How Many Genes Do We Have?
Science
| February 20, 2008
| Tim
Actually, nobody knows for sure, the answer seems to be: "Not many more than a roundworm":
When analysis of the draft human genome sequence was published by the International Human Genome Sequencing Consortium on February 15, 2001, the paper estimated only about 30,000 to 40,000 protein-coding genes, much lower than previous estimates of around 100,000. This lower estimate came as a shock to many scientists because counting genes was viewed as a way of quantifying genetic complexity. With around 30,000, the human gene count would be only one-third greater than that of the simple roundworm C. elegans at about 20,000 genes (2).
Studies since the publication of the draft genome sequence have generated widely different estimates. An analysis by scientists at Ohio State University suggested between 65,000 and 75,000 human genes (3), and another study published in Cell in August 2001 predicted a total of 42,000 (4).
Although the number of human genes is still uncertain, a winner of GeneSweep was announced in May 2003. GeneSweep was an informal gene-count betting pool that began at the 2000 Cold Spring Harbor Laboratory Genome Meeting. Bets ranged from around 26,000 to more than 150,000 genes. Since most gene-prediction programs were estimating the number of protein-coding genes at less than 30,000, GeneSweep officials decided to declare the contestant with the lowest bet (25,947 by Lee Rowen of the Institute of Systems Biology in Seattle) the winner (1).
What does this mean? A hint: Since there are tremendous visible differences between a human and a roundworm, and apparently not that much more genetic information, what does that imply?
To me, it seems to imply that the main differences are in the organization of the genes. It's not how many different shapes of Lego blocks you have, it's how they're stuck together.
We're told over and over that humans and monkeys have a 99% similarity in chromosomes. To some, this implies we're no different than monkeys. But I notice that, then, the main difference then between a humans and monkeys concerns our chromosomes, not our genes:
Humans have 46 chromosomes while the other apes have 48 chromosomes. Sometime, way back when, on the way to Homo sapiens, the monkey chromosomes 11 and 12 fused to form what is now human chromosome 2. There are also eight major inversions in human chromosomes when you try to match them up with chimp chromosomes. Chromosome pairing is necessary for fertilization and the development of the egg. [1]
Notice: Monkeys and humans cannot mate because they have different numbers of chromosomes and different configurations, and chromosomal pairing is necessary for fertilization.
What is the definition of "species", dear reader? Do you know it?
As I was taught it, a "species" is "a classification of related organisms that can freely interbreed." [2] In other words, if two animals can interbreed (e.g. wolf and dog), they are said to be in the same species.
Charles Darwin's main claim to fame is that he addressed the question of "The Origin of the Species". The answer we are told today is that species develop because of genetic mutation -- not through changes in chromosomes. Yet the obvious answer, sitting right in front of us, seems to be that it is, in fact, changes in chromosomes which produce new kinds of animals which can't interbreed with others -- new species.
The differences between these two mechanisms are not trivial.
Genetic differences account for the differences, say, between red-haired people and blond-haired ones. Or between small dogs and larger dogs. Or between varieties of finches. Genetic changes happen by mutation, and can be slowly accumulated over time, as dog breeding nicely demonstrates.
Nobody has yet produced a new species by such changes, nor pointed to a concrete example of such.
Chromosonal changes happen all at once -- in one individual -- and can produce huge differences. Again, consider the difference between a human and a organutan. Or the difference between a normal adult and a mongoloid. We all know of examples of such changes which prevent long-term interbreeding. (Horse and donkey, for example, can produce only one generation.)
The idea that species are produced primarily by chromosomal tangling, shearing, etc. would be, I suspect, would unsettle many.
For one, there goes Darwinism.
Two, it would make a lot more sense of what see in the fossil record, with newly-formed species appearing full-blown, and little evidence of change beforehand or afterwards. (Billions of years of no-trilobites, then *bam* -- trilobites! Then layer upon layer of fossil trilobites with *no* significant changes.)
Three, it would leave us with an even bigger puzzle: Since significant chromosomal changes don't allow mating with the other members of the species, how is the new species produced? The change must happen in more than one individual in the same location or lifetime, or there must be a short series of partial changes happening in quick sequence among a small breeding group.
Either way, I suspect the theological problem would be that such an occurrence would be found to be hugely improbable, statistically. Perhaps not, but, if so, I suspect most materialist biologists would run screaming from such a specter. (Or have already.)
So, once more in parting:
1. Differing chromosomes prevent interbreeding
2. Inability to interbreed is what defines different "species"
Therefore species are produced primarily by chromosomal -- not genetic -- differences. This seems obvious.
If so Darwin and his followers are profoundly mistaken, and leading science down a blind alley. Otherwise, let me know if you can poke holes in this.
I'll try to write more later, but a few quick comments;
1. Female mules can breed with male horses to produce more mules.
2. Darwinism posits random variation (genetic) and natural selection. I'm curious which modern (last 20 years, say) geneticist is asserting that point mutations account for the majority of genetic variation? A change in chromosome number is a form of mutation.
