Beeblebrox, I really did not find Ben’s criticism of your idea particularly “condescending” in tone, but I did find your response to him to be so:
First, he said a sequence, which doesn’t imply a single sequence. Of course, the cellular machinery required to back-translate a protein does not exist. But I think asking “Do you even know what a codon is?” was inappropriate in tone, at least outside the Pit.
ambushed, I have read both Dawkins (the Selfish Gene) and Gould (several papers and books), and while I found Dawkins’s arguments fascinating, I think his ideas also have some logical flaws. And for the most part, I really liked Gould’s perspective. I definitely will check out the book by Dawkins you recommended, but I’d be interested in hearing why you dislike Gould’s theories. Is there any type of consensus about these two authors in the scientific community?
No, it doesn’t. The current consensus is that the computing power- not the complexity, mind you, but the computing power- of a bacterium or a single neuron is more or less like that of a pocket calculator. Are you familiar with Koshland’s work on bacterial chemotaxis?
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The sequence in question would have to be a sequence that would code for the protein needed for dealing with the environmental stress. And yes, I know what a codon is. Why do you ask?
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I know what “signal transduction” is. It’s just that (if I’ve read you correctly) you’ve said that some sort of signal transduction is being bandied about as a possible engine of directed evolution. I was hoping you could explain your ideas in more detail.
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Phosphorus, not potaSSium.
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I’m sorry you found my post to be condescending. I was merely pointing out the flaws I see in your ideas as you have described them thus far, and I was asking for more details on how you might resolve those potential difficulties.
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Have you ever heard of exon shuffling before? It’s a fairly basic concept in molecular genetics.
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Precisely.
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I don’t appreciate being called names in GD. I suggest you apologize.
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The reason it happens is because the transposons have flanking sequences that are recognized by a transposase.
I think that you may be right there, because what you can’t do is take the next generation plants further north and gain another leap in cold-tolerance (suggesting that it is merely some sort of mechanism that the parent plant uses to ensure a better chance of passing on it’s genes, rather than those genes changing on the fly)
Yes, prions cause several diseases, but it turns out that in yeast they can transmit acquired traits to offspring. I explained this a few times in the past, when people brought up Lamarck, but I can’t find it in the search right now.
In a nutshell:
Prions are like ice-9 from Cat’s Cradle: a protein misfolded into a prion will catalyze the transformation of other protein molecules of the same type into prions. In yeast, the proteins which suppress the genes responsible for certain traits can become prions in response to environmental pressure. Once these proteins are tied up in the form of prion aggregates, they can’t suppress the genes anymore, and the traits become active.
These traits are then passed on to offspring, because prions from the parent yeast will contaminate the daughter yeast cells and cause their proteins to become prions too. When the environmental pressure is removed, the prion plaques can dissolve, and the yeast will revert to the negative, inactive trait (which they can also pass on to their offspring, since there are no longer any prions present.)
You are absolutely correct. Ben, you have my whole hearted apologies. In no way should I have taken my bad mood out on you. My actions were absolutetly inexcusable.
Whoops
But what triggers the activation of the restriction enzyme? Why does it splice it out in the first place?
Ben, my earlier post was inexcusable in tone. I am profoundly sorry that I even wrote it. I can only ask for your forgiveness.
I would also like to apologize to all of you. Please do not judge me over this one incident. It will not happen again.
-Beeblebrox
Directed mutation, as it is called, is a phenomenon by which bacteria do indeed become hypermutable when they reach stationary phase. It has never been observed in anything but bacteria. I should know, I worked with Susan Rosenberg, who is one of the leaders in this field. This debate has kind of been done before, between me and jorolat in two threads a few months ago in Great Debates.
Your problem, Beeblebrox, is that you underestimate the power of random mutation. Most people immediately equate random mutations to random point mutations across the genome, which are often silent and very rarely would produce gross changes.
Random mutation is much more than that. All organisms, even humans, undergo large scale genomic changes at random. Chromosome translocations, transpositions, inversions, duplications, and deletions are all relatively common spontaneous events. This can serve to bring already formed genes together, forming genes with new functions. It is seen throughout the genome. Also, exon shuffling, as Ben talked about, is a great way of organizing protein domains into new combinations. It is again known to happen with a relatively high frequency.
Large scale genomic change happens quickly – it can cause the speciation of two populations of Drosophila in only a few decades.
Also, we can add to the above selector genes and homeotic genes. These genes have been duplicated (common spontaneous event) during evolution and have led to things like limb transformations and body segment duplications and deletions. These gross changes happen relatively frequently, as seen in the ultrabithorax and Antennapedia mutations of Drosophila (to name two quite famous ones).
People have looked for the reverse flow of information from protein -> genome for many, many years now. The fact of the matter is that for higher organisms it has never been observed. It would be quite a story if it was, and no scientist is saying that it is not a distinct possibility. It does not, however, seem to be the main driver of evolution. All of the evidence (and there is a mountain of it) points to spontaneous mutation.
Beeblebrox : another word of advice. Ben is extremely knowledgeable about these things. He is not being condescending to you – he is just pointing out flaws in your arguments. Unfortunately, this topic is somewhat of a touchstone for evolution-deniers, and we all kind of tend to leap on it to show the flaws in the argument. His tone is valid – a degree in molecular biology may get you so far, but realize that many of us around here have more than that and may know a little more than you in some fields.
Yes, there is a general consensus on this issue; see the quote below by John Maynard Smith. Dawkins’ ideas are seen almost universally as being far more fruitful, accurate, and scientifically sound than Gould’s.
Stephen Jay Gould possesses a very keen intellect and is clearly a major expert within his narrow field of expertise. And anyone who has read him comes away with the clear impression that Gould can also write with notable grace, wit, and insight.
But outside his own narrow field of expertise of paleontology, he is not much respected by the scientific community. Gould allies himself with those few lingering ultra-environmentalists (in the sense of nurture vs. nature, not ecology) whose avowedly Marxist prejudices on human and animal behavior have long been discredited by mainstream scientific research. In short, Gould suffers from some significant political biases in his scientific work.
Consider the following extract from a paper published in Harvard’s Salient:
(Just for the record, I certainly do not believe that Marxist science is flawed just because it is Marxist! Rather, it is flawed because it is predicated on a thorough-going bias).
Here are the words of John Maynard Smith, easily one of the world’s most respected and distinguished evolutionary scientists:
Gould has published other works of dubious scientific validity, such as The Mismeasure of Man. Unfortunately, his scientific views outside of his narrow specialty simply cannot be trusted.
I’d like to reiterate what edwino said. In higher, multicellular organisms, large scale genomic changes can be a major factor in evolution. In plants, for example, there’s a lot of evidence that polyploidy and subsequent re-diploidization has been resposible for driving many speciation events.
Polyploidy is the wholescale duplication of a genome. It is quite common in plants. Examples of polyploid plants include:
[ul]
[li]potato - autotetraploid[/li][li]wheat - allohexaploid[/li][li]banana - triploid[/li][li]sugarcane - (something really complicated)[/li][/ul]
Maize is the canonical example for re-diploidization. About 11 million years ago, two closely related grass species hyridized to form an allotetraploid. Not just one gene, not just one chromosome, but the entire genome was duplicated. Over time, sufficient mutations (including additional chromosomal rearrangements) accumulated, such that modern maize once again acts as a diploid.
Well. I see a lot has happened since my last post here
First, to reiterate what some posters have already mentioned, re: this:
Regrettably, there is no evidence to support that an adaptive response by an organism to its environment is translated backward from phenotype to genotype; or, more specifically, from protein molecules backwards to DNA. The flow of information from genotype to phenotype is unidirectional.
However, to reiterate what I mentioned earlier about developmental influences, not every instance of a change in phenotype is based in genetics. The molecular organization of the cell surface in ciliate protozoans, for example, acts a template for the new surface upon cell division; thus nongenetic alterations to the cell’s surface will be passed on to the next generation. Similarly, the cytoplasm of an egg cell can be altered by the mother’s physiological state, which can, in turn, affect the phenotype of the developing organism. Such maternal effects typically only persist for a generation or two, but they do occur.
Also, re: experiments with tobacco plants, it is hyposthesized that some such environmental shocks can result in the interrupted sequencing of DNA, resulting in extra copies of the earliest-copied genes (that is, the sequencing is interrupted and starts over, resulting in the duplication). This may account for some of the observed occurances of environemtal influences being carried over from generation to generation (depending largely, I would think, on which genes were being duplicated).
I would also like to restate what tracer, et al., wrote earlier: mutations may be random, but natural selection isn’t. Environmental factors are what determine the relative value of a given mutation at any given time. Under a different set of circumstances, the same set of mutations will be selected for differently. This, however, doesn’t mean that natural selection is in any way directed; it simply means that what is considered an advantageous mutation for an organism at a given point in time is determined by the prevailing conditions.
The truth is, there is much we don’t know about what happens between “protein” and “complex phenotype”.
To nitpick, this is not an example of maternal effect. This is an example of epigenetic inheritance. Maternal effect is a phenomenon by which the mother sticks stabilized ribonucleoproteins into the egg. Since nuclear transcription only starts after a few cell divisions in most embryos, those RNPs act as the genetic program for the first bit of embryo development. These are often quite important genes determining embryonic polarity and size, which are contributed only by the mother. Mitochondrial inheritance can also be thought of as maternal effect.
I would also be less dogmatic about saying that no information passes from protein to DNA. There are a number of examples of transposon upregulation and hypermutability due to stress. This is certainly not the directed action that Beeblebrox is looking for, but it is certainly true that proteins do affect the genome at times. While this is most often seen in lower organisms, gene amplification of MDR channels in cancer cells comes to mind with the selection given by chemotherapy.
Note that this in defense of my example, not a nitpick of yours!
To quote Futuyma,
Also, from a “Dictionary of Biology” (by M. Thian and M. Hickman):
Mitochondrial inheritance sounds more like maternal inheritance (that is, characters inherited through the female line only) than a maternal effect.
“Epigenetic” merely refers to processes whch occur during development, whether influenced by the mother or not (at least, that’s my understanding of the term).
Darwin’s Radio has come up in another thread, so I thought I’d restart this DR-esque discussion. I hope no one objects!
Anyway, bearing in mind that it’s been a few months since I read it, my take on DR was that it makes me cringe a little bit. Imagine that George Lucas really believed in the Force. Imagine, too, that he wanted to convince his audience that the Force was real, and that soon mainstream science would accept the Force and we’d have Jedi-like people running around. So in the course of Star Wars, we have Obi-Wan Kenobi teaching Luke about the Force, and talking about Maxwell’s unification of electricity and magnetism and Grand Unified Theories and whatnot. Lucas would also provide an extensive glossary on physics in which he’d talk about various exotic particles that mediate the strong nuclear force, etc. etc. Then Star Wars is a big hit, and people are really wowed by the level of technical detail, and everyone is excited about this whole Force idea… but somehow Lucas never got around to explaining how, exactly, his definitions of the strong nuclear force and electromagnetism add up to an argument for the existence of The Force™.
As best I remember, DR was much the same way. We get a huge technical glossary and intro to molecular biology, and there’s a lot of talk about endogenous retroviruses and whatnot, and Bear assures us that one day soon the old fogies will realize that he’s right about directed evolution, but somehow he never explains why, exactly, we should believe that the existence of endogenous retroviruses means that the genome can figure out that the human race needs pheromonal communication and photophores, figure out what proteins would be needed to acheive that, back-calculate what DNA sequences would be needed to produce those proteins, and communicate all this to different members of the species so that the highly evolved superbabies are all born at once. In other words, how does Bear explain all the objections I raised above in my earlier post? I remember a lot of impressive talk about molecular biology, but I don’t remember seeing anything that would connect it to Bear’s thesis. It’s as if he wanted to prove that Atlantis really existed, and the Atlanteans had nuclear energy, forcefields, telepathy, etc. and their civilization was sunk by a volcano- and then he provides us with an extensive glossary on the terminology of vulcanology.
Anyway, I was never a big fan of Darwin’s Radio either. I didn’t really agree with Bear’s explanation and the speed of the change seemed a bit far fetched (extreme understatement). I was also annoyed that the “new humans” or whatever were that same old hackneyed “superior being” . I always found the idea that Vonnegut put fort in Galapagos of people evolving into something like otters to be far more plausible.
I have read this thread a couple of times since my last post on it, and have had a chance to rethink my views. I believe that edwino may be right about me underestimating the power of random mutations. I still believe there are mechanisms that cause adaptation independant of the ones assosciated with what we think of as random mutation (of course I can’t cite any), but these are more likely to be described as some VERY interesting polymerases. I no longer think that these would be the driving force behind evolution. I was looking for a “Holy Grail” that just wasn’t there. However, let’s just say that I wouldn’t be too suprised if we found something in the next twenty years that blew our freakin’ minds.
Oh, Ben, I want to apologize again for my earlier post in this thread. The fact is that you do come across as a bit snide in some of your posts. Combine this with a few too many and a somewhat imperfectly remembered B.S. in molecular biology that has been collecting dust for the last three and a half years, mix, and BOOM you get my earlier eruption. I just humbly ask that you refrain from making such comments as “Super Straw Man Powers Activate!” CreationismThread
-Beeblebrox
“In the beginning the Universe was created. This has made a lot of people very angry and been widely regarded as a bad move.”
Had an email conversation (2 or 3 back and forth) with Greg Bear. You see, there was this fascinating article in Nature last year about a protein called syncytin. Syncytin is a working protein with an hypothesized role in placental formation in humans. It perhaps mediates cell fusion in formation of the syncytiotrophoblast, the syncytial outer layer of the placenta involved in uterine invasion. The cool thing is that this protein is actually the env protein of the human endogenous retrovirus HERV-W. The even cooler thing is that HERV-W integrated only a few million years ago, after the branching of Old and New World monkeys. Only Old World monkeys have HERV-W (and presumably syncytin). I wrote a proposal (as an academic exercise) to try and correlate syncytial trophoblast formation (a highly variable process which is not present in many mammals) with HERV-W and working syncytin. Kind of wacky, but an academic exercise. Greg Bear was excited by the whole thing and he had read the paper.
As Ben said about the book. It reflects some good ideas, but it generally made me cringe. Endogenous retroviruses are a very interesting article of whole scale genomic change. The possibility that a series of retroviruses is acting as a “evolutionary engine” which is almost intelligent is far fetched to say the least. If I turned off the biology section of the brain, it did make some good reading, though.
Rather than the times of higher stress, isn’t it a necessary consequence of the mathematics of population that the greatest number of mutations (both within specific species, and within higher divisions) would occur during times of relatively lower stress? The explosion takes place slowly over the long periods without major changes. The “good times” lower the bar on what is harmful, and what is beneficial. Total populations grow larger, and variances accumulate in the low stress environment. The catastrophe just winnows the variations into extremes by adaptation. The remaining population is now segregated by variances. Speciation results after the fact, in different ecological niches.
Another matter, forgive my ignorance.
The diversity of large species has had major swings over time, with whole ages of domination by one order or another. However, I have never seen a quantitative description of the diversity of the microscopic species over time. Since the larger species represent environment for some, I suppose those particular examples will follow the same trends, but I wonder about the group as a whole. Is diversity constantly increasing? Is genetic information conserved across extinction events? Was dinosaur flu an ancestor to Hong Kong flu? Where did it live during the intervening ages? Or was it turkeys?
On the subject of protein to DNA influence, I cannot speak with any knowledge of the chemistry, but it does seem that a generalized mechanism of design information passing through this “channel” would have to promulgate its own survival as an immediate characteristic. That seems to me to predict an easily reproducible system in all subsequent descendent populations. I don’t see any evidence of that in what little I have read on inheritance mechanisms.
In other words, if Darwin’s Radio is broadcasting, there ought to be a whole lot of receivers tuned in. Where are they? If they are not there, why broadcast?
Tris
“It is even harder for the average ape to believe that he has descended from man.” ~ Henry Louis Mencken ~
I really really have a problem with the idea of a cellular computer that can “decide” when to cause an evolutionary change. It just doesn’t make sense.
I imagine this computer is fairly complex, right? So it would be succeptable to breaking down given a few bad mutations. But since most organisms aren’t going to evolve and thus aren’t going to use the computer, there is no selective mechanism to maintain the computer. If you lose an important protein you are usually dead. But if you lose your computer all that happens is that you don’t evolve.
OK, so you go extinct while the lines that conserved the computer adapt. But this type of species selection would have to happen all the time. It just seems to me that a faculty that is not neccesary for survival by each and every generation is going to be lost quickly.
On the other hand, the notion that organisms get chunks of new genes via viruses is interesting. Perhaps this could be important for evolution…as long as we realize that the tranfered genes are most likely to be junk. But every now and then you might get a brand new enzyme added to your genome.
Triskadecamus, I will try and answer some of your questions:
This is actually reminiscent of an interesting phenomenom in fruit flies (my organism of choice). As with most animals, flies have a family of proteins called chaperones which refold denatured proteins. Proteins can be denatured (unfolded) by any one of a number of stresses, most typically heat shock. Point mutations also may cause a protein to partially unfold. In a normal, non heat shocked fly, chaperones are engaged in refolding proteins with point mutations, thus suppressing genetic variability in a population. When the organism is heat shocked, the chaperone system gets overwhelmed by a huge influx of heat-denatured proteins, and cannot refold all of the mutated proteins. The mutated proteins are allowed to stay in their original configuration, removing the suppression of genetic variability. This basically means that a mutation which ordinarily would decrease fitness has no effect. If this mutation increases fitness in a heat shocked animal, it is unmasked during the heat shock. This gives a fly population a mechanism to adapt to temperature shift within one or two generations.
I read Jared Diamond’s excellent book Guns, Germs and Steel a few months back. He reinforces the point that we have coevolved with diseases from ancient times. Moreover, new diseases often come from animals with which we have close contact. TB perhaps jumped from cows to humans. AIDS came from monkeys. Flu jumps from a number of domesticated animals – swine flu jumped from pigs and Hong Kong flu from chickens. This is caused (at least in influenza) by a well studied phenomenom called antigenic shift, an event which happens a few times every century that often results in pandemic flus. Viruses and bacteria, as they are so adaptable, probably would be much more prone to survival of a large extinction event than their host. Since we see this jump often in modern times, chances are it happened in the past.
I will also add that no evidence for any kind of process even remotely resembling Lamarckian evolution has ever been found, despite lack of trying. It would be extremely interesting, of course, and have staggering implications. Even biologists are limited by simple tenets of information theory. The genome is a read-only device (except for a handful of exceptions). Environmental cues are complex. The genome is complex. The machinery that would be needed to translate these envirnomental cues into genome modifications would be large and complex. We see nothing of the sort.
Beeblebrox:
Thanks. As the inventor of the Pan Galactic Gargle Blaster, you are mine.
I would disagree. There are some things you have to remember:
There’s a difference between the rate at which mutations take place, and the rate at which they become “fixed” in the population. “Genetic drift” refers to the process by which a gene spreads throughout a species until all individuals have it. At that point it’s fixed, because all offspring must have the gene, and it’s become a part of the species’ genetic heritage. If you have a lot of individuals, you will have a lot of mutations taking place, but they can’t all become part of the genetic heritage of the species, because, if nothing else, those mutations will be competing against each other.
Furthermore, if you look at genes across species to see when and how they change, you see that times of greater selection pressure doesn’t cause a change in the total number of mutations so much as it causes a change in the ratio of voiced to silent mutations. An example comes from the leaf-eating colobus monkeys. At the point in evolutionary history when the monkeys started eating leaves, they needed a good way to extract nutritional value from the leaves. One way to do this is to let bacteria in their digestive tracts break down the bacteria, and then the monkeys can digest the bacteria and harvest the pre-digested nutrients. The enzyme, lysozyme, which digests the bacteria is one which is normally found in tears, where it protects the eyes from infection. Once the monkeys started eating leaves, a mutation took place which caused lysozyme to be expressed in the stomach, and further mutations slightly modified lysozyme to optimize it for its new environment. If you compare lysozymes across species, you find that for the most part the differences between the lysozyme genes are silent mutations which don’t affect the protein at all, or are neutral mutations on the surface of the enzyme which don’t affect its function. But when you look at the colobus monkey lysozyme, you find that it has a disproportionate number of mutations in critical parts of the enzyme, and if you calculate the time at which they took place, they all happened at the time the monkeys started eating leaves.
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I would argue that this isn’t the case. If you took a bunch of mice and raised them in a rat utopia where they had no predators and free food, there would still be intense competition for sex. In “good times” individuals will still try to get ahead of other members of their species.
I suspect that questions of “good times” and “hard times” have less to do with natural selection than species selection. If a meteorite causes a mass extinction, the species which survive tend to be ones which had a random quirk that just happened to make them well-adapted to new conditions (even something as trivial as living far from the impact.)
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Large populations generate an evolutionary inertia, because it’s harder for mutations to spread throughout the entire population and become “fixed.” Evolution goes fastest in small, inbred groups.
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The problem is that if you take a teaspoonful of dirt from your backyard, it might contain 10% known species and 90% unknown species. It’s not that people are uninterested in those microorganisms; it’s that you can’t study a bacterium in the same way you can cage a yak and take photos of it. You need to culture microorganisms in order to study them, and that means that you can’t study the organism unless you hit upon the right set of conditions for growing them in quantity.
This situation has been changing lately, though, with the advent of single-cell PCR techniques which enable us to extract DNA from the soil sample and sort it out into different species. Microorganism censuses are now being performed, and no doubt will become more popular in the near future. This technique is particularly useful for extremophiles, which grow in acidic or high-temperature (even above the boiling point of water) conditions.
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If I understand you correctly, then you’ve hit upon one of my big problems with the DR scenario. During the long periods of stasis when the “radio” isn’t in action, there’s no selectional pressure to preserve it. It should erode very quickly, just as a high-fruit diet destroyed the primate gene for synthesising vitamin C.
BTW, Tris, I wanted to thank you for suggesting Wonderful Life; it was quite good.
