| | Ms. Isanhart wrote:
Do you plan on responding to Marcus's post #154? While I was intrigued with your original response in answer to my question regarding bacterial resistance, Marcus's answer in the above mentioned post is a direct contradiction to your argument.
First, Marcus is much too busy being both Science Leader and Science Follower of his own "Society For Fact-Free Science" to read my posts and comment thoughtfully on them. I've noticed that in place of cogent arguments, he prefers to substitute exclamation points ("Wrong again!" "Not information loss, adaptation!"). He is clearly unable to think abstractly -- it reminds me of arguments I have with economic interventionists. I'll demonstrate that a price control on, say gas, leads to shortages. And they'll say, "OK, well, what about price controls on housing? Eh??? Answer that Mr. Grammarian!!" They sometimes even use as many exclamation points as Science Leader.
I'm not sure why you find that sort of argument convincing on any level.
Second, his examples are all old, well known examples from both the ND and the ID literature, and are what is now being referred to (by ID and general non-ND people) as "Icons of Evolution." I.e., "Sacred Cows" or critically unexamined phenomena that turn out NOT to be so convincing as proof of Neo Darwinism when one actually takes the time to look closer. It turns out that these Icons were initially interpreted in the light of ND theory, and the old guard dislike any sort of new spin being put on their interpretations.
I took a long time to explain the issue of bacterial resistance to antibiotics (and, by implication, insect resistance to pesticide), and to explain it in light of a larger theory that looks at the way information must be encoded/decoded in order for the organism to get anything done. I also tried to create analogies (protein vs. text) which are not only standard in biochemistry today, but which are no longer even being taken as analogies by a growing number of biochemists. DNA is not like a code; it is a code. (Because information qua information requires a code, as well as a sender and a receiver.) Sorry if you find it "enigmatic." The concepts are rather simple, and have wide application.
I'll try to explain again, this time addressing some of these Icons of Evolution.
1. There are several different methods that bacteria use to resist antibiotics. Some bacteria have built into them a resistance to some antibiotics. The resistance comes from an enzyme (a type of protein) that alters the drug and makes it inactive. This type of resistance does not "build up" through mutation. To my knowledge, no one knows that the enzyme is actually for; it's just there.
Some researches apparantely think its primary purpose is to attack molecules involved in some other cell function; in their opinion, the resistance to the antibiotic is simply fortuitous.
Other bacteria become resistant through a virus that transfers the gene for resistance. The virus may have picked up the gene from an already naturally-resistant bacterium. Still other bacteria can be deliberately made resistant by splicing into their DNA the gene that encodes the information for producing the enzyme.
The gaining of antibiotic resistance in these ways is obviously non-Darwinian, and certainly adds no new information, at least not to the "biocosm" as a whole. Simply to transfer some algorithmic steps from one software program and insert it cleverly into another software program indeed adds information to the first program, but this is not the same as writing a really new program with new steps: there's no net gain of information.
A net gain of information is what's required by the theory of evolution. Humans are not bacteria that have made clever adaptive use of pre-existing bacterial structures; they have entirely new abilities (and I'm just speaking biochemically, let alone mentally).
Some bacteria, however, start off as sensitive to an antibiotic and mutate to become insensitive. We know how this is done for many bacteria. The question for Neo-Darwinian Theory (NDT) is whether this is a satisfactory model for describing (i) origin of species from non-living matter, and (ii) appearances of completely new species, with new body-plans and new abilities that didn't exist before.
Scientists have long studied how, e.g., streptomycin and other mycin drugs keep bacteria from growing, and how a nucleotide substitution in the bacterium's DNA (a "point mutation") can desensitize the bacterium to the antibiotic. A molecule of the drug attaches to a matching site on an organ of the bacterium called a ribosome and interferes with its making of protein. With the drug molecule attached, the ribosome is unable to put the right amino acids together when it makes protein. It makes the wrong proteins; it makes proteins that don't work. The bacterium can't grow or divide and can't propagate. The ribosomes of mammals don't have the site at which the mycin drugs can attach, so the drugs can't harm them. Because the mycins can stop bacterial growth but not harm the host, they make useful antibiotics.
A point mutation can desensitize the bacterium to the antibiotic, not by conferring a brand new ability (which requires new information coding for new proteins), but by degrading an already-existing function in such a way that the specific shape of the binding site is altered. When this occurs, the antibiotic can no longer attach itself to the ribosome.