3. For what it's worth, the notion that divergences in species among animals starts with a very small population is consistant with the "mitochondrial eve" hypothesis which asserts that all our mitochondrial DNA comes from a single maternal ancestor.
4. It's important to restrict such assertions to animals. Plants are a lot more tolerant to unusual karyotypes, and have been demonstrated to have some speciation mechanism that has at least not been demonstrated in animals to my knowledge and not related to chromosome number. Most of the fruit you eat has had its chromosome number artificially multiplied to increase fruit bulk.
Female mules typically produce horse offspring. Sorry.
A change in chromosome number is a form of mutation.
I don't disagree. But it's certainly not the kind of small-scale mutation usually being discussed -- for example, Dawkins' notion of a "selfish gene". An accumulation of small mutations, not a few large leaps.
Thanks for the link, though I didn't see much there about other large-scale chromosomal changes beyond non-disjunction.
Lets say that you have a chromosome replicated so that an animal now has a few extra chromosomes.
I'd agree it's the cause of at least some divergence of species as you claim, and possibly most of them. I'd agree that it's important. But what good is the simple replication of already present chromosomal material?
Granted, most people have a few mutations which are beneficial with one copy but harmful with two. For instance, women may be able to see in four channels of color if they have a mutation in one of their genes for their red cones. But if they have two copies of the mutation, they won't be able to see a large portion of the red spectrum and will be red-green colorblind. The same holds true for men with a single copy of the mutation. If that chromatic material were somehow replicated, that would allow an organism the opportunity to 'discard' the unneeded genetic replications and keep the beneficial mutations that co-existed with other crucial genes.
(also, some crucial genes, like those involved in the creation of mitotic spindles, seem to have multiple copies of themselves in eukaryotic genomes, according to what my Cell Bio professor told me)
Also, simple divergence of a small population might allow for a population to adapt itself to some other local niche.
I'm not arguing with the importance of what you're describing. It just seems to fit rather nicely into the Darwinist paradigm as far as I can tell, though it does seem to strike a blow to the gradualists.
Lets say that you have a chromosome replicated...
The word "replicated" does not occur in the post above. Instead, note the words "tangling", "shearing", and "fused".
I agree that a merely replicated chromosome doesn't necessarily have a huge impact. (Though it can have some -- such as with males with an extra Y chromosome.) That's why I haven't said anything much about it.
I'm not arguing with the importance of what you're describing. It just seems to fit rather nicely into the Darwinist paradigm as far as I can tell, though it does seem to strike a blow to the gradualists.
It doesn't fit into the classical Darwinian paradigm at all. Not even slightly. (Though I have no doubt that, if it were suddenly proven, most scientists would claim it was "obvious" all along. Everything is wrong until it's obvious.)
Wikipedia (italics in original):
In the 1930s, Darwinian natural selection was combined with Mendelian inheritance to form the modern evolutionary synthesis, in which the connection between the units of evolution (genes) and the mechanism of evolution (natural selection) was made. This powerful explanatory and predictive theory has become the central organizing principle of modern biology, providing a unifying explanation for the diversity of life on Earth.
The idea that genes are the units of evolution are the "central organizing principle of modern biology." Almost everything -- molecular clocks, selfish genes, genetic drift, discussion of finch beaks as a perfect example of the steps needed to produce new species (etc.) all focus around the gene -- not changes to chromosomes.
Darwinianism IS gradualism, Ryan. (Though, again, if disproved, I have no doubt most would suddenly claim otherwise, and begin the rewrite. Darwinism is not, as far as I can see, falsifiable.)
Darwin coined the term natural selection to describe the process by which organisms with favorable variations survive and reproduce at a higher rate. An inherited variation that increases an organism's chance of survival in a particular environment is called an adaptation. Over many generations, an adaptation could spread throughout the entire species. In this way, according to Darwin, evolution by natural selection would occur. [1]
Small changes accumulate gradually by conferring a competitive advantage. That's certainly not the same as posing one or two large jumps -- such as the fusing of two chromosomes -- which might suddenly create a vastly different animal, on or past the verge of being able to mate with most or all other members of its specie. Even Stephen Jay Gould (who is today not favored) never took it that far.
Another pervasive misunderstanding of punctuated equilibrium was that it invoked large-scale mutations, the sort invoked by Richard Goldschmidt in The Material Basis of Evolution. According to Dawkins, punctuated equilibrium "has no connection with macromutation and true saltation [a large jump in visible traits], but rather "followed from long accepted conventional Darwinism," namely Mayrian allopatric speciation. [2]
You may think the two ideas compatible but Dawkins (and Gould, I'd argue) whose names are synonymous with evolution, certainly didn't seem to think so.
And, again, whereas a small change to a gene is generally considered probable, and over time such changes can compete -- I suspect we will find that a large positive change is vastly more improbable, especially when you consider the small population numbers involved (such as the size of a single troop of monkeys).
Moreover, it would mean that the mechanisms of evolution -- a stunning and radical change to the chromosomes -- would not be a repeatable process we observe today. IDers, for example, point out that bacteria have trillions of short-lived individuals who are quite susceptible to genetic mutation -- yet don't seem to be producing new species. As non-Darwinian evolutionist Pierre Grasse noted:
What is the use of their unceasing mutations, if they do not change? In sum, the mutations of bacteria and viruses are merely hereditary fluctuations around a median position; a swing to the right, a swing to the left, but no final evolutionary effect. Evolution of Living Organisms (1977) p.87
Bacteria, the study of which has formed a great part of the foundation of genetics and molecular biology, are the organisms which, because of their huge numbers, produce the most mutants. This is why they gave rise to an infinite variety of species, called strains, which can be revealed by breeding or tests. Like Erophila verna, bacteria, despite their great production of intraspecific varieties, exhibit a great fidelity to their species. The bacillus Escherichia coli, whose mutants have been studied very carefully, is the best example. The reader will agree that it is surprising, to say the least, to want to prove evolution and to discover its mechanisms and then to choose as a material for this study a being which practically stabilized a billion years ago! Evolution of Living Organisms (1977) p.87 [3]
Whatever event first produced these bacteria seems to have been a one-way ticket.
Finally, if every form of "evolution" (change from one specie to another) can be called "Darwinian", then Darwinism itself has no meaning -- good heavens, even Intelligent Design proponents are evolutionists. Are they also then Darwinists?
And if all forms of evolution are really Darwinism, then what's the acrimonious war all about? Shouldn't the people who are saying the current reigning theory is full of holes be given some credit, should specie production be found to boil down more to sudden, large-scale changes to chromosomes rather than an accumulation of changes to genes and alleles -- or another non-Darwinian mechanism?
The man who first made me think about chromosomes was a biology professor (whose web page I have long since lost now) in New York who proposed that chromosomes had something to do with evolution. Sadly, he also had several web pages devoted to describing the persecution he received for dissenting from neo-Darwinism. You may think such changes fit neatly into Darwinism, but evidently his self-described Darwinian contemporaries did not.
And if Darwinism merely points down the assertion that evolutionary changes are "blind and unguided", with no specific, falsifiable mechanism, then it's nothing more than a religion.
(And, given the advent of Darwin Day, I'd say that's probably just about right in most cases.)
And if Darwinism merely points down the assertion that evolutionary changes are "blind and unguided", with no specific, falsifiable mechanism, then it's nothing more than a religion.
Finally, if every form of "evolution" (change from one specie to another) can be called "Darwinian", then Darwinism itself has no meaning
Darwinism as I understand it is typically contrasted to Lamarckism (or, alternately, the immutability of species and the belief that humans and monkeys do not, say, share a common ancestor.)
Darwinism would be contradicted by directed mutation or inherited acquired characteristics as opposed to variation and selection.
And there's some evidence for both, I'd argue. inheratance of DNA methalation would be one source for this.
But I'm not aware of Darwin himself proposing any genetic mechanism to be proved or disproved.
Interesting cites. I'll look into them later. When did this professor have his falling out with his contemporaries? We certainly were taught in college that evolution was more than just point mutations and I graduated in 2000.
Re: Grasse
What is the use of their unceasing mutations, if they do not change?
I'm not particularly impressed that he has to ask this question. Even microbes are subject to regular predation by viruses, which would favor adaptation to the local pathogenic environment, among other things. Which is adaptive, and thus evolutionary whether the organisms have stabilized or not. Also, some are more pathogenic than others, which is also an adaptation. Ewald has proposed an interesting theory for the environments which encourage coexistance or pathogenesis. But I'm open to the notion that E.Coli are fairly well adapted to their environment. And if some new bacterial species were generated by E.Coli, I'm not sure by what process we'd discern it.
Sorry this is breif and less than a comprehensive response.
Darwinism would be contradicted by directed mutation or inherited acquired characteristics as opposed to variation and selection.
Indeed it would. But that's certainly not the only way Darwin's theory could be contradicted.
If I make even a simple proposition, say "Bob murdered the deceased with poison", there are numerous ways I could be wrong. It might have been a different person, the cause of death might have been natural, the poison might have been administered by accident -- the alleged victim might even still be alive.
The core of Darwin's differences with his opponents, it seems to me, is nicely summed up in this short paragraph from his last chapter:
But the chief cause of our natural unwillingness to admit that one species has given birth to other and distinct species, is that we are always slow in admitting any great change of which we do not see the intermediate steps. The difficulty is the same as that felt by so many geologists, when Lyell first insisted that long lines of inland cliffs had been formed, and great valleys excavated, by the slow action of the coast-waves. The mind cannot possibly grasp the full meaning of the term of a hundred million years; it cannot add up and perceive the full effects of many slight variations, accumulated during an almost infinite number of generations.
