Background (to be deleted when PNT is acceptable): I really want to let Chiro free play in his thread Evolution Simplified, as he has a nice approach. A detailed response to NJ’s msg 46 would probably derail a very good thread. However, there are sufficient misunderstandings and other issues in that post that I feel it appropriate to address the details. I’m not entirely sure how a PNT in a case like this would work - so I’d appreciate an admin’s assistance in putting a solid PNT together. I think the issues are worth addressing. Biological Evolution would be a good place if we can get a reasonable topic established.
Quotes are from the cited message by nemesis_juggernaut.
I think any evolutionist, by necessity, eventualy will have to rest their claims on the transfer and mutation of genes. The reason why they are so adamant on this point is that the theory would collapse without it.
I’m not sure this is an accurate characterization. I fully concur that evolution would be in trouble without a demonstrable mechanism of inheritance. It would also be in trouble if there were no inheritable variations arising in a population. The good news is that we do in fact have a very good understanding of both mechanism and process. We can watch gametogenesis and meiosis in vivo under a microscope, and we have direct lab and field observations of the action of random mutation and natural selection. No inference required. “Evolutionists” don’t need to be adamant about anything - their understanding of these two elements is based on direct observation of fact; not inference.
Mathematician and molecular biologist, Harold Morowitz, calculated the odds that just one paramecium arranging DNA by chance, is: 1 in 10 to the billionth power. To help aggrandize the enormity of this improbability, 10 to the 50th power is considered, ”absolute zero.’ When you reach absolute zero, it is so improbable that we might as well say that it is impossible. That's just to arrive at any lifeforms at all.
This is a serious mischaracterization of Morowitz’s work, and is a prime example of why people need to be careful of who, what, and from where they get their information in these discussions. Morowitz is a respected origin-of-life researcher. His dissension arises from his contention that membranes formed before other cellular components. IOW, he’s a “membrane-firster” as opposed to the “RNA Worlders” like Leslie Orgel
et al. Somehow I doubt you’ve actually read Morowitz’s book,
Beginnings of Cellular Life: Metabolism Recapitulates Biogenesis (Yale Uni Press, 2004), where he lays out his arguments. Bottom line: he argues that lipid bi-layer membranes represent a minimum energy state, and hence could form
spontaneously providing a snug, secure environment where other chemical processes could occur and be concentrated. In other words, he completely accepts the chemical origin of life - just argues about the order of occurrence. Since I don’t have the book on hand at the moment, I can’t verify that the alleged calculations you allude to are in it, but I strongly doubt it - at least not in that form. Hopefully someone with access to a decent library can verify this. The point is kind of irrelevant anyway, so this is just a brief cautionary note about sources.
But since the First Cause can never be witnessed again, lets just speak about already extant beings for the time being. The fact is most mutations are silent. They are mostly benign deletions from copying errors in the genes. Its important to note, however, that the only reason most mutations are benign is because of specific cells that serve to repair mutations. In fact, it is their only function. Therefore, in all actuality, all mutations are truly harmful, especially if these specific cells, themselves, are the product of a mutation.
This is not entirely accurate. Most mutations (changes in the genome) are benign because they are neutral with respect to the environment. IOW, if they don’t affect the relative fitness of the organism or aren’t actually expressed, they are invisible to natural selection. “Deleterious”, “beneficial” and “neutral” are terms that describe the action of particular mutations with respect to the environment. Neutral in one environmental context may be deleterious or even beneficial in another. “Environment”, in this case, is not only the macro-scale landscape where the organism as a whole lives and interacts, but also the genetic environment inside the individual organism itself. IOW, the other genes at work affect how the mutation is treated.
Beyond that, you are gravely mistaken on both what constitutes a mutation and how the cellular machinery acts to minimize and/or repair mutation. Perhaps a brief primer is in order.
1. A mutation is simply a copying error in any DNA sequence in any cell. It can be caused by multiple factors, and there are multiple types. It is estimated that such errors occur as much as 20,000 times per day in every single cell in the human body. Unrepaired mutations in germline cells can be inherited if the mutated cell is the “lucky” one that gets fused with its counterpart during gametogenesis. Unrepaired mutations in somatic cells can cause cell death, cancer, or a few other diseases/infirmities, depending on type and severity.
2. The reason we’re still alive, in spite of all the lousy copying, is that organisms have developed exceptionally good error-correction chemistry. These error correction processes are not based on cells - most of them are enzymes such as glycosylases and DNA polymerases. We have, for instance, over 20 different genes encoding these genetic fixers, each of them capable of repairing multiple types of mutations. Even if one of the genes encoding a particular repair enzyme is itself mutated, there is sufficient redundancy to “repair the repairer” without problem - most of the time.
There would be nothing to stop these free radicals from culturing rogue, mutated cells without their assistance.
I’m sorry, but this makes absolutely no sense whatsoever. A free radical is a collection of linked atoms at least one of which contains an unpaired electron. Obviously, free radicals are highly volatile because they are able to bind with other atoms fairly easily. Sometimes this can disrupt cellular processes because radicals can chain-reaction-like create other free radicals to the point it has a more macroscale effect. There are, of course, enzymes such as superoxide dismutase and others that counteract the effects.
I think you may possibly be confusing prions with mutations. Prions are normal proteins that for some reason have changed their three-dimensional shape. They can “corrupt” other normal proteins of the same type by forcing them to configure to the prion’s new shape. It’s sort of a “chain of infection” rather than a mutation, per se. Bovine spongiform encephalitis (mad cow disease) is one example of what can happen when the system goes crazy. Proteasomes are the enzymes produced to limit or eliminate prion infection. The problem with BSE, for instance, is that its prion configuration is highly resistant to proteasome destruction. If this isn’t what you meant, I’m sorry but I have no clue what you’re talking about here. Perhaps you can clarify?