When I say "binding site," think "lock and key." A lock is a binding site -- a receptor -- with a highly specific shape. A key must be shaped in exactly the right way or it won't fit into the lock. In fact, the specificity is so high with a good lock and key system, that we all know the annoyance of having problems opening our doors when we have a new copy of a key made; it's still a little "rough around the edges" and so won't match precisely with the lock until we fuss with it (or take it back to the locksmith's). The specific shape of all the little nooks and crannies inside the lock is governed (in the ribosome's lock) by various sequences of DNA. To desensitize the bacterium, a point mutation in the DNA of the ribosome can occur which destroys the highly specific shape of the lock. If you wanted to "adjust" your door lock in such a way so that it could no longer be opened by your door key, how would you do it? You could add brand new information to the system by removing the lock and inserting new, different one -- but that's difficult, time consuming, and expensive. Wouldn't an easier, more cost-efficient method be to use the little metal nail file you have in your purse and file away some of the specific notches in the lock? If you file away long enough -- if you remove some of the specificity of the shape of the lock -- your highly specific-shaped key will no longer fit. Right? You don't even have to be too careful where you file something away: there are going to be at least several different sites (nooks and crannies) in the lock that suffice for this change. In this example, would you say that you've added information to the lock, by making it a more highly specific one, or would you say that you've taken away already existing information, making it a less specific lock?
In the bacterial ribosome, the point mutation that changes the specificity of the ribosome lock could occur along one of several different sites, which changes the shape in a random, unpredictable way, along one of several corresponding "nooks and crannies" within the ribosome lock -- precisely analogous to your filing away some nooks and crannies with your door lock, which changes any one of a number of different sites in a random, unpredictable way. If we admit that the door lock loses information, then we must admit that the ribosome lock loses information. They both lost information because they both degraded their previous specificity.
Now, to lose information by losing specificity might be a good strategy for a short-term advantage in life; survival, after all, is the name of the game. A wife who wants to prevent her philandering husband from entering their summer home, might decide to file away some of the lock on the front door just out of spite: she can't get back in, but neither can that bastard! Short-term gain. Same for the bacterium. It gained a short-term advantage in survival at the expense of the specificity of a part of one its essential organs for survival. Is there a "cost" associated with this? Yes. Loss of specificity does affect negatively the way in which the bacterium performs; it's less fit in certain ways, though the immediate gain is worth more. In the case of mycin drugs, the bacterium's overall performance is degraded. It's been known since the late 1960s that ribosomes with this sort of resistance are more sluggish at translating RNA codons into protein. It traded-down an advanced, specific, complex feature -- efficient translation -- for a short-term survival benefit. Do you blame it?
A change in structure through mutation allows the protein to avoid binding to an antibiotic, while still performing it's usual function!!! (The normal function is not to bind to antibiotics!!!) No loss of information, but an adaptation for survival.
I have no idea what he means when he says that the "normal function is NOT to bind to antibiotics" as if a ribosomal lock teleologically evolved knowing that it would someday be attacked by a poisonous key. I suspect that he doesn't know what he means, either. I've noticed a curious tendency on his part to use proportionally more exclamation points as he gets on shakier ground. Anyway, there's no contradiction between "loss of information" and "adapation for survival." In fact, it's a very common scenario in the biocosm. ID merely denies that this is evidence of the kind of evolutionary process that can turn bacteria into tree shrews (with a whole bunch of new protein and new functions); a tree shrew into a chimp (with yet more novel proteins and abilities); and a chimp into a human. A computer is not merely a typewriter whose functions have been "adapted" to some other use. Computers may have some things in common with typewriters, but they also exhibit novel, highly specific abilities and characteristics that you don't get simply by rearranging the parts of a typewriter, or combining a typewriter with some other example of already existing techology.
There are also other types of "gain of information" (as you call it) drug resistances that evolve by aquiring a pump, or adapting an existing pump to exclude the antibiotic/ drug from the cell.
