Now, let's address your points, individually. First, allow me to be clear that I am in no way a biologist, or even a medical student. As such, most of the terms you used were outright foreign to me. You asked about "dead retroviruses" - I had to look it up. The best way I could grasp the concept, is that your question was regarding empty or "dead" sequences, found in the innermost parts of the human genome. Is this correct so far, or have I missed the point?
You are correct. A retrovirus is a type of virus that travels from one cell to another (or from an individual to another), carrying with it a piece of RNA coding for the proteins required for its replication and further dissemination. Unlike a standard virus, which just infects a cell, proliferates and goes on its merry way, a retrovirus reverse-transcribes its RNA into double-stranded DNA, which then integrates in a host cell's genome at a random point.
So let's imagine that a chromosome has the following sequence :
a b c d f g h i j k l m n o p
and that a retrovirus integrates itself between the k and the l, then the chromosome would be altered to
a b c d e f g h i j k (retroviral sequence) l m n o p
When that cell replicates, the retroviral sequence will be replicated along with it. That is one reason why diseases like AIDS are so hard to cure; the HIV sequence having integrated into the host's CD4 cells cannot be removed. All we can hope for is that we'll manage to kill all the cells carrying the viral sequence, or prevent the virus from being expressed efficiently.
Naturally, such a genetic parasite does not benefit the host and any damage to the viral sequence will be positively selected. So we might see a descendant of the infected person above carrying this sequence :
a b c d e f g h i j k (retro*iral se*uence) l m n o p
There are now new inactivating mutations in the retroviral sequence, and the poor thing is "dead". (Well, poor thing... good riddance, if you ask me!)
Further down the line, we could see the great-great-great-greatn grandchildren of that person carrying a sequence like
a b c d e f g h i j k (r**ro*iral se*uen*e) l m n o p
and so on and so forth. The longer we wait, the more degenerate the retroviral sequence will become because there is no advantage to its being repaired. Let's note that the other regions of the chromosome (the other letters, here) do get repaired when they are mutated, because when they don't it reduces the carrier's ability to reproduce.
Each species of plant or animal on Earth carries a lot of such retroviral remnants, in various states of disrepair.
Trivia time: we sometimes adopt retroviral genes because they offer some advantage. The process is called exaptation (a word worth a lot when playing Scrabble!) and the placental animals' ability to carry a baby to term over the course of long months is due to genes called syncitins, which have a retroviral origin.
That's correct. There are DNA transposons, which are basically mobile DNA elements that cut themselves free from one position and insert themselves elsewhere, and RNA transposons (or retroposons) which work like retroviruses: they stay in place in a chromosome but make an RNA copy of themselves, an RNA copy that gets reverse-transcribed into DNA and inserts itself elsewhere. Almost half of the human genome is made of such elements, because they're really like genetic weeds. Luckily they, too, tend to accumulate mutations and stop functioning. (We also have defense mechanisms involving their silencing, but that's another subject).
Never, of course, and that's a common misconception about the process of evolution. Species are not fixed entities, with abrupt transitions from one to the other (although on the geological scale, some species do change rather quickly). The process is more like a child growing up. There is no moment where a baby turns into an adult; it's a long process, with a lot of intermediate steps. In hindsight, we can prove that the adult James, all hairy and burly was originally the adorable little Jimmy with his big round head; their genes are the same, they share fingerprints, and those are definitely grandpa Bob's ears. We do not need to see the moment of transition to be convinced that Jimmy gave rise to James, and we understand that we shouldn't even expect to, as the process takes too long. It would be the same with a beard: when does stubble on a chin become a beard? Is there a moment where adding just one hair makes a difference? I don't think so. And yet we can determine, by understanding how beards grow, that at some point a full beard was just stubble on a chin.
With the evolution of species, it is the same. Only it doesn't take days (as with the beard) or years (as with the baby) but hundreds of thousands of years.
Not necessarily. Moving genes are something we observe everywhere, and while retroviruses are a more efficient way to transport genes from one species to another via lateral transfer, transposons can also do it -perhaps by piggy-backing on ordinary viruses. One type of transposons, called Space Invader, was particularly active in that regard a few million years ago.
Yep, a pseudogene is definitely a dead-end (although some people insist on their being very important, as they provide raw material that could be reactivated at some point. There are some examples of that, true, but to me a pseudogene is essentially dead for the time being.)
They're very interesting when it comes to evolution, however, especially when it comes to showing that species are closely related. Let's set aside the more than 6,000 pseudogenes that were created by the integration of processed exons and focus on "real" genes that stopped working. One good example is that of a gene called Gulunolactone oxidase (or GULO).
The protein coded by GULO is the last enzyme used in a chain of reactions that allow animals to make ascorbic acid (vitamin C) out of glucose. Most animals have all the enzymes required therefor, and produce ascorbic acid; it means that to them, "vitamin C" is not a vitamin at all; they don't need to find it in their food.
But see how evolutionary pressures can work: if a species lives long enough in an environment that provides it with enough ascorbic acid (which was the case with our simian ancestors, living on a diet rich in fruit and veggies), there is no need to synthesize it from within the body. And if perchance a mutation was to inactivate GULO, there would be no consequence to an individual. No advantage either, of course, so there is no reason for the mutation to propagate within the species; but here we face another aspect of the evolutionary process, which is genetic drift.