Just as a cliff is excavated one small rock at a time, so also Darwin argues that numerous slight changes accumulating over millions of years produce a new species.
In contrast, consider the fusing of two monkey chromosomes to form human chromosome #2.* Whatever individual first possessed that might have appeared markedly different than its parents. That's precisely the sort of difficulty Darwin is right here (and his successors, in previous quotes) is saying his theory removes by posing the accumulation of innumerable small changes, akin to a cliff being slowly eroded out a hill.
(And see the other quotes I supply above -- Dawkins also insists that Darwinism implies gradualism -- and that even punctuated equilibrium is still gradualism because it implies a multitude of slight changes happening in a smaller -- but still considerable -- period of time.)
(* And how would this individual have mated, having had a differing number of chromosomes, and no-where for chromosomes #11 & #12, among its potentials mates, to pair up with? (And now having an "extra" chromosome with no clear match?) While it's not hard to see how an extra chromosome would pose no difficulty (it's simply left out in the cold, while its twin gets busy) this seems a bit more difficult -- though I don't claim expertise, certainly.)
While looking for a few more quotes regarding gradualism, I discover Dawkins, red-handed, attempting to define "gradualism" in mainly theological terms:
In Darwin's time what he was fighting against was, well really, closet creationists who thought that god gave evolution kind of a helping hand over difficult jumps. So that's the sense that Darwin was a gradualist, and in that sense Steve Gould was too. Punctuationism is gradualism in the sense in which Darwin was a gradualist.
The the test here (which differs a little from the previous quote I cite above) for "gradualism" simply comes down to: "What do you believe about God and the meaning of difficult jumps?" Your inner thoughts on the likelihood of such things occurring without purpose determine the categorization of your proposed mechanism! Since Gould was a nice safe agnostic, his theory fit within "gradualism"!
Hilarious!
Total tangent (as Dawkins gives a better, more testable and less laughable explanation in the previous quote), but telling nonetheless. That's pretty much a confirmation of what I said above, that the key feature of Darwinism, for many seems to have become not some specific testable mechanism, but a general sense that no purpose operates here. (And hence, that Darwinism is no longer, for such people, a scientific proposition, in Karl Poppers' sense of the word.)
By the same token, I guess, since I'm willing entertain the possibility of a "helping hand" should we ever face the sufficiently improbable, I would guess my argument here could not be a form of gradualism, and hence not Darwinism. ;-)
Grasse: What is the use of their unceasing mutations, if they do not change?
Ryan: I'm not particularly impressed that he has to ask this question.
Keep in mind that he penned this in the 1960s or 1970s, nearly 40 or so years ago -- and that this sentence has little context.
My point in citing the quote was not regarding the short-term usefulness of various genetic modifications (which is easy to make a case for, such as the ability of dogs to adapt making them useful to humans, or the size of finch beaks varying to help them gather different foods in different periods of availability) but the larger point that these changes don't seem to result in any sort of recent new species, despite ample time in which to do so.
As I said before, whatever produced e coli seems to have been a one-time event, not an ongoing change we can observe happening right now, as Dawkins and co insist.
... if some new bacterial species were generated by E.Coli, I'm not sure by what process we'd discern it.
Well, for one, we should see totally new bacteria appearing on a yearly basis. Not merely strains, but whole new species of bacteria. (How many apes have ever lived? I would suspect it would be a minuscule fraction of the # of individuals of bacteria produced in a single year. And given bacteria's even greater susceptibility to mutation, we should see far more speciation.)
As I understand it, the current reigning theory would suggest we could then use "molecular clocks" and morphological tests to link these constantly-appearing new bacteria to their progenitors.
Please note that I'm NOT suggesting that new species of bacteria never appear. (Though I'd welcome an example. Even the famed nylon-eating bacteria is merely a strain.) Just that it's not nearly as frequent as we'd expect given the current popular model of evolution as the accumulation of small mutations of the sort bacteria (and other animals) regularly exhibit.
Since significant chromosomal changes don't allow mating with the other members of the species, how is the new species produced?
A single chromosomal inversion doesn't nessicarily cause sterility. It can reduce fertility among hybrids (unions between those with the change and without it.) There are a lot of writings on evolutionary biology which posit some kind of isolation as contributing to speciation for this reason. So chromosomal inversion and speciation resulting from it would fit in with a kind of gradual (i.e. "stepwise" process.)
link
I haven't had time to research what happens when two chromosomes combine yet, except to find that the platypus has numerous sex chromosomes and doesn't pair those chromosomes, but instead 'chains' them.
The word "replicated" does not occur in the post above. Instead, note the words "tangling", "shearing", and "fused".
and etc. ;)
An inversion wouldn't nessicarily cause a jump straight to sterility and you'd mentioned that "chromosomal pairing is neccessary for fertilization." The question of what results a fused chromosome has in terms of non-gradual speciation are still relevant, but I haven't had time to research those yet.