We now know that genes are composed of DNA strands, a magnificently complex molecule. DNA is an encoded message or language. The language has four letters, which form 64, three letter words. The function of the gene acts as a blueprint to tell the cell how to build a particular protein, of which I already described in a previous post how astronmically improbable it is just to arrive at one protein.
Sort of. The language analogy can be a very useful explanatory tool if it’s not taken to extremes as you do here. It’s not a language - it’s a collection of molecules that simply because of their chemical composition can’t form any other way. Because of its chemical properties, it does somewhat act like a template, and all of the various enzymes and factors in the cell are geared toward making use of it (if I can be pardoned a bit of anthropomorphic language). When we get down to the details, however, terms like “code”, “language”, “message” are highly misleading. IOW, the analogy breaks down at the chemistry level.
As far as the probability argument goes, in a trivial sense you’re correct. The odds of coming up with a specific protein on a random basis is pretty astronomical. However, given the fact that multiple protein configurations can perform the exact same function, arriving at a functional protein gets a lot easier. There’s a great deal of wiggle room for exons to encode a wide variety of amino acids that combine to perform the same function. It’s not unlimited by any stretch, but pretty wide latitude in general. This is one of the reasons that mutations are usually neutral - even if a mutation changes a gene expression a bit, it doesn’t necessarily have to be “terminal” as long as the gene still expresses amino acids that together perform the original function. In fact, it’s this ability to vary and still be functional that allows for the existence of “beneficial” mutations.
Anyway, the genes are provided with basic instructions for creating protein insulin, myoglobin, hemoglobin, etc. Though most mutations are neutral, a very large percentage is devastatingly harmful.
I won’t disagree that some mutations can be harmful. As you mention, cancer is a good example. However, I do disagree that “a very large percentage is devastatingly harmful.” You seem to be contradicting your previous statements concerning the neutrality of most mutations. Most of the time, especially in critically important sections of the genome, the genetic repair mechanisms are pretty good at fixing what’s broke. In some other areas, such as non-coding regions, mutations can actually build up without much effect. This is one of the possible explanations for the Alu repeats, for instance.
In the most rare occasions, a mutation can be beneficial. This kind of mutation is not truly advantageous, however. For instance, many evolutionists use Sickle Cell Anemia as a prime example of a good mutation.
I’m not sure I’m following you. Why would a beneficial mutation
not be advantageous? As to your second point, I don’t think you’ll find too many people saying that sickle cell anemia is a “good” mutation, at least not taken out of its environmental context (remember, environment includes the other genes). Even then, most of us would (I think) characterize sca as deleterious - but less so than malaria infection. It is certainly very deleterious in its own right outside of malaria-endemic areas. Here’s the rub: sca is fatal if homozygous. In Central Africa, life expectancy of a child homozygous for sca is five years (from Sergeant GR 2005,
Mortality from sickle cell disease in Africa, BMJ 330:432-433). It’s obviously very different in the West, where supportive measures can be implemented. Malaria also has a high mortality rate if untreated in endemic areas. It is responsible for at least 10% of infant mortality, and as much as 25% of mortality in children 1-4 (see Hempel J 1999,
Malaria in Tropical Africa - Estimated Incidence and Mortality), throughout Central Africa. Sickle cell is not an example of a “beneficial” mutation. It’s used as an example of how a
deleterious trait can be maintained as a polymorphism in a population over time. Kids with sickle cell disease die. Kids with malaria are likely to die. Kids that are heterozygous for the sickle cell
trait may not be healthy, but given the relative protection gained against malaria, they usually live long enough to reproduce - and pass on their crap-shoot genetic legacy.
What they fail to realize is, the more individuals that procreate, the greater and more frequent the disease will be, and the less the immunity will be. The ”immunity’ will literally be bred out of existance.
As I just explained above, the
trait is maintained in the population. The disease itself is a byproduct of this polymorphism. You are confusing genetic disease with parasitical/bacterial/viral disease, I think. You can’t change the level of immunity conferred by the trait unless somehow the parasite (in this case) evolves to “get around” the sickle cell structure. One possible reason why this hasn’t occurred is that there are more than sufficient victims without the trait that it hasn’t been a significant selection pressure on the parasite.
Aside from this, its as if no one has taken into consideration how terrible this disease really is? So, you don’t have Malaria, but now you have Sickle Cell Anemia?
That’s just the point: heterozygotes with the trait don’t develop the disease. They’re a bit anemic, but not fatally so. The folks (primarily kids) who develop full-blown sca die without extensive support. Period.
So, that's how I disagree that mutation could be the propulsion of macroevolution. In other words, it effects reproduction because the more people breed, the more this disease will effect us by removing the immunity. Therefore, I don't agree that SCA, or any other mutation, could be advantageous.... (I'll be cautious here): There are no truly advantageous mutations that I know of and I've heard lots of testimonies on it.
Unfortunately, this conclusion doesn’t follow from the argument very well. The example you cited, sickle cell anemia, doesn’t cause changes in immunity to malaria. Possession of the trait in a heterozygous condition does. Since it’s a genetic trait, rather than an immune response,
Malaria falciparum parasites haven’t evolved to get around it. Indeed, malaria can live quite comfortably in a heterozygote’s bloodstream and be transferred via its normal vector. The carrier simply doesn’t develop a full-blown malaria infection.
Discussion of advantageous mutations will have to wait a bit. However, as you said “that you’ve heard of” may be an indicator that you haven’t been following the literature very closely.
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