..Unbelievable Y chromosome differences between humans and chimpanzees
Quote:Indeed, at 6 million years of separation, the difference in MSY gene content in chimpanzee and human is more comparable to the difference in autosomal gene content in chicken and human, at 310 million years of separation.
So much for 98 percent. Let me just repeat part of that: humans and chimpanzees, "comparable to the difference ... in chicken and human".
The human Y chromosome began to evolve from an autosome hundreds of millions of years ago, acquiring a sex-determining function and undergoing a series of inversions that suppressed crossing over with the X chromosome1, 2. Little is known about the recent evolution of the Y chromosome because only the human Y chromosome has been fully sequenced. Prevailing theories hold that Y chromosomes evolve by gene loss, the pace of which slows over time, eventually leading to a paucity of genes, and stasis3, 4. These theories have been buttressed by partial sequence data from newly emergent plant and animal Y chromosomes5, 6, 7, 8, but they have not been tested in older, highly evolved Y chromosomes such as that of humans. Here we finished sequencing of the male-specific region of the Y chromosome (MSY) in our closest living relative, the chimpanzee, achieving levels of accuracy and completion previously reached for the human MSY. By comparing the MSYs of the two species we show that they differ radically in sequence structure and gene content, indicating rapid evolution during the past 6 million years. The chimpanzee MSY contains twice as many massive palindromes as the human MSY, yet it has lost large fractions of the MSY protein-coding genes and gene families present in the last common ancestor. We suggest that the extraordinary divergence of the chimpanzee and human MSYs was driven by four synergistic factors: the prominent role of the MSY in sperm production, ‘genetic hitchhiking’ effects in the absence of meiotic crossing over, frequent ectopic recombination within the MSY, and species differences in mating behaviour. Although genetic decay may be the principal dynamic in the evolution of newly emergent Y chromosomes, wholesale renovation is the paramount theme in the continuing evolution of chimpanzee, human and perhaps other older MSYs.
Just glancing at the ideograms, they don't even look like homologous chromosomes!
Obviously they are; there's a whole lot of homologous sequence in there including functional genes. But the structure of both human and chimpanzee Y chromosomes has evolved incredibly fast compared to the rest of the genome.
The central question: beyond its interest for Y chromosome structural evolution, what does this result say about the evolution of human (and chimpanzee) phenotypes?
Option 1: Maybe nothing. The main mechanism for the rapid structural evolution was probably autologous recombination. Imagine that the Y chromosome wriggles around and different copies of repetitive sequences get together with each other.
The molecular mechanisms that enabled this wholesale remodelling of ampliconic regions merit consideration. Although the chimpanzee and human MSYs do not normally participate in meiotic exchange with a partner chromosome, the mirroring of sequences in the ampliconic regions provides ample opportunity for ectopic homologous recombination within the MSY. This recombinational proclivity is well documented in the human MSY, where it has repeatedly given rise to large-scale structural polymorphisms during the past 100,000 years of human history as well as to Y-chromosomal anomalies that cause spermatogenic failure and sex reversal in current generations. We suggest that ectopic homologous recombination between MSY amplicons has similarly accelerated structural remodelling of the MSY in the chimpanzee and human lineages during the past 6 million years.
That leads to rapid structural evolution, but not necessarily any functional changes.
Option 2: Massive changes in gene regulation. Then again, widespread relocations of genes have a way of stripping them apart from upstream (or downstream) elements that may regulate their expression. Besides that, chimpanzees have lost several genes entirely, while humans have picked up a few that weren't in the common ancestor. So there's a potential for phenotypic evolution from these changes, possibly reverberating through the genome.
In aggregate, the consequence of gene loss and gain in the chimpanzee and human lineages, respectively, is that the chimpanzee MSY contains only two-thirds as many distinct genes or gene families as the human MSY, and only half as many protein-coding transcription units.
That's pretty amazing. They speculate that the most important phenotypic correlates of these genetic changes may be related to sperm or testicular function, which certainly is a target of rapid evolution elsewhere in the chimpanzee and human genomes.
Option 3: Hitchhiking. OK, this isn't different or mutually exclusive from the above, but it's worth remembering that it only takes a single advantageous mutation to fix the entire Y chromosome in the population. That event carries with it whatever strange mutations might be on the same copy as the initial advantageous change. This kind of event may have happened dozens or even hundreds of times on the chimpanzee and human lineages. Indeed, if it was common enough, hitchhiking can drive its own dynamic, since it tends to fix lots of slightly deleterious variations that later have to be repaired or accommodated.
An interesting possibility: Maybe the extreme evolution of the Y chromosome in the emerging human and chimpanzee lineages explains the unusual similarity of their X chromosomes.
I'm thinking back to the story about chumans and the divergence of chimpanzee and human lineages ("The dawn chumans"). Patterson and colleagues (2006) suggested that the two lineages had undergone some kind of hybridization event long after they began to diverge. This surprising hypothesis was meant to explain why the X chromosome shows a substantially lower level of genetic difference between humans and chimpanzees, compared to the average autosomal locus. I don't think that a late hybridization is necessary to account for X chromosome similarity. A large ancestral effective population size implies a wide variance in coalescence times in the ancestral population; the average on the X will be lower than the autosomes, and if there was any hitchhiking the X would be lower still.
But...that X chromosome similarity might have a different explanation. A fraction of the human Y chromosome continues to recombine with the X. Imagine an initially rapid divergence of Y chromosomes within the chuman population. For a while, there might have been a strong selection pressure on the ancestral X to equip it for the structural diversity of the Y. Possibly an inverse relation would have emerged: the as the Y becomes variable (possibly in partially isolated subpopulations), the X adapts to that variation until reproductive isolation finally occurs.