Chromosomal rearrangements are thought to be important in speciation because sometimes they can disrupt meiosis in hybrids, thereby causing sterility (7–9). Drosophila species have been studied extensively with regard to chromosomal rearrangements and their fitness consequences, both in the context of direct effects of inversions (10–12) and effects associated with allelic differences between genes contained within them (e.g., refs. 13 and 14). One of the most common types of rearrangement, the paracentric inversion, is not considered to play a role in speciation, because hybrids of parents differing in these gene arrangements are fully fertile and viable. Recombination is prevented effectively between different arrangements, although it still occurs readily across uninverted regions of these chromosomes.link 2001
Tim - The idea that genes are the units of evolution are the "central organizing principle of modern biology." Almost everything -- molecular clocks, selfish genes, genetic drift, discussion of finch beaks as a perfect example of the steps needed to produce new species (etc.) all focus around the gene -- not changes to chromosomes.
link
While I personally think that mutation rates are too variable based on environment to work as clocks, it makes sense to use them rather than having to sequence an entire genome before work can begin. Perhaps Dawkins ignores things like chromosomal inversions. I'm not familiar with his work. But I can find piles of articles on such processes in both research abstracts and educational materials. Are you saying that they're sparse, or just that a group is or was ideologically opposed to such things.
Perhaps this is some recent revolution that occurred just a little while before I went to school.
From our results, we propose a preliminary genic model whereby inversions may contribute
to the speciation process, thereby explaining the abundance of arrangement differences between closely related species that co-occur geographically. We suggest that inversions create
linkage groups that cause sterility to persist between hybridizing taxa.
link (received for review June 1, 2001)
Likewise, there does seem to be some evidence that some "neo-darwinists" are exclusive gradualists (as opposed to facultative gradualists ;-) ), as well as those two terms can be defined.
Well, for one, we should see totally new bacteria appearing on a yearly basis. Not merely strains, but whole new species of bacteria.
First, the term 'species' here is rather arbitrary since the ability to breed is no longer the criterion for a species. So "speciation" in bacteria is a different word, a different catagory than the term applied to animals. Even in non-sexual species, a large quantity of DNA can be integrated directly into the bacterial chromosomes. I don't claim to be well versed in microbial taxonomy, but the term 'species' is, as well as I understand it in this situation, mostly a semantic classification and not an objective statement. We could just as easily re-label each strain as "a new species" as we could classify or re-classify pluto as a planet and then we would "have new species." What I'm trying to get at is; what underlying observable physical change is Grasse looking for that he did not find? Without that explanation, the phrase "no new species of X microbe" means nothing whatsoever.
I can understand his point that because E. Coli is so well adapted to its environment, that not many changes are required of it and that it might therefore a poor model (or none of that may be true). I don't think the current definition of genetic relatedness of species was even used back in the 1970s. Using the term 'species' which means different things in different situations is grounds for confusion.
From a 2001 article related to microbial taxonomy;
Currently, full-genome sequences for multiple isolates of a single microbial species are rare, implying that genetic typing is still performed by methods that are inherently suboptimal.
...In addition to the shortcomings of current genetic typing methods, researchers involved in the aforementioned fields of microbiology that employ these methods to genetically characterize organisms tend to use different vocabularies, experimental methodologies, and modes of data processing and interpretation. This is a problem since communication of data is obstructed because of a general lack of standardized genetic typing procedures. Except for primary DNA sequences, typing data frequently suffer from limited interlaboratory reproducibility. In light of these issues, an integrated experimental and theoretical approach to taxonomy, evolutionary and population genetics, and epidemiological typing of microorganisms is vital.
... The definition of species is a primary underlying concept; however, it is controversial and is undergoing continuous refinement....
...When the diverse microbial world is considered, many species of microorganisms have been described on the basis of phenotypic characteristics without any clues to their phylogenetic status being available....
...For bacteria, a species was defined as an entity in which members have a DNA-DNA homology value of at least 70% ...
...This genospecies concept can be replaced by the alternative but more general phylogenetic species concept proposed by Cracraft (17). According to this concept, a species is a "group with a common origin that is composed of the smallest diagnosable cluster of individual organisms within which there is a parental pattern of ancestry and descent." It has been proposed that a microbial species should correspond to a discrete typing unit to be valid (109). In contrast to the genospecies concept, the discrete typing unit concept does not imply any given level of phylogenetic divergence and refers only to the criterion of genetic discreteness. Consequently, this approach relies heavily on the quality of genetic typing data. The criterion of genetic discreteness can be adhered to in a strict manner, in which case the species definition is clear-cut. On the other hand, species can be considered "condensed nodes" in an "otherwise cloudy, confluent taxonomic space"...
...Taxonomists using the strict species definition have been accused by population geneticists of arbitrarily imposing divisions in a continuum...
...At least four fundamental mechanisms can give rise to variation used to define evolutionary genetics: mutation, hypermutation, genetic recombination, and selection. ...
...in recent years evidence has accumulated supporting the view that microbial genomes have far greater mutational flexibility than was previously assumed. Microbial mutation rates vary not only among species but also among different genes of the same individual and even within the same gene at different time points...
...Although this is perhaps counterintuitive, genetic recombination can decrease the level of genetic variation under some conditions...
link(2001)
from my comment; While I personally think that mutation rates are too variable based on environment to work as clocks...
The bolded portion of my above comment should have been deleted.
So that we're comparing apples to apples so to speak, we should ask what would happen if the definition of species used for animals (the ability to create fertile offspring) were applied to bacteria. The ability of a species to genetically recombine with another in the presence of a functional repair mechanism is a decent analogy, though slightly laxer than the one used for animals. Different body types, mating patterns, geographical separation and so forth are enough to prevent free interbreeding in animals though we wouldn't care about these problems in microbes.
The experiment below demonstrated that resistance to recombination between E. Coli with a common ancestor could develop in less than ten years.
There doesn't seem to be an impregnable barrier to recombination even between micro-organisms of entirely different genera. Having to juggle billions of bacterial species would not make for a very functional taxonomy, though.
...The biological species concept emphasizes the roles of sex and recombination in maintaining evolutionary cohesion (1, 3). This concept is often problematic for organisms, such as bacteria, that do not reproduce sexually. Indeed, some may question the validity of bacterial species given their lack of regularized sex and recombination. Nonetheless, bacteria do undergo genetic exchange via plasmid-mediated conjugation, virus-mediated transduction, and (in some groups) transformation (4, 5). Therefore, the potential for recombination may be one useful metric, among others, for delimiting bacterial species, even if it is not sufficient in all cases...
...Recent attention has focused on the genetic basis of species differences in both eukaryotes (9, 10) and bacteria (11). To date, this work has been largely statistical and has not considered the special importance of genetic factors that can modulate recombination....
...Four populations of Escherichia coli B were propagated for 20,000 generations...
... The evolving populations were founded from a single asexual clone, and mutation was their only source of genetic variability. They were propagated for some 20,000 generations in a simple, defined environment. The ancestral strain, and most derived lines, have functional MMR pathways, but some lines spontaneously evolved mutator phenotypes caused by defects in MMR (24). In this study, we examine two lines (designated A-1 and A+2) that retained functional MMR throughout the 20,000 generations of experimental evolution, two other lines (designated A-2 and A+3) that became defective for methyl-directed MMR around generation 3,000 and remained mutators throughout the subsequent 17,000 generations, and their common ancestor (designated Anc)...
...These data indicate that each mutator line independently diverged from the ancestor to an extent that was sufficient to create a barrier to recombination...
...In conclusion, these data support all of our predictions concerning the effects of MMR on recombination rate, with the minor exception that MMR slightly impedes recombination even among self-crosses; this last effect has been observed previously in yeast (15). These findings thus support three key components of a recent model (16, 28) that postulates an important role for MMR in speciation: (i) populations that evolve defects in MMR undergo rapid genetic divergence from other populations because of their mutator phenotypes; (ii) this accelerated sequence divergence does not impede recombination as long as the MMR system remains defective; but (iii) on reacquisition of a functional MMR system, the accumulated sequence divergence presents a genetic barrier to further recombination. Of course, the magnitude of the barrier to recombination in our experiments is much smaller than the barrier between such clearly distinct species as E. coli and Salmonella enterica (13, 14, 16), which have diverged from a common ancestor for approx 130 million years (29). Nonetheless, our findings indicate that an incipient barrier can evolve rapidly, during only 20,000 generations (less than 10 years under the experimental conditions)....
...We have demonstrated experimentally the plausibility of this model in which speciation is promoted by mutations that destroy MMR (accelerating sequence divergence) followed by reacquisition of functional MMR (reducing subsequent recombination). There is a high incidence of MMR deficient mutators among natural isolates of E. coli and Salmonella (20, 21). Ongoing retrospective (phylogenetic) studies, aimed to determine how often functional MMR genes have been reacquired by gene transfer, will be critical to assess the importance of these events in nature...
Mutation, recombination, and incipient speciation of bacteria in the laboratory (June 22, 1999)
A single chromosomal inversion doesn't nessicarily cause sterility.
Err, I don't recall suggesting it would. In fact, I suspect all sorts of chromosomal mutations might be viable. That's why I suggested the rather-more-dramatic example of a chromosomal fusion which (among others) differentiates humans and apes.
I'm only suggesting it might pose a pretty nasty puzzle -- obviously, an individual did experience such a change and reproduced. How did it mate with its "normal" peers -- or another similarly mutated individual?
... the platypus has numerous sex chromosomes and doesn't pair those chromosomes, but instead 'chains' them.
