Relay-Version: version B 2.10 5/3/83; site utzoo.UUCP Posting-Version: version B 2.10.2 9/18/84; site phri.UUCP Path: utzoo!watmath!clyde!burl!ulysses!mhuxr!mhuxn!ihnp4!pesnta!phri!roy From: roy@phri.UUCP (Roy Smith) Newsgroups: net.origins Subject: Re: So simple, even a creationist can understand! Message-ID: <327@phri.UUCP> Date: Sun, 14-Jul-85 22:38:07 EDT Article-I.D.: phri.327 Posted: Sun Jul 14 22:38:07 1985 Date-Received: Sat, 20-Jul-85 02:48:14 EDT References: <2156@ut-sally.UUCP> <347@scgvaxd.UUCP> Organization: Public Health Research Inst. (NY, NY) Lines: 66 Keywords: Natural Selection > *How* do the beneficial mutations get amplified by Natural Selection? A perfectly reasonable question. Let's suppose that due to a single nucleotide being wrong in my DNA, the hemoglobin in my blood tends to crystalize when it shouldn't (we're talking sickle cell anemia, here). I'm weaker, slower, etc. than you are. I'm less likely to survive to puberty than you are because I can't compete for food or run away from attackers as well as you can. Even if I reach sexual maturity, I'm less likely to father children (and pass on my mutated DNA to my progeny) than you are because when we fight over a woman, you are likely to win. Thus, this random mutation gets *selected against*. I can't think of such a striking example in the other direction, but the idea is the same. Suppose a random mutation causes my hearing to be slightly better than yours in some way. I'm more likely to hear an attacker in time to save myself than you are. When hunting, I'm better able to tell where my prey is. In this case, the effect is small (as it is with most beneficial mutations). However small the advantage is, I am more likely to propagate my DNA than you are. This mutation gets *selected for*. Actually, the vast majority of mutations are harmful. This doesn't change the basic idea, though. The harmful ones get weeded out because they either don't survive or don't reproduce as well as the wild-type (non-mutated) organisim. When talking about mutations, one needs to make a differentiation between phenotype and genotype. Phenotype refers to the observable characteristics (the phenomena you can measure) of a system. Genotype refers to the genetic makeup; the two are only loosely related. Small changes in genotype can produce large changes in phenotype (as in sickle cell anemia). Conversely, large changes in genotype can produce little or no phenotypical changes. Mutations are changes in the genotype. Evolutionary pressure is applied, however, because of changes in phenotype. The single base change mentioned earlier is a genotypical change. This genotypical change produces the sickle cell phenotype. Which brings us back to what appears to be a contradiction. If sickle cell anemia is bad for you, why *hasn't* natural selection selected it right out of existence? You have two sets of genes which make hemoglobin, one given to you by your mother, the other by your father. The sickle cell phenotype is recessive. That means that you only exhibit the symptoms if *both* of your copies of the gene are defective. If only one copy has the sickle cell genotype, you are said to the have sickle cell trait; you can pass it on to your children but you don't have the symptoms yourself. Well, it turns out that having sickle cell trait is actually beneficial. If you have the trait, you make both the good and the bad kinds of hemoglobin. It turns out that this is sufficient to make your red blood cells function properly and you don't get sick. However, the parasite that causes malaria lives in your red blood cells, and *it* can't tolerate the mixture of good and bad hemoglobin. So we have an interesting situation. People with sickle cell trait have protection against an often fatal disease so the trait gets selected *for*. On the other hand, two people with sickle cell trait have a 25% change of their children having the anemia, so it gets selected *against*. Which of these factors stronger? Check back with me in a few million years and I'll let you know. -- allegra!phri!roy (Roy Smith) System Administrator, Public Health Research Institute