In a nutshell, genetic drift is a change in the genetic profile of a population attributed to the fact that not everyone reproduces at the same rate. If we have a huge population, the genetic pool stays pretty much the same, because a statistical distribution is likely to balance things out. But the smaller a population is, the more likely it is that we'll see divergences from the expected distribution. (Imagine a population of three females with black hair and three males with red, blond and black hair. If for some reason the guy with blond hair has fewer children that his friends, the next generation will have fewer genes for blond hair. Should he perchance die before he has children, the blond hair gene would disappear altogether! It wouldn’t happen in a big population with thousands of guys with blond, red or black hair.)
And so, likely due to genetic drift, the GULO mutation spread in the population. The mutation had no consequence because of the rich diet, and eventually all primates descended from that mutated founder population carried it. We apes can still perform all the transformations leading from glucose to gulunolactone, but we can't go one step further because our gulunolactone oxidase sequence has fallen into disrepair. We miss large part of the gene, and in the parts that remain we have lots of individual mutations that make the whole thing nonfunctional.
What's that got to do with the price of fish? Well if we look at the GULO pseudogene (it gets a P at the end when it's dead, so let's call it GULOP) from humans and chimps, we see that both species carry the same genetic "corpse". Apart from a few individual mutations that accrued since our splitting from a common ancestor, the GULOP sequence is at the same place, and lacks the same parts.
It could very well be that chimps and humans independently lost the GULO gene because of their respective diet rich in vitamin C, of course; and in fact, other animals including the guinea pig lost their GULO gene too. But we're not just talking about losing GULO; we're talking about losing it in exactly the same way. The most reasonable explanation is that the gene was mutated in an ancestor, and that its remnant can still be seen today (getting more and more degraded as we compare more distantly species of primates).
Indirectly, by selection. You're right: barring the occasional environmentally-induced mutation (GAMMA RAYS!!!
) the genome is not usually much affected by the environment; it certainly does not "adapt" to circumstances. What happens, though, is that mutations occur at random in any population and that depending on environmental conditions, certain genes will prove more advantageous than others; the carriers of such genes will leave more fertile offspring after them, and the proportion of "more useful genes in these circumstances" will augment relative to others in the genetic pool. This, in turn, will affect the way the species looks like. We see this effect at a smaller scale (and a much reduced time span) with selective breeding, where natural selective pressures are replaced by the whims of Man; that's how we can turn a grey wolf into a chihuahua.
It was indeed a canid. And if we go further back, we'll find a caniform ancestor which was the great-grandfather of canids, bears, raccoons, seals and all that branch of the order carnivora. The other branch of the carnivora is that of the Feliforms, where we find felines, civets, and also (strangely enough) hyenas. Despite its rather dog-like shape, the hyena is closer to cats than to wolves.
But then again, species are just a name we assign to a group of animals that habitually breed together and leave fertile offspring. A species is a useful category that allows us to know what we're talking about, but it is not an isolated thing; it is one step in a long series of reproductive events. The plasticity of what a species is can be illustrated by our current discussion on whether the dog is a subspecies of wolf (
Canis lupus familiaris) or its own species (
Canis familiaris). Both can breed and leave fertile offspring, but don't habitually mate; the dog has been selected for so long by its human partner that it seems reasonable to view it as it own thing. (I don't have a bone in that particular fight, as it's all rather academic).
As species get further and further estranged, they lose their ability to interbreed; being more or less isolated genetically, they select certain genes and accumulate certain mutations that eventually make them as incompatible as ratchets using metric units or imperial units. When their number of chromosomes changes, either by fusion or by separation, species become downright incapable of producing fertile offspring; in other cases, they may produce babies that are just barely fertile (usually with one sex being sterile and the other not. According to Haldane's law of hybrids, when this happens in mammals, it is always the male that is infertile). Lions and tigers are like that: female ligers or tigons can be fertile, but never the male (and ligers and tigons are both animals that suffer from developmental problems).
That is an immunological issue, not a species-related one. We can't even receive organs from another human without using immunosuppressive drugs. It all has to do with our acquired immune system (the one that uses B and T cells and produces antibodies). That system is not genetically pre-determined, unlike our innate immune system. In the case of the acquired system, our developing body sees its B cells and T cells cut and swap the components of genes coding for its B cell receptor (BCR) and T cell receptor (TCR), producing cells with a unique BCR or TCR. When these receptors recognize our own tissues, they are forced to die (otherwise we'd suffer from auto-immunity). That means that our complement of B cells and T cells reaching maturity will not recognize and attack our own tissues, but they will recognize and attack foreign tissues, whether they come from a fellow human or from another animal.
(Identical twins are an exception, as they have the same genes and therefore the same molecular markers on their tissues.)
Addendum: Grafts can also be performed from one person to another, but for the operation to be a success in the long term we must use people who are genetically close, especially for a category of genes involved in tissue identification that are called HLA. But even in that case, people must use immunosupressants.
Addendum to the addendum: some tissues can be grafter without problem (like the cornea) because they are not subject to much immune surveillance).
That’s fair; if the evidence is not sufficient to convince you, then the burden of proof rests on whoever provides it. They must either bring more of it, explain it better, or answer questions in a more satisfying way. And at the end of the day, you’re the one who decides if you agree with the evidence or not.
) the genome is not usually much affected by the environment; it certainly does not "adapt" to circumstances. What happens, though, is that mutations occur at random in any population and that depending on environmental conditions, certain genes will prove more advantageous than others; the carriers of such genes will leave more fertile offspring after them, and the proportion of "more useful genes in these circumstances" will augment relative to others in the genetic pool. This, in turn, will affect the way the species looks like. We see this effect at a smaller scale (and a much reduced time span) with selective breeding, where natural selective pressures are replaced by the whims of Man; that's how we can turn a grey wolf into a chihuahua.