Interesting!
But I can find piles of articles on such processes [chromosomal inversions, etc.] in both research abstracts and educational materials. Are you saying that they're sparse, or just that a group is or was ideologically opposed to such things.
I'm saying that the standard theory I've heard is and has been focused on the gene as the "central unit of evolution" (see quotes above) -- not primarily chromosomal changes as the means of speciation. (I'm not saying, for example, that nobody has ever written about chromosomal mutation.)
And yes, I'm also suggesting that the chromosome as the "central unit" of evolutionary change could (perhaps I'm wrong -- this idea is new to me) have troubling implications for some. Again, look into Dawkins' disgust at the idea of saltation. As a New York Times writer put it:
NOT content with rebutting creationists, Mr. Dawkins presses his arguments against those who claim to have invented serious alternatives to the generally accepted ''neo-Darwinian'' view. The theory of punctuated equilibria, for example, proposes that the rate of evolutionary change varies, so that sometimes change is rapid, sometimes none occurs at all. Evolution by jerks, or rapid steps, has been confused with evolution by saltations, or leaps, in which major change would occur in a single generation. Mr. Dawkins accuses Mr. Gould, the leading propagandist of the punctuational view, of misleading people by using ''saltation'' to describe two very different processes. Orthodox theory rules out leaps, but emending it to allow for a lot of rapid steps [rapid gradualism] means only a change in emphasis. [As reposted on Dawkins' site]
And it seemed Gould would have agreed:
The Cambrian Explosion was an example of rapid gradualism. Here, I explicitly remember an essay by Gould explaining it this way. In fact, he provided arguments as to why the Cambrian Explosion was very gradual (relative to the lives of the animals involved, not in terms of geological time).... Gould makes brief statements about the Cambrian Explosion NOT being an example of saltation. However, in Dawkins doesn't feel that Gould is emphasizing the point enough. [1]
I'm not sure how much material I'll have to cite here to make the point that standard Darwinism, as it is understood by leading exponents, leaves room for no large jumps of the sort that chromosomal changes are (it seems to me) capable of producing.
Notice how such theories are called "non-Darwinian" and opposed vigorously, on seemingly ideological grounds (Dawkins' anger at Gould's failure to clarify is akin to that of a partisan fighting a war, not that of one scientist who simply cannot decipher a cryptic phrase by another).
I suppose at this point I should also mention the case of John Davidson, professor emeritus of biology at U Vermont. I've just discovered his Evolutionary Manifesto which suggests a "semi-meiotic" mechanism for evolution. I'm not finished reading it, and I'm certainly not an expert in the field, but it looks approximately like the sort of thing I've been pondering and suggesting here. (Perhaps Davison is the professor I stumbled upon in the past?)
He seems to believe such a mechanism would be properly labeled as "saltation", and it seems his peers were indeed rather opposed to something he wrote. It would seem he received a pay freeze lasting over a decade, was relieved of teaching responsibilities, and had an inquiry launched into his views.
So, um, yes, unless that's all fiction, or unless his views are obviously cracked in some way I'm not detecting, it would seem such ideas do generate ideological resistance.
First, the term 'species' here is rather arbitrary since the ability to breed is no longer the criterion for a species.
Quite right. I realized that shortly after posting. But one would expect something more significant than a few mutations -- the 70% threshold sounds like a reasonable arbitrary line. Examples still welcomed.
I see we've been posting in parallel!
The experiment below demonstrated that resistance to recombination between E. Coli with a common ancestor could develop in less than ten years... Having to juggle billions of bacterial species would not make for a very functional taxonomy, though.
So in other words, the resulting bacteria might have passed the "specie" test applied to larger animals, but it would still be considered e coli if only because failing to do so would give one a taxonomical headache?
I may be misunderstanding it, but it seems to me that the implication here is a bit arbitrary. Let me explain: First, two populations of bacteria were created from clones and allowed to live separately for many generations. Some lost their ability to do MMR (DNA mismatch repair). Those individuals/lines experienced significant genetic drift, but were still able to recombine with divergent DNA. (Understandably. Borrowing from network work, we might say their DNA was in "promiscuous mode.") Later, a mutation would switch MMR back on, again protecting their DNA from significant changes, and locking them into a mode in which they were too different from the other population to mate (recombine).
That seems somewhat arbitrary because it seems if we then dumped them in with the other population (say, they came into proximity again) individuals would AGAIN experience a mutation which turned MMR off, allowing them again to recombine with the other population, resulting in general drift right back towards compatibility.
In other words, their inability to mate is just a temporary phenomenon. It's as if, using our analogy, you could put monkeys and humans together, and again get them producing fertile offspring again. If that could happen, would we really have different "species"?
What I'm saying, I guess, is that perhaps speciation isn't speciation if said animals could still possibly mate with each other.