Could this have been the proximate cause of human-chimpanzee reproductive isolation? The sex chromosomes are often implicated in speciation through Haldane's rule. It's a bit of speculation, but not too far from some discussion within the paper, particularly the relation between Y chromosome variations and infertility
The human Y chromosome began to evolve from an autosome hundreds of millions of years ago,...
Quote:The human Y chromosome began to evolve from an autosome hundreds of millions of years ago,...
Now we've got humans evolving for hundreds of millions of years... I assume you have some sort of evidence for such a claim? That would be, of course, some item of clothing or tools or personal hygiene items from, say, around 100,000,000 BC or thereabouts...
We ARE related of course. But the relationship amounts to similar design and/or genetic re-engineering, and not evolution.
Nobody really believe in it any more and it's basically about lifestyles and not science
Face it, even if I HAD said something like that, it would still make sense compared to evolution and evoloserism.
We ARE related of course. But the relationship amounts to similar design and/or genetic re-engineering, and not evolution.
Monday February 12, 2001
The potentially-poisonous Japanese fugu fish has achieved notoriety, at least among scientists who haven't eaten any, because it has a genome that can be best described as "concise". There is no "junk" DNA, no waste, no nonsense. You get exactly what it says on the tin. This makes its genome very easy to deal with in the laboratory: it is close to being the perfect genetic instruction set. Take all the genes you need to make an animal and no more, stir, and you'd get fugu. Now, most people would hardly rate the fugu fish as the acme of creation. If it were, it would be eating us, and not the other way round. But here is a paradox. The human genome probably does not contain significantly more genes than the fugu fish. What sets it apart is - and there is no more succinct way to put this - rubbish.
The human genome is more than 95% rubbish. Fewer than 5% of the 3.2bn As, Cs, Gs and Ts that make up the human genome are actually found in genes. It is more litter-strewn than any genome completely sequenced so far. It is believed to contain just under 31,780 genes, only about half as many again as found in the simple roundworm Caenorhabditis elegans (19,099 genes): yet in terms of bulk DNA content, the human genome is almost 30 times the size.A lot is just rubbish, plain and simple. But at least half the genome is rubbish of a special kind - transposable elements. These are small segments of DNA that show signs of having once been the genomes of independent entities. Although rather small, they often contain sequences that signal cellular machinery to transcribe them (that is, to switch them on). They may also contain genetic instructions for enzymes whose function is to make copies and insert the copies elsewhere in the genome. These transposable elements litter the human genome in their hundreds of thousands. Many contain genes for an enzyme called reverse transcriptase - essential for a transposable element to integrate itself into the host DNA.
The chilling part is that reverse transcriptase is a key feature of retroviruses such as HIV-1, the human immunodeficiency virus. Much of the genome itself - at least half its bulk - may have consisted of DNA that started out, perhaps millions of years ago, as independent viruses or virus-like entities. To make matters worse, hundreds of genes, containing instructions for at least 223 proteins, seem to have been imported directly from bacteria. Some are responsible for features of human metabolism otherwise hard to explain away as quirks of evolution - such as our ability to metabolise psychotropic drugs. Thus, monoamine oxidase is involved in metabolising alcohol.
If the import of bacterial genes for novel purposes (such as drug resistance) sounds disturbing and familiar, it should - this is precisely the thrust of much research into the genetic modification of organisms in agriculture or biotechnology.
So natural-born human beings are, indeed, genetically modified. Self-respecting eco-warriors should never let their children marry a human being, in case the population at large gets contaminated with exotic genes!One of the most common transposable elements in the human genome is called Alu - the genome is riddled with it. What the draft genome now shows quite clearly is that copies of Alu tend to cluster where there are genes. The density of genes in the genome varies, and where there are more genes, there are more copies of Alu. Nobody knows why, yet it is consistent with the idea that Alu has a positive benefit for genomes.
To be extremely speculative, it could be that a host of very similar looking Alu sequences in gene-rich regions could facilitate the kind of gene-shuffling that peps up natural genetic variation, and with that, evolution. This ties in with the fact that human genes are, more than most, fragmented into a series of many exons, separated by small sections of rubbish called introns - rather like segments of a TV programme being punctuated by commercials.
The gene for the protein titin, for example, is divided into a record-breaking 178 exons, all of which must be patched together by the gene-reading machinery before the finished protein can be assembled. This fragmentation allows for alternative versions of proteins to be built from
the same information, by shuffling exons around. Genomes with less fragmented genes may have a similar number of overall genes - but a smaller palette of ways to use this information. Transposable elements might have helped unlock the potential in the human genome, and could even have contributed to the fragmentation of genes in the first place (some introns are transposable elements by another name). This, at root, may explain why human beings are far more complex than roundworms or fruit flies. If it were not for trashy transposable elements such as Alu, it might have been more difficult to shuffle genes and parts of genes, creating alternative ways of reading the "same" genes. It is true that the human genome is mostly rubbish, but it explains what we are, and why we are who we are, and not lying on the slab in a sushi bar.
• Deep Time by Henry Gee will be published shortly in paperback by Fourth Estate. He is a senior editor of Nature.
Not owning a time machine, I would not really be in a position to say who exactly had been doing any genetic engineering in the day of Alley Oop.
I'm implying that to be one possibility, amongst two or three, and that does not include evolution which I view as mathematically impossible. One possibility not to be overlooked is that prior to the flood, the more advanced creatures of the Earth were able to somehow or other modify their OWN morphology from one generation to the next. That's what Gunnar Heinsohn's studies of Neanderthals would suggest
I'm implying that to be one possibility, amongst two or three, and that does not include evolution which I view as mathematically impossible.