It's not I who call it "gain of information." I merely accept as plausible what I know both from biochem and information theory. The relation between the two sciences is not especially new, though many people are hearing about for the first time mainly through the efforts of ID people. Bachlus is free to provide concrete examples in which a new ability was gained as result of adding information that wasn't already there in some unexpressed form already. Here are the constraints he's under if his examples are supposed to prove evolution by Darwinian processes:
1. The variation must be small. No big jumps allowed.
2. The variation must be truly random. Point mutations are truly random, so they fit the bill. Other sorts of changes -- misnamed "mutations" -- such as transposition, recombination, deletion, etc., do represent quick, often large-scale changes to the way in which information is expressed by the genome; but there's no evidence that these are random. Many of them are regulated by intermediates, such as enzymes; some are regulated and, apparently, controlled by some other (as yet not understood) means: "master" control switches. This may all be very mysterious, but it's a very different sort of thing from a truly random copying error made during DNA replication. NDT guys were very excited when DNA was discovered because they believed that accidental substitution of one or more rungs of the DNA ladder (the nucleotides) at last provided a "unit" of variation, as well as a minimal size for change: no variation can be smaller than 1 nucleotide substition. It solved a problem that had plagued the theory since Darwin's day. So now, we're going to hold them to it: either it's a random single-nucleotide substition (or many of them; as you wish), or the process is not truly random, and therefore, not truly Darwinian.
3. The small, random variation must increase information in the genome. I've explained this proviso many times. New information = new sequences = new proteins = new abilities (not there before, and not merely transferred form one part of the genome to the other, or one part of the biocosm to the other, or already existing but unexpressed.).
NDT guys are fond of hand-waving explanations. They claim, for example, that we can extrapolate small positive changes in an organism over a long time to get big changes; the latter being merely accumulated small changes. All evolution for them is simply "the taking over of existing structures by means of random mutation and a super-breeder that weeds out the undesirables and preserves the desirables vaguely called Natural Selection (when you really look into the latter, you'll see not only how vague it really is, but how unsatisfied even the hardcore old guard in evolutionary theory have found that term to be). Their scenario for the evolution of an organism -- say the eukaryotic cell -- is something like this: It starts off as an invented primitive form on one side of a long hallway, and through small baby-steps -- each step being selected for it by Natural Selection, and each step advantageous to its survival -- it crosses the hallway and winds up on the other side looking very different. Aside from whether or not such a primitive form ever really did exist, it's the actual crossing of the hallway that's problematic. That scenario completely mischaracterizes what's involved in going from point A to B. The organism doesn't cross a nice, smooth, comfortable hallway with nice smooth carpeting; it has to cross the biochemical equivalent of a 10-lane superhighway with no speed limit; with barbed wire set up on the near side and trenches with spikes and poison gas on the other. And it has to do it, not once, but as many times as there are proposed "steps" in some purported evolutionary process; and it must be done by each necessary element of some process. For years, NDT proponents could get away with assuming all sorts of ad hoc processes, "forces," etc., without needing to do any calculations of the odds of such things happening. When mathematicians first did this for them -- in the 1960s at a place called the Wistar Institute -- the biologists didn't believe it. "You've merely misunderstood our theories" they said. Then they believed it but said that odds are simply irrelevant. Then both the math and physics guys told them that they had better start taking things like odds seriously or risk not being taken seriously as scientists. Then they believed it and took the odds seriously and tried to find a way around it (see Dawkins' book "Climbing Mount Improbable"). Now they are busy rejecting information theory and its overall application to evolution. Again, the math and physics -- their "big brothers" -- tell them "Grow up. We're making great use of this common field of applied mathematics. So should you." Some of them are coming around to it and at least recognize the problems posed by information theory to NDT. I'm sure more will follow.
In the 1960s, a very famous biologist named Sol Spiegelman did an important experiment. He wanted to see what would happen to DNA replication in vitro (in a test tube). He made a soup of unactivated mononucleotides, added some enzymes, and threw in a DNA "template." As expected, the little molecule started whirring away, copying itself again and again. What wasn't expected was that the DNA chain became shorter and shorter, until it reached a minimal length. The shorter, simpler DNA strands, of course, can reproduce faster than the longer, more complex ones. So the short DNA eventually outcompeted the longer ones and took over the "population" of DNA in the test tube. Could this be any sort of model of evolution? DNA that gets simpler and shorter over time? Obviously not. The only place that DNA can increase complexity and maintain this increase in complexity is within a cell. Conclusion: DNA by itself is useless as an explanation for what drives evolution. To be of any value, DNA needs an already existing cell.