Without my caveat, it raises some real-life questions: Presumably, Europeans and Native American Indians were separated by at least tens of thousands of years (not just ten). Yet I'd bet both populations would have been found to both have something recognizable as "E. Coli" living in their guts. ;-)
What do you think?
On the other hand, if what I'm saying is true, then it may be that E. Coli can only travel so far from some central functional "norm", around which the mutations will invariably rotate -- "a swing to the right, a swing to the left." At any given moment, a few individuals could be found who couldn't mate, but all it takes is an MMR flip before the law of averages comes back into play. If so, that would certainly explain why long-separated populations might still have something recognizable as "E. Coli" in their guts.
Thanks for an interesting and stimulating discussion!
I'll have to check out John Davidson. It's amazing how absolutely fascist scientists can be at times.
So in other words, the resulting bacteria might have passed the "specie" test applied to larger animals, but it would still be considered e coli if only because failing to do so would give one a taxonomical headache?
So far as I can tell. A lot of taxonomy is done for the sake of functionality and convenience. And functionally back when Grasse wrote it made a lot of sense to catagorize microorganisms based on what they could metabolize. A lot of taxonomic tests revolve around things like gram stains, substances that can be broken down or metabolized, etc.
In other words, their inability to mate is just a temporary phenomenon.
Well, to be clear their ability to 'mate' (conjugate) was gone before the experiment even started. Sorry if my editing made that unclear. The issue here was with increased difficulty recombining due to divergence (recombining is more forgiving. But it seems to fit the 'fertile offspring' requirement better. )
And while a member of the strain might regain the ability to conjugate and eventually even recombine at normal rates, I'm not sure that the entire strain would go that direction if it had established itself in some new niche.
But an even weaker standard is applied to animals.
Tigers can breed with lions and produce fertile offspring.
Polar bears can breed with Alaskan brown bears and produce fertile offspring.
But because the two cannot interbreed in nature, they are considered separate species.
link
Thanks for an interesting and stimulating discussion!
Likewise!
Yet I'd bet both populations would have been found to both have something recognizable as "E. Coli" living in their guts. ;-)
What do you think?
Sounds like a safe bet.
My interest here is; to what degree does the environment of its host set the limits on what the bacteria would adapt towards? If you set up a cycle where a population regularly contaminated its drinking water with feces (an environment which preferrs rapidly multiplying pathogens who sacrifice their hosts) how quickly would some strain of E. Coli adapt to take advantage of the opportunity?
My guess is that they'd evolve relatively quickly in that direction. Whether it would likely be a conjugating population or a clonal strain, I don't know.
Also, regarding chromosomal arrangement, my college microbio textbook (Brock, biology of microorganisms, most recent revision 1997 c.9 p 343) asserts the following which I thought might be of interest to you;
although there may be no general rules governing gene location, there do seem to be some constraints. Many bacteria have a similar organization of genes near the origin of DNA synthesis, and similarities also exist at the terminus of DNA synthesis. Also, in at least some Bacteria, including E. coli, it appears that for certain genes or regions it is advantageous for the direction of transcription to be the same as that of the movement of the DNA replication fork. In these cases, an inversion mutation can be very deleterious to the organism.
The pattern of gene location along the chromosome may give clues to the evolution of the chromosome, and it seems clear that in many bacteria, transopsition and other large-scale rearrangements have been important.
I'm not sure whether the focus on the gene as a central unit of evolution might be a case of 'looking for your keys under the lamp post because that's where the light is.' Genes seem significant, knowledge of them produces results and they were more tractable to work with back when it was an effort to simply map a gene. (E.Coli's genome was only mapped in '97)
In 2000 they were just wrapping up a 'working draft' of the Human Genome Project to produce chromosomal maps of a handful of reference organisms. It may be that scientific focus will change towards gene arrangement and 3D structures now that we have the technology to work with those kinds of things.
Jeff Hawking has a similar criticism of using PET scans to measure the brain's blood flow during tasks. It seems like people often organize their knowledge around the tests that they're capable of doing.
transopsition = transposition
transopsition -> transposition
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I'll try to write more later, but a few quick comments;
1. Female mules can breed with male horses to produce more mules.
2. Darwinism posits random variation (genetic) and natural selection. I'm curious which modern (last 20 years, say) geneticist is asserting that point mutations account for the majority of genetic variation? A change in chromosome number is a form of mutation.
3. For what it's worth, the notion that divergences in species among animals starts with a very small population is consistant with the "mitochondrial eve" hypothesis which asserts that all our mitochondrial DNA comes from a single maternal ancestor.
4. It's important to restrict such assertions to animals. Plants are a lot more tolerant to unusual karyotypes, and have been demonstrated to have some speciation mechanism that has at least not been demonstrated in animals to my knowledge and not related to chromosome number. Most of the fruit you eat has had its chromosome number artificially multiplied to increase fruit bulk.
Posted by: Ryan W. on February 20, 2008 03:50 PM