Genes combinations that result in dark hair will naturally be more prevalent than light hair, because dark pigment will overpower light pigment. However, things get more complicated if there are survival advantages in having light-colored hair; or if sexual selection favors light hair. Then you would eventually see light hair dominating the population, in ways mendelian genetics can not explain on its own, at least not with any precision.
Ah, now I can see how you're getting confused.
You used the terms "recessive" and "dominant" in reference to Mendelian characteristics, but now you use the term "dominating" with respect to population genetics. In population biology, genes and genotypes are talked about in terms of proportion or frequency, not dominance.
And your example, you are wrong. Gene combinations that result in dark hair need not be more prevalent in a population, just because of how the genes are expressed. It may be that, in a particular population, genes for hair pigment are rare. Individuals with a high dose of pigment genes will have darker hair (that's Mendelian dominance), but they might not be prevalent in the population.
And so, in response to my question about explaining dominance of the cystic fibrosis wild-type gene, you answer with
There are a few theories. Resistance to cholera being the most prevalent, it seems.
which the answer to the question of
persistance of the mutant type in the population.
But the reasons for the Mendelian inheritance pattern was clear when it was discovered that CF is caused by mutations in the CF transmembrane conductance regulator (CFTR) gene expressed in certain epithelial cells, the most common a 3 bp deletion termed deltaF508. The function of this protein is to regulate other ion channels and pH, among other processes.
So, individuals lacking functional CFTR tend to "leak" fluids, and in the lungs this leads lung disease typical of CF. However, as long has a person has at least one gene that produces a functional CFTR, they won't exhibit the phenotype of CF. Therefore, if you have two normal genes, you don't get CF; if you have one normal and one mutant, you don't get CF; only when you have both mutant alleles will you develop CF.
That is a classical Mendelian inheritance pattern; we can describe CF solely in terms of the biochemistry, molecular and cellular biology of CFTR.
We can
add to the story by noting that some known derived from evolutionary theory greatly spread the discovery of the CFTR gene, in that homologies to related proteins and chromosomal organization among humans and model organisms helped track the specific DNA sequence and to understand gene function, but ultimately, the gene could have been found using just human pedigrees.
Harder, but doable.
We can explain the persistence of the gene by noting that it seems, in heterozygotes, to confer some resistance to cholera. The cholera pathogen isn't in and of itself deadly, but it triggers fluid loss to the extant that victims die from dehydration. However, since heterozygotes don't have as many functional CFTR proteins (because they have a mutant gene), they are less responsive to cholera.
About the only thing that evolutionary theory adds to the story is that, using methods of molecular evolution, the deltaF508 has been dated to around 50,000 years ago.
Really, until you get a proper grasp on Mendelian and population genetics, you'll have a hard time making any headway about randomness in evolution. This kind of statement,
Mendelian genetics might predict that the probability of gene "X" showing up in the population is 25%. If reality was that simple, you might as well roll a 4-sided die, to try to predict who will have it or not.
suggests you confuse the two, because with Mendelian genetics it really as simple as rolling a 4-sided die (actually, it's two independent coin flips - the law of independent assortment); and Mendelian genetics tells nothing about the probability of a gene showing up in a population, only the probabilities of genotypes (and phenotypes) in the offspring of specific crosses.
You might want to read this:
http://plato.stanford.edu/entries/population-genetics/
The rich and healthy have adapted a survival strategy, where they don't need to reproduce as much, because their children are more likely going to be healthy and survive.
The sick and poor have adapted a strategy where they just try to have as many children as possible, in hopes that some of them will survive.
That summary over-simplifies the matter, some-what. There are a lot of complicated other aspects involved. But, is that a good start?
Way over-simplifies. You're starting with the outcome, and assuming that the populations deliberately chose strategies to achieve that outcome.
But that's not how evolution works. Organisms simply go on with their lives, and if their way of living is productive in a given environment, they'll more likely reproduce than not reproduce.
It may be more simply that rich and healthy make better choices about lifestyle - that impulse control thing I linked to earlier. They stay in a work to build a nest egg before having kids because it makes them feel secure. Perhaps people with little regard for the future, instead of saving money go out and party and have unprotected sex because they just don't care about the future, that way ending up with more kids. These people don't think about the future, their not going to think about health care.
Or perhaps the original observation is flawed - people have as many kids as they can afford, and rich people can afford more kids. Poor sickly guys don't get laid much.
Really, I most the questions I asked were rhetorical. But this one tells me that you don't understand selection.
Organisms don't adapt (or did you adopt, because adapt has a different meaning here) strategies to maximize survival, instead the different "survival strategies" are selected for or against by the environment.
A couple years ago, I took an exercise physiology class; this shortly after taking a quantitative genetics class. In the ex. phys. class, I was struck by the different meanings of "adaptation".
In exercise physiology, adaptations are the things your bodies does in response to exercise; to adapt to repeated stress - increased cardiovascular capacity, for example. In quantitative genetics, though, the adaptation is predetermined - some people are better adapted for distance running (like, say, Kenyans) and no amount of training is going to make them good sprinters.
Physiological adaptations are things you can change about yourself, genetic adaptations are the things you are lucky (or unlucky) enough to have been born with.
Here, I'm using physiological adaptation to be pretty much equivalent to "phenotype" and genetic adaptation as "genotype"; when you say "rich and healthy have adapted a survival strategy", it sounds more like a physiological adaption, not a genetic adaptation. Not something that is necessarily heritable.
Selection acts the physiological adaptation, but transmission occurs through the genetic adaption. Physiological adaptations get you through immediate environmental changes, but genetic adaptations persist over generations in a common environment.
It's not about just the children; evolutionary selection generally acts across multiple generations.
Though, for quick-and-dirty purposes, you could define "all-natural" as any life forms where humans have not intentionally altered the course of their evolution.
It wasn't all-natural as opposed to life forms I was curious about; it's the application fitness landscape in your statement.
Certain genes made some life forms easier to domesticate, than others. Those that were domesticated found their forms being altered (fruits would be larger, for example, and dogs better able to sniff-out foxes...). Genes that allowed for these preferred alterations would tend to survive and reproduce more effectively, among humans, than those without the favored features.
That's domestication, but not artificial selection. Domestication in many cases may be better explained in terms of co-evolution.
But what makes artificial selection a Darwinian process?
Taffer said:
Perhaps a better way to describe selection is that skews the associated probabilities of survival in one direction or another?
Consider it this way - you can count cards at Vegas to skew your odds that will beat the house. That's the genotