belt (W. Greenland), the 3.24 Ga Pilbara region (W. Australia), the ∼3.2 Ga Barberton Greenstone Belt (South Africa; 2), the ∼2.7 Ga Matagami area (Abitibi Greenstone Belt, Canada), and the Proterozoic (∼2.2 Ga) Ongeluk Formation (South Africa). The consistency of fluid inclusion data suggests that Archean and early Proterozoic seawater may have been more saline, and potentially stratified, compared to modern seawater.

Note: Ga (for gigaannum) – a unit of time equal to 109 years.

Weiss, M., Sousa, F., Mrnjavac, N. et al. The physiology and habitat of the last universal common ancestor. Nat Microbiol 1, 16116 (2016).
Weiershäuser, L., Spooner, E.T.C. Seafloor hydrothermal fluids, Ben Nevis area, Abitibi Greenstone Belt: Implications for Archean (∼2.7Ga) seawater properties. Precambrian Research, Volume 138, Issues 1–2, 2005, Pages 89-123.

It's amazing that the ocean was actually more salty than today -- my intuition couldn't have been more wrong.


text:
State of extracted DNA
A well-known and commonly-done experiment is to extract DNA from strawberries or other fruit by first mashing the fruit of choice, adding the mush to a mixture of water, salt, and detergent, and then adding isopropanol. DNA then precipitates out.
How intact is the DNA obtained from this experiment? Does the experiment introduce breaks or other forms of DNA damage? Is the DNA intact enough to be sequenced and for one to be able to identify what organism it came from?

For many sequencing methodologies, DNA fragmentation is actually necessary.

Yes, normal DNA extraction protocols fragment genomic DNA.  In my experience, extracted DNA tends to have a size distribution on the order of 10 - 20 kilobase pairs (kbp), independent of the protocol and source organism (assuming a chromosome size >> 20 kbp).  This seems to be corroborated by what I can find online -- see the gel below from Successful tips of DNA extraction and PCR of plants for beginners

Figure 1. Agarose gel electrophoresis of DNA samples extracted from horticultural plants. M, molecular weight marker. Modified from Kasajima et al. (2013)

as well as this gel from ThermoFisher

Genomic DNA purified with the Genomic DNA Purification Kit
Agarose gel (0.7%) electrophoresis analysis of undigested (odd lane numbers) and EcoRI digested (even lane numbers) DNA samples.
M – Lambda DNA/HindIII Marker [top band is 23130 bp]
1, 2 – human blood
3, 4 – human lymphocytes
5, 6 – human placenta
7, 8 – mouse liver
9, 10 – Hedera helix
11, 12 – Haemophilus influenzae
13, 14 – E.coli ER2267
15, 16 – Bacillus subtilis

The consistent size of extracted genomic DNA across organisms is a physical constraint rather than a genetic one.  When unwound and unprotected by the cell and nuclear envelopes, chromosomes are subject to the shearing forces of pipetting and vortexing.  Consider a mile-long length of high-test fishing line.  Coiled in the box or around a reel, the line is strong and stable.  If you laid the line out end-to-end, however, there would be many places along its length where the line gets snagged, knotted, and torn.
As hinted by canadianer, DNA fragmentation is necessary for most sequencing methods (specifically whole-genome shotgun sequencing, not sequencing of specific PCR amplicons).  As an example, Illumina sequencing platforms generally require libraries with fragment size distributions between 300 and 600 bp, and fragments larger than 1000 bp are sequenced inefficiently.  So, after DNA extraction, additional steps are required to further reduce the average DNA fragment size prior to sequencing adapter ligation.  The most common method of genomic DNA fragmentation for short-read sequencing is sonication, though enzymatic methods are also used in some kits.
Recently, long-read sequencing technologies have been developed to overcome the difficulty of assembling short reads.  Nanopore platforms can sequence DNA fragments that are 100s of kbp long.  To prepare these extremely long libraries, special care must be taken to not shear the DNA during extraction.  The Journal of Visualized Experiments provides a good guide on how to extract and process high-molecular-weight DNA:
Gong, L., Wong, C. H., Idol, J., Ngan, C. Y., Wei, C. L. Ultra-long Read Sequencing for Whole Genomic DNA Analysis. J. Vis. Exp. (145), e58954, doi:10.3791/58954 (2019).


text:
What microbial contaminant grows blue on L-agar/L-broth and is resistant to carbenicillin?
We are trying to grow liquid cultures of Mycobacterium smegmatis as a host for bacteriophages, but we have been having issues with contamination. Our latest attempt went like this:

Tuesday 1 pm: Added 20 ml 7H9 broth, 2 ml Albumine-Dextrose solution, 0.02g CaCl2, one colony from master M. smegmatis culture was added to 100 ml Erlenmeyer flask. Incubated in a shaker at 35° C.
Wednesday 6pm: Added 20 ul of carbenicillin (should have been added from the top, but the carbenicillin arrived a day late)
Thursday 1pm: liquid culture is turbid white and clumpy as expected.
Friday 2pm: Culture is still turbid white and clumpy. Inoculated a streak on left half of L-agar plate.
Saturday 3pm: Streak plate shows streaks of yellow-white colonies (as expected), but also a blue diffuse contaminant which smells very bad. This is similar to what we've seen in our previous attempt at growing this culture

Now, the question is: What could this blue contaminant be? The original culture protocol used Cycloheximide to control for fungal growth, but ours has not arrived yet.
A related question is. Where could it have come from?
Master M. smegmatis culture

Liquid M. smegmatis culture

Contaminated streak plate

Pseudomonas aeruginosa is a likely candidate. This is a common skin organism and cultures/colonies often have a blue/green sheen. Pure cultures generally have a fruity/ester smell.
The blue/green pigment is a combination of pyoverdine and pyocyanin.
Of note is that it is also commonly antibiotic resistant having intrinsic antibiotic resistance to a range of antibiotics, including the penicillin group


text:
Prothrombin time when extrinsic pathway is turned off
I was searching for an answer that "why do we need intrinsic pathway when there is fast extrinsic pathway" and i found the answer in the following link:
http://www.pathologystudent.com/?p=3197
It says that the factor X produced in the extrinsic pathway turns off the extrinsic pathway and activates the intrinsic pathway. As the extrinsic pathway is turned off so, we need intrinsic pathway to continue the clotting process. But if the extrinsic pathway is stopped then how do we get prothormbin time because prothrombin time is for extrinsic pathway?

In order to understand the importance of both pathways, you first need to be clear about what is meant by them respectively. Clotting activation from tissue factor (TF) is known as the extrinsic pathway, so you've got that one right.
The intrinsic pathway doesn't involve FX
The intrinsic pathway does not (as often misunderstood) refer to the clotting cascade downstream of factor X (FX) which involves FV, FVIII and thrombin. Rather, the intrinsic pathway is a system which is able to initiate the clotting cascade without any tissue factor being present. It is triggered by the assembly of high molecular weight kininogen, prekallikrein and FXII on collagen. This is also known as contact activation, and sets off a small cascade producing active FIX (FIXa), which can then assemble with circulating FVIIa in order to produce FXa and thereby set off the rest of the clotting system.
The extrinsic and intrinsic pathway are separate ways towards a "common pathway"
So think of it this way: The extrinsic pathway produces FXa in one way (TF), the intrinsic pathway produces FXa in a different way (HMWK+prekallikrein+FXII). There isn't really any interaction between these two. Once FXa is produced from either of these two, it will start to set off what you could call the "common pathway", i.e. it will produce thrombin, which will activate co-factors that will then lead to more production of FXa and propel the entire thing forward faster and faster until it reaches what we know as the thrombin peak.
The intrinsic pathway is not important for haemostasis in humans
Aside from this, you should know that the intrinsic pathway exists, but it doesn't bear much significance in a living human. This is demonstrated by genetic FXII deficiency - you would expect it to produce haemophilia if FXII and therefore the intrinsic pathway was important (just like FVIII and FIX), but it doesn't (read here: http://en.wikipedia.org/wiki/Factor_XII#Role_in_disease).
The principle behind the initiation pathways and the common pathway
So to summarise: You fell victim to a misunderstanding and a bad explanation on that site you linked. The extrinsic pathway doesn't "turn itself off", and the intrinsic pathway doesn't "take over". What really happens in a human is that the intrisic pathway doesn't really do anything. Rather, the extrinsic pathway will produce a little bit of active FXa. But that is enough to produce a little bit of thrombin. And that bit of thrombin will then produce small amounts of FIXa and co-factors (FV and FVIII). These will start to produce more FXa, which will produce more thrombin, which will produce more FIXa and co-factors, and so on.
What the article you refer to is trying to mention are the inhibitory systems that will be set off alongside all of this. Think about it - if thrombin increases its own production perpetually, how does it know when to stop? These systems which ensure that clotting does stop are known as anticoagulation pathways. They are just as amazing as the coagulation pathways themselves, and they are extremely well-geared towards shutting off exactly the right clotting factors at exactly the right time, to ensure that a clot forms in the wound but only there and nowhere else.
Edit: It turns out people do use more complicated definitions of "intrinsic" and "extrinsic" - the problem being once again that everybody can define words as they like. This is rather based on the distinguishing of the two ten-ases, TF-FVII (extrinsic tenase) and FIX-FVIII (intrinsic tenase). In this understanding, the physiological process does indeed start off by the extrinsic pathway (i.e. mechanisms which generate extrinsic tenase), which will kick off the amplification cascade of the intrinsic pathway (i.e. which produces intrinsic tenase). It is true that this way, the contribution of the "extrinsic pathway" is minor once the "intrinsic pathway" is active, but even so, it does not "shut itself off". What turns the extrinsic pathway off is the layer of material which gets deposited on top of the exposed subendothelial surface, preventing access to TF!


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Why do you need the intrinsic pathway when you have faster extrinsic pathway?
There are two pathways in blood clot fromation; the extrinsic pathway and the intrinsic pathway.
The extrinsic pathway is faster than intrinsic pathway because it has less number of steps. So, why do we need intrinsic pathway then?

in general there are very few functions in organisms which have a single mediation - redundancy is typical in biology at the level of gene action.  it makes the system robust

This question embodies two unjustified assumptions that keep cropping in questions. 1. How do you know that a pathway with fewer steps is faster? You don't. It depends on amounts of enzymes and their catalytic characteristics. 2. How do you know that a slightly faster faster pathway will have an advantage? Again you don't. Other factors may be limiting or more important. Moral: when you have written your question out, read it and consider the validity of your assumptions.

In short: The extrinsic cascade reacts to damages of the blood vessel, the intrinsic pathway reacts to damages of the walls. But as with all things, the long version is ways more complicated:
The extrinsic pathway is activated when you damage tissue and factor VII come in contact with tissue factor (also known as factor III). Tissue factor is located in the membrane of the cells and is only released when the cells are damaged.
Then the cascade starts and delivers a very fast large amounts of active thrombin, which then converts fibrinogen to fibrin to build a block of the damaged blood vessel. The step from the thrombin is common between both pathways.
The intric pathway is also called the "contact pathway", which starts when the factor VII comes in contact with collagen or anionic surfaces.
The main advantage of this pathway is the strong amplification of the initial signal from the intrinsic pathway by a factor of about 1000 fold. The intrinsic pathway is also co-activated by active thrombin (which stands at the end of the cascade) meaning it is also a powerfull feedback loop to make the initial reaction much stronger. This also overcomes weak activation which where the active thrombin will be inactivated by Tissue Factor Pathway Inhibitor.
The coagulation cascade has a pretty nice article in the Wikipedia.
Interestingly it is now believed, that the start of the intrinsic pathway plays no or almost no role in vivo. There are people which "suffer" from a deficiency in factor XII which is necessary to start the intrisic cascade. These people have absolutely no problems with their coagulation, so the first steps are not necessary (any more?). This article presents findings, that it stabilizes a thrombus:"The intrinsic pathway of coagulation is essential for thrombus stability in mice."
Here are some further articles about the intrinsic pathway:

In vivo roles of factor XII.
Factor XII: what does it contribute to our understanding of the
physiology and pathophysiology of hemostasis & thrombosis.

Do you mean extrinsic pathway by "initial signal"?

Nope, ny initial signal I mean the initial signal from the intrinsic pathway. Activation of Factor XII which in turn activates Factor XI and so on. Each step of the cascade magnifies the signal.

The extrinsic pathway is activated by extrinsic trauma , that makes blood escape out from the vascular system , and then after the formation of a small amount of fibrin , a substance called Tissue Factor Pathway Inhibitor ( TFPI ) is released , this inhibitor prevent more activation of factor x , it’s thought that TFPI is responsible for preventing more un-needed fibrin , but if the injury need more fibrin to cure , at this point the intrinsic pathway will be activated to form more needed fibrin

Welcome to SE Biology. On this site we're looking for answers in which explanations or assertions are supported by references, preferably with links. Without these neither the poster nor anyone else can tell whether or not you are correct, or learn any more about the topic. See the Help for "how do I write a good answer?".


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Events after Endothelial interruption
What are the physiological events that occur after there is endothelial interruption in the blood vessel?
What does endothelial interruption mean here? And what could be the physiological events?

Are you sure it is endothelial interruption ? Do you mean injury ?

Our teacher gave us this question as an assignment so, i think i should ask him about "endothelial interruption". Thanks


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Why is prothrombin time test not used for heparin
Prothrombin time test is used for the monitoring of warfarin but not heparin. Why is this used for warfarin monitoring and why is it not used for heparin monitoring?

Thats because the mechanism of action is different between warfarin and heparin.
Warfarin inhibits the formation of prothrombin (also known as factor II) by inhibiting the metabolization of vitamin K (for extensive details have a look at the Wikipedia article about Warfarin).
Heparin inhibits the blood coagulation by binding to antithrombin III which functions as a inactivator of active clotting factors as factors V, IX, X, XI and XII. It also binds calcium which is important for the blood coagulation. For more details see the Wikipedia under Heparin.
Therefore Heparin interferes with the formation of Thrombin and the test does not work. A nice image of the coagulation cascade can be found here, which also shows the points where Heparin interferes. The test can be done with Batroxobin, see here.

So, heparin stops the formation of thrombin and warfarin stops the formation of prothromibin. But i still don't get it that why is PT test not used for heparin monitoring?

Because you can measure how much thrombin activity is left when the synthesis is inhibited (for warfarin), but when it can't be activated (for Heparin), you will not measure anything. You don't knock-down coagulation completely with Wafarin. The last link in the answer above explains the test.

The answer and reasoning by Chris are incorrect. Heparin DOES effect both the PT time and APTT time because it affects factors in the final common pathway. Heparin activates antithrombin 3 which inactivates activated factor x (factor xa) and thrombin (AKA activated factor ii). These factors are involved in the final common pathway: activated factor x converting prothrombin to thrombin which converts fibrinogen to fibrin. Both the APTT and PT rely on the final common pathway which follows on from either the intrinsic pathway (in APTT) or extrinsic (in PT).
HOWEVER, heparin does have a much greater effect on APTT and so this is why this is used. Indeed at therapeutic concentrations PT is within normal range due to a minimal increase. However, in a heparin overdose PT will become significantly high.
I am not sure of the reason for heparins greater effect on APTT but it may be something to do with heparins mechanism of action - in addition to inactivating factor xa and thrombin, antithrombin 3 (which heparin activates) inactivates other factors (xia and ixa apparently) which are part of the intrinsic pathway (which is measured in APTT) but not the extrinsic pathway (measured in PT). I think the fact it affects multiple factors in the APTT test causes a synergistic affect so affects it more compared to the PT where it only affects two factors (xa and thrombin) so there isn't the synergistic effect.
I thought of this explanation using an explanation I found of why low molecular weight heparin (LMWH) does not have as much of an effect on APTT as unfractionated heparin (UFH). LMWH's, unlike UFHs, activation of antithrombin 3  only really causes inactivation of factor xa so the synergistic affect of effecting multiple clotting factors involved in APTT does not happen (like it does with unfractionated heparin). However, for whatever reason in real patients LMWH is as effective at anticoagulation as UFH.
Source of last paragraph : https://fritsmafactor.com/post/low-dose-heparin-and-ptt


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Parthenogenesis in Bees
Parthenogenesis is defined as:
"A type of asexual reproduction in which egg develops without fertilization to form a new individual."
If parthenogenesis takes place in bees, a drone or male bee is produced.
My question is that parthenogenesis is the development of EGG into new individual so, how can egg be developed into male because egg won't have that "Y" chromosome required for male offspring?

Because the "Y chromosome" has nothing to do with sex determination in bees.  Instead, the number of X chromosomes determines the sex.  With only one X chromosome, the egg will develop into a male.  This is called a haplodiploid system of sex determination (the male bees are haploid, having only half the number of chromosomes).
EDIT: I should add that there are many systems of sex determination, not just XY or the haplodiploid system.  See the Z-W system (males are ZZ and females are ZW), the X0 system (the males are diploid for all but the sex chromosome), and temperature-dependent system of sex determination.

@MuhammadRafique: I have edited my answer to be slightly more accurate and provide additional information.

The Cape honey bee in South Africa can create female offspring without the queen being mated. Female stick insects can also produce female offspring without males, all daughters will however be clones of the mother. I guess this is a last resort to ensure survival in difficult times until a male is found to mate with.

can you add some references to this?


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Reproductive isolation causing evolution
My course book says about reproductive isolation that it does not allow the interbreeding among the individuals of different species. It also says that it is a cause of evolution.
How is this cause of evolution?

could you quote what the book says and tell us what book that is?

Reproductive isolation isn't exactly a cause of evolution, but rather a cause of speciation. Reproductive isolation allows for two cohorts of one species to be reproductively separated. In this case, evolution via random mutation or mechanisms like genetic drift allows for the differentiation of the two groups, up to the point that the two cohorts and their respective gene pools have evolved to be completely different species.
Truly defining a species is still debatable (via the Biological species definition, Morphological, etc) but reproductive isolation is definitely a mechanism involved in speciation.


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How to wash the column during protein purification with GST tag?
I have been working with GST tagged proteins for the last 4 years and after loading the cell lysate into the column I was washing it with 20-30 column volumes of PBS and sometimes my proteins were eluted very pure sometimes with a lot of impurities.
A few times I tried washing with NaCl gradient (0-400 mM) but later decided not to do that because it may denature the protein and some of my proteins may not refold.
What do you suggest for washing step?
Note: I don't have any UV detector to see the washouts/flowthroughs/elutions.

Use your plate reader to see the elution peak by collecting 100 ul or so as you are washing and eluting. You can also set up a Bradford-type colorimetric assay in a disposable microplate and add aliquots as you're washing and eluting to check for the presence of protein.

Bradford idea is really good actually, I will try that in my next purification. Thank you!

You're quite welcome. I did that before we got a little Biorad FPLC with a UV flow cell. If your lab does lots of purifications you might want to check it out - they're fairly inexpensive (as I recall) and you can just set the program up and walk away until it's done.

The standard when purifying GST with Glutathione agarose beads is to use STE buffer (10 mM Tris-HCl (pH 7-7.5), 150 mM NaCl and 1 mM EDTA) for washes and we have had no problem with this in our lab!


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Seed Germination
Is my understand of how seed germination comes to be and what it entails correct?
Seed germination: As the seed matures it loses water and enters dormancy (a state in which it’s metabolic processes slow down dramatically) after which it is dispersed.  Once the seeds have been dispersed and if they have landed in an area that meets the requirements (sufficient water, warmth, and oxygen), they may begin to grow into seedlings or they may remain dormant.  If they have not landed in a suitable area they can remain dormant for hundreds or thousands of years and wait until they are transported to a suitable area to resume growth.  Eventually once the seeds have landed in a suitable area, the seed resumes the process of growth when the seed is able to absorb, the process of resuming growth after being dormant is called germination. The water causes the seed to swell and breaks open the seed coat. The stored food in the endospore or cotyledons begins to break down, and nutrients are made available to the embryo. The food and the presence of oxygen allow cellular respiration to occur, which provides energy to the embryo for growth. The first part of the embryo to appear outside the seed is a structure called the radicle, which starts absorbing water and nutrients from its environment, eventually the radicle develops into the plant’s roots. The hypocotyl is the region of the stem nearest the seed. In many plants, it is the first part of the seedling to appear above the soil. In some dicots, as the hypocotyl grows it pulls the cotyledons and the embryonic leaves out of the soil. Photosynthesis begins as soon as the seedling’s cells that contain chloroplasts are above the ground and exposed to light. In monocots, the cotyledon usually stays in the ground when the stem emerges from the soil.

You're not accounting for anything other than "the happy path" here. For instance, not all seeds care about warmth or oxygen, and not very many can last for hundreds or thousands of years, and those that do often require more than transportation to another area to germinate. Otherwise, it sounds fairly accurate.


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What could the etymology of Phallodriline be?
I'm reading about a series of gutless worms described in several papers as phallodrilines. A search in the World Register of Marine Species shows that there is a subfamily called "Phallodrilinae", but then, in at least one paper this term is used to collectively describe gutless worms in several taxa including Oligochaeta, Annelida, and Clitellata. Since they're also described as club-headed I'm assuming that "Phallo-" is from the Latin for penis, but what would be the rest?

I'm voting to close this question as off-topic because it seems to be entirely about etymology rather than biology.

Phallus in Latin means penis, while drilus is the New Latin word for Greek

δρῖλος (drîlos)

which means both worm or erect penis.
Here you can check some sources corroborating my claim:
Merriam Webster dictionary
Wiktionary: δρῖλος (drîlos) means verpus
Liddel & Scott Lexicon
Drîlos meaning penis in Greek

-o- linking vowel indicates Greek. -i- is Latin, unless the second word starts with a vowel (many -ectomy words for example). This is irrespective of declension or gender. Weird I know.
In fact, Latin phallus is from φαλλός.
The second part is worm δρῖλος (drilos). Actually it can also mean penis, but let's gloss over that...


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Where do birds and squirrels go to die?
This may sound like a silly question, but I have been wondering about this for a while. I live in a suburban neighborhood with a lot of trees. A lot of trees means birds and squirrels. You can hear them all day and cant leave the house without seeing them.
So why don't we see dead birds and squirrels more often? I only really see them after they have been hit by a car.
My first thought was that nature was just really efficient at cleaning them up. Flies, foxes, and maybe birds of prey get to them before I notice. But that would have to be awfully efficient. When I see a dead squirrel in the road it can take weeks for the sun and the flies to remove it entirely. A fox would have trouble getting in to my backyard (lots of trees but it is fenced in), and I rarely ever see a hawk or a falcon in my area.
My second thought was that there may not be as many birds and squirrels as I think. Yes, there are a lot of them, but maybe I am seeing them same ones over and over again? Squirrels don't really travel THAT far from their homes so maybe I just see the same 10 squirrels all of the time, which makes me overestimate their numbers.
There is a store near my house that always has hundreds of pigeons hanging out in the parking lot. They fly up to the power lines and occasionally fly down for what I assume is left over food or trash. I'm guessing they aren't there at night, but during the day you can always see them. Why wouldn't you see more dead pigeons in an area with so many pigeons? I know they have relatively long lifespans but still, some of them must die of unnatural causes.
Does anyone have any idea where they go?

A major cause of squirrel death is predation:

Survival and mortality of the Arizona gray squirrel (Sciurus arizonensis)
Causes of red squirrel (Sciurus vulgaris) mortality in England

You won't see those bodies, for obvious reasons.
Disease, starvation, and harsh weather are other major causes of death. Squirrels dying in these ways are probably likely to die in their nests or otherwise hidden places. Again, no visible bodies.
So that leaves being hit by cars as the major cause of mortality where you'd have a chance of seeing bodies. You've already noted that you do in fact see these bodies, so there's no contradiction there. I'll add that depending on where you live, roadkill can be cleaned up by scavengers more or less quickly -- in areas where buzzards, coyotes, crows, etc are common, they can be cleaned up quickly, but in more urban and/or colder areas they may last longer.

I live in Georgia about 15 miles outside of Atlanta. While it is kind of close to the city, my neighborhood is surrounded by trees. Im not sure what would prey on squirrels in my area aside from foxes and birds. Thanks for the answer, but partial credit because I still dont know where the birds go!

@bsayegh: Well, humans (at least those raised in Appalachia and suchlike places) do prey on squirrels.  Squirrel stew is quite tasty :-)  Dogs and cats probably get a number, too.

@bsayegh - birds (hawks, owls, etc) are major, major predators of squirrels.  Foxes are important but cats are probably much more so. Coyotes, opossums, weasels, snakes - all common around Atlanta. So there is no shortage of squirrel predators. As for birds -- this is why Stack Exchange recommends asking one question per post. But the general answer is the same, except that pigeons being about half the mass of squirrels scavengers are even more important.

When a squirrel dies in a nest, the other squirrels who use the nest leave the remains there. The deceased body adds insulation and structure to the nest. I read where when a drey (squirrel nest) is removed it is not uncommon to find the skeletal remains of more than one squirrel.
As for the birds, I had a bird hit my window (female cowbird) and she died instantly of a broken neck. I have a big back yard and I walked half way out into the yard and laid her to rest on the grass in the sun. Less than an hour later, she was gone. I do see hawks and other raptors over my yard and I'm sure that's what took her...either way someone enjoyed a good meal that day...

Hi Joanne. Interesting info about dead squirrels in dreys. However, we're looking for answers here that not only comment on info they've heard/read/learned about, but we actually want and require that you support your answer with something more tangible. Please find a journal article, online article, encyclopedia article, etc that supports the claims you make, and explicitly mention/link your source in your answer. In doing so, visitors will know that they can better trust the information you provide or look up your source to make the judgment about how factual claims are themselves.Thanks


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Why is an intron (or exon) still called intron (exon) if retained in (excluded from) mRNA?
In most explanations, the sections of RNA removed during splicing are called introns, and the remaining segments that are stitched together are called exons.  That is, introns and exons are defined in terms of the splicing process.
But I've come across several counter-examples.  For instance:
From A simple answer for a splicing conundrum:

Exons without these elements [exonic splicing enhancers (ESEs)] are
generally not recognized and tend to be excluded from the mature
mRNA.

And from Wikipedia on alternative splicing:

Intron retention: A sequence may be spliced out as an intron or
simply retained...

In what sense is an exon still an exon (and not an intron) if it tends to be excluded from the mRNA?  In what sense is an intron an intron if it included in an alternatively spliced mRNA?

Try searching for “alternative splicing”. It’s not a question of nomenclature.

You must know that:

Introns are non-coding regions of an RNA transcript, or the DNA encoding it, that are eliminated by splicing before translation.
An exon is any part of a gene that will encode a part of the final mature RNA produced by that gene after introns have been removed by RNA splicing.

Now, about the exceptions, alternative splicing: Here,

particular exons of a gene may be included within or excluded from
  the final, processed messenger RNA (mRNA) produced from that gene. There are numerous modes of alternative splicing observed, of which the most common is exon skipping. In this mode, a particular exon may be included in mRNAs under some conditions or in particular tissues, and omitted from the mRNA in others.

Apparently, this greatly increases the biodiversity of proteins (since there are differences in their amino acid sequence and, often, in their biological functions) which might explain why it is so common.
So in this case, it becomes easier to understand if you use 'coding' and non-coding' as the difference instead of 'spliced' and 'not-spliced'.

EDIT- The coding region of a gene:

In DNA, the coding region is flanked by the promoter sequence on the 5' end of the template strand and the termination sequence on the 3' end. Although this term is also sometimes used interchangeably with exon, it is not the exact same thing: the exon is composed of the coding region as well as the 3' and 5' untranslated regions of the RNA, and so therefore, an exon would be partially made up of coding regions. The 3' and 5' untranslated regions of the RNA, which do not code for protein, are termed non-coding regions.

I had previously forgotten about the UTR's, so I have included that. Now, if there is a definite sequence where coding regions are found, it points out to the fact that coding regions must be intrinsic. Another point in favour:

The evidence suggests that there is a general interdependence between
  base composition patterns and coding region availability.The coding
  region is thought to contain a higher GC-content than non-coding
  regions. There is further research that discovered that the longer the
  coding strand, the higher the GC-content. Short coding strands are
  comparatively still GC-poor, similar to the low GC-content of the base
  composition translational stop codons like TAG, TAA, and TGA.

Thanks.  I am still not 100% clear.  Given your comment, I think it boils down to this:
Is whether a region is coding or non-coding, a property that exists regardless of whether it is included or not in the mRNA?
In other words:
Are regions inherently coding or non-coding, and the splicing process selects for that?  Or, does the result of the splicing process itself determine whether a region is encoding or non-encoding?
If it is the former, then what exactly is it that gives a region its coding property?  If it is the latter then the questions I asked above remain.

A biologist (but not geneticist) friend suggested that:
"An exon is any region that is included in at least one of the alternative splices, and an intron is a region that is included in none of them."
Regarding intron retention, he hadn't heard of it, but on further inspection said:
"It's looks looks like an aberrant case and shouldn't detract from the main definition"
Would you agree with this?

RNA splicing ultimately determines what part of the sequence becomes translated and expressed.  So, exons (since they code) should, usually, be included in mRNA. Your friend's statement seems alright to me, though I still suggest exons to be defined on the basis of coding regions.