avocationist
Posts: 173
Joined: Feb. 2006
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Chris, going back over some posts I found your co-option one, and I just want to say that I have reread it and take note.
Russell,
| Quote | | Surely, when you say such and such model has been "largely abandoned" - you can cite at least one review of the relevant literature by a relevant scholar of the field to substantiate that claim. |
I really can't evaluate a paper of the length that you have given. If you could summarize it, or bring out its main points...
Why dismiss Mike Gene so easily? His 5-part essay on the flagellum is pretty readable and has references at the bottom of each section. I didn't see a date. I wanted to see if it was later than the paper you cited.
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2. Is there any reason to think the type III export system, complete with the ancestors of flhA, flhB, fliR, fliQ, fliP, fliI and others, existed as a "cooptable part." Thus far, the answer is no, as there are good reasons to think the type III system evolved from pre-existing flagella.
a. The bacterial flagellum is found in both mesophilic and thermophilic bacteria, gram-positive and gram-negative, high GC and low GC content bacteria, and spirochetes. Type III systems seem to be restricted to a few gram-negative bacteria. That is, if we look at the sequenced genomes from the various groups cited above, we can find the genes for the bacterial flagellum but not the type III system genes.
b. Independent evidence suggests the type III system is recent. It is not only restricted to gram-negative bacteria, but to animal and plant pathogens. In fact, the function of the system depends on intimate contact with these multicellular organisms. This all indicates this system arose after plants and animals appeared. In fact, the type III genes of plant pathogens are more similar to their own flagellar genes than the type III genes of animal pathogens. This has led some to propose that the type III system arose in plant pathogens and then spread to animal pathogens by horizontal transfer.
c. When we look at the type III system its genes are commonly clustered and found on large virulence plasmids. When they are in the chromosome, their GC content is typically lower than the GC content of the surrounding genome. In other words, there is good reason to invoke horizontal transfer to explain type III distribution. In contrast, flagellar genes are usually split into three or more operons, they are not found on plasmids, and their GC content is the same as the surrounding genome. There is no evidence that the flagellum has been spread about by horizontal transfer.
d. It's much easier to envision the evolution of the type III system from flagella than vice versa. For starters, evidence has surfaced that the basal body of the flagellum already works to secrete proteins other than the flagellar proteins, including virulence factors. Thus, the basal body is already poised to evolve into a type III system from the start. Evolution apparently would only have to duplicate and tweak the type III virulence protein secretion activity already existing in flagella. . In my opinion, this view is far more parsimonious than to propose that something like the type III system evolved long ago, was lost by all bacteria but gram-negative animal/plant pathogens and then was used to evolve the flagellum so that horizontal transfer could spread flagella far and wide (despite the lack of evidence for such transfer).
Thus, it should not be surprising that the scientific opinion has been converging on the notion that the export machinery evolved from the flagellar machinery [5-7].
There is yet another interesting aspect to all this. Since evolving from some flagellum, the type III transport system appears to have lost its ability to engage in rotary transport. The flagellar motor is composed of five proteins: MotA, MotB, FliG, FliN, and FliM. We'll discuss this more below, but right now it is worth pointing out that the type III systems have no homologs for MotA, MotB, or FliM. The Mot proteins are essential components of the motor, as they are membrane proteins that fulfill two functions: they transport ions to provide the energy for rotation and serve as the stator against which the rotor (FliG, FliN, FliM) moves. What's more, the type III rotor components have significantly changed. The type III homolog of FliN shares sequence similarity only with in its C-terminal 80 amino acids. And the sequence similarity between the FliG homologs are almost non-existent. Furthermore, there have been significant changes in FliF. FliF forms the MS ring (the "mounting plate"), which is associated with and above the C-ring composed of FliG, M, and N. FliF in flagella is composed of 500+ amino acids, but in the type III homolog, both the C- and N-terminal domains thought to be involved in forming the MS ring are missing. All that is left in common between them is a central region of about 90 amino acids.
Here we find another reason to recognize the significance of the flagellum-to-type III system evolution. Type III systems have apparently lost their ability to rotate. Thus, we can't think of type III systems as something pre-adapted to rotate, as all the rotary information has been lost. To argue that the type III system could reacquire the ability to rotate, as the flagellum does, is to essentially violate Dollo's Law, which states: "evolutionary change manifested at any level higher than the genetic is irreversible, and that anatomical structures or functions once lost cannot be regained." [8] Yet by proposing that the flagellum once existed as a type III system and later acquired the ability to rotate is not hardly any different that proposing type III systems could reacquire the ability to rotate and violate Dollo's Law.
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| Quote | | Saying, "I think it's extremely unlikely" does not amount to "refuting". |
OK, maybe refuting isn't the word, but Behe has made good arguments to show that the compiling of the flagellum from disparate parts is not likely. I spent a bit of time and didn't find them. We are not talking about absolute proof, but rather establishing that intelligent design is a reasonable supposition.
| Quote | | Are you being quite serious here? Evolution is an iterative process. Mutations build on one another. If one mutation leads to better vision, that presumably is beneficial in and of itself. Subsequent mutations leading to more brain development capable of using the better vision then become favorable, etc. Also, did you know that skull formation is responsive to brain formation? |
OK, there may be some systems in which this can work to a degree, but I think that my objection still stands. There is an awful lot of very exacting interface and construction in the different systems. Are we just assuming they can cobble themselves together? We not only get a fortuitous mutation, but it includes the construction kit also?
| Quote | | It demonstrates the one system is almost certainly related to the other by the process of "co-option" that Behe has "refuted" by declaring it unlikely. |
Well, unfortunately, we really don't know that, and it is hardly certain when there is good reason to think the type 3 was not a precursor. I'm not sure Behe is against all co-option, just doesn't think it can work to put together an IC system.
| Quote | | But the point stands: an evolving system can have a series of selectable functions without the "final" function being selected from the very beginning. |
So it could get a couple of proteins to do something, and then get a few more, cobbled together which will now do something entirely different, and somehow the genome has decided to code for putting them together, and then along comes another protein or set of proteins, which do yet something else again, and this is now added to the first two, which now has a completely new function, and all the old functions for these three systems are still also being covered (presumably they are still needed) while each time this two and now three and now four and now five-part set assumes a completely new role, while somehow not abandoning the old role, and all fitting together perfectly. Not only each new added part but also each set of two-parts, and three-parts, and four-parts - presumably all things the cell still needs?
| Quote | | apparently in vain. Is that your version of an apology? |
No my dear, when I feel the need to apologize it will be much sweeter. If you didn't say it, I won't insist. I am pretty sure I saw it. Maybe it was someone else. As for Spetner, I got an answer from him, but it appears he still didn't understand what he did. He corrected me to say that yes, Dawkins did the calculation, but did not calculate the likelihood of the event happening in the lifetime of the alien. However, I sent him another letter pointing out that where Dawkins said that he also used a different phrase, i.e., perfect hand, not perfect deal.
| Quote | | Oh really? What would you estimate is the similarity between yourself and a human with Down syndrome? |
Gosh, I don't begin to know how to answer this. there are a lot of genes on a chromosome, and I don't really know what happens or why when you have that extra chromosome, but I don't think the situation is comparable.
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The genetic similarity between us and chimps is exxagerated I am sure, |
| Quote | | and I'm sure that you are sure, and that your certainty is based on... nothing at all. |
How can we be 99.4 the same as a species with 1/3 our brain size? a species with a different form of locomotion? a species which cannot speak?
Here's what a guy who calls himself an 'interventionist' (humans and domesticated plants and animals were deliberately genetically altered by human-like aliens) has to say:
We are taught that by every scientific measure humans are primates very closely related to all other primates, especially to chimpanzees and gorillas. This is so ingrained in our psyches it seems futile to even examine it, much less challenge it. But we will.
Bones. Human bones are much lighter than comparable primate bones. For that matter, our bones are much lighter than the bones of every “prehuman” ancestor through Neanderthal. The ancestor bones look like primate bones; modern human bones do not.
Muscle. Human muscles are significantly weaker than comparable muscles in primates. Pound-for-pound we are five to ten times weaker than any other primate. Any pet monkey is evidence of that. Somehow getting “better” made us much, much weaker.
Skin. Human skin is not well adapted to the amount of sunlight striking Earth. It can be modified to survive extended exposure by greatly increasing melanin (its dark pigment) at its surface, which only the black race has achieved. All others must cover themselves with clothing or frequent shade or both, or sicken from radiation poisoning.
Body Hair. Primates need not worry about direct exposure to sunlight because they are covered from head to toe in a distinctive pattern of long body hair. Because they are quadrupeds (move on all fours), the thickest is on their back, the thinnest on the chest and abdomen. Humans have lost the all-over pelt, and we have completely switched our area of thickness to the chest and abdomen while wearing the thin part on our backs.
Fat. Humans have ten times as many fat cells attached to the underside of their skin as primates. If a primate is wounded by a gash or tear in the skin, when the bleeding stops the wound’s edges lay flat near each other and can quickly close the wound by a process called “contracture.” In humans the fat layer is so thick that it pushes up through wounds and makes contracture difficult if not impossible. Also, contrary to propaganda to try to explain this oddity, the fat under human skin does not compensate for the body hair we have lost. Only in water is its insulating capacity useful; in air it is minimal at best.
Head Hair. All primates have head hair that grows to a certain length and stops. Human head hair grows to such lengths that it could be dangerous in a primitive situation. Thus, we have been forced to cut our head hair since we became a species, which might account for the sharp flakes of stones that are considered primitive hominid “tools.”
Fingernails & Toenails. All primates have fingernails and toenails that grow to a certain length and then stop, never needing paring. Human fingernails and toenails have always needed paring. Again, maybe those stone “tools” were not for butchering animals.
Skulls. The human skull is nothing like the primate skull. There is hardly any fair morphological comparison to be made apart from the general parts being the same. Their design and assembly are so radically different as to make attempts at comparison useless.
Brains. The comparison here is even more radical because human brains are so vastly different. (To say “improved” or “superior” is unfair and not germane because primate brains work perfectly well for what primates have to do to live and reproduce.)
Locomotion. The comparison here is easily as wide as the comparison of brains and skulls. Humans are bipedal, primates are quadrupeds. That says more than enough.
Speech. Human throats are completely redesigned relative to primates. The larynx has dropped to a much lower position so humans can break typical primate sounds into the tiny pieces of sound (by modulation) that have come to be human speech.
Sex. Primate females have estrous cycles and are sexually receptive only at special times. Human females have no estrous cycle in the primate sense. They are continually receptive to sex. (Unless, of course, they have the proverbial headache.)
Chromosomes. This is the most inexplicable difference of all. Primates have 48 chromosomes. Humans are considered vastly superior to them in a wide array of areas, yet somehow we have only 46 chromosomes! This begs the question of how could we lose two full chromosomes, which represents a lot of DNA, in the first place? And in the process, how could we become so much better?
| Quote | | Anyway, I wonder: is there any reason why a Martian Linnaeus, say, would assign us to two different genera? |
So maybe the above is an answer.
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