Where did the "already existing" cell come from? How did it manage to "find" a suitable DNA molecule? Why should it incorporate it? Was it all by chance? Nonsense. Calculate the odds. Is there some natural affinity, chemically, on the part of DNA for a cell, or on the part of a cell for DNA? Nonsense. Prove it if you claim it. Demonstrate it in a laboratory. What would the ensuing protein synthesis of DNA+cell be good for, if there's no already existing organism? If there isn't an already existing organism, why would DNA+cell produce a given protein that has NO use to anything EXCEPT some already existing organism? Why is there a gene that codes for all eyes -- the "ey gene" -- including camera-type eyes, whose age in the evolutionary chain vastly antedates the physical existence of camera-type eyes? That's like opening up an ancient Druid burial ground and finding the blueprint for a Nikon 35mm camera. What's it doing there? Why do humans, buffaloes, and bean nodules all have identical hemoglobin molecules? We descended from bean nodules and buffaloes -- common ancestry? I don't think so. "Convergent" evolution? You mean variation+natural-selection, independently evolved hemoglobin in humans, hemoglobin in buffaloes, and hemoglobin in beans, three different times? Each time arriving at exactly the same structure?
Bachlus then waxes loudly on another icon of evolution, the apparent advantage conferred on certain persons who have sickle-cell anemia. This is the situation: It was noticed many years ago that persons carrying one gene affected by the sickle-cell mutation (which substitutes one amino acid, valine, for the normal acid, glutamic acid, in coding for the hemoglobin molecule) had a much higher resistance to endemic malaria than those who had normal hemoglobin genes. Those with both genes affected by the sickle-cell mutation usually (not always, but usually) get the full blown disease and die from that, rather than dying from malaria. The evolutionary "just so" story goes like this: this is Natural Selection at work, conferring advantages to those with a randomly produced variation in their genes; conferring a disadvantage who had the audicity at one time -- i.e., before a malaria epidemic -- to claim they were normal. This proves that Natural Selection culls out advantages from the environment. The NDT is proven once again!"
Not so fast.
1. No one, certainly no ID person or other anti-NDT person, ever denied that organisms frequently trade-down: they give up a long term advantage for a short term one, especially if that short one is immediate physical survival. We see that in certain kinds of bacterial resistance; we see it in certain kinds of insect resistance. What we don't see is this short-term survival trade-down as creating a new species. Same bacteria/insect; different strain. No wasps from fruit flies or (following Darwin's assertion) whales from bears. Furthermore, these trade-downs are almost always accompanied by degradation of some other function in the organism. That makes sense; that's what we would expect in trades that involve a loss of specificity and a concurrent loss of information.
2. The advantage is very short-term, indeed. Unlike the bacterium, which can confer its immunity to streptomycin to its offspring, if a person with the single mutated gene has offspring with another person with a single mutant gene, there's a 1-in-4 chance that one or more of their children will inherit both mutant genes and contract the full blown sickle cell anemia. No survival advantage in that to the species as a whole.
3. Those with a single mutant gene can (though they need not) suffer from weakened symptoms of the sickle shaped red blood cells. It obviously only confers an advantage to those who have zero complications from having a few sickle-shaped cells polymerize and squeeze through the capillary system. Those are the lucky ones. The sickle cells (with the malaria parasite) are sent to the liver which weeds them out, along with the parasite.
4. Even the lucky ones are not necessarily immune to malaria. They can have weakened and fewer symptoms, though they can much more easily survive an attack of the plasmodium parasite.
The whole case is analogous to that of "industrial melanism" in which the population of certain white moths near industrial centers in England became black to blend in better with the soot that had deposited on buildings, trees, etc. No one claims that the white moths "turned into" black ones. the black moths were already there in the population as a minority. The minority was selected out, in the short term, because they could hid themselves against soot-covered objects better than white moths could. When the moths are moved to different non-sooty locations, the "gene frequency' for white moth vs black moths returns back to its original state. This is variation-around-a-mean by means of the environment suddently being hostile to one part of the population, and friendly to an already existing minority than can now flourish. NO NEW SPECIES. Nothing new was created; no new information to moth genomes or the biocosm as a whole. Clearly not a model of how we can go from chemicals to life, from life to bacteria, from bacteria to chimps, and from chimps to man.
Lastly, Bachlus posts another icon of evolution, the usual drivel about the "inefficiency" of the vertebrate eye (which is, supposedly, "wired backward," with the neural connections facing outward, toward the light). I've already posted above an interesting (if heavy going) article by Michael Denton on the vertebrate eye. It does, indeed, display an optimum design, though it's rather superior and far more subtle than what one would expect from a 3rd year engineering major at MIT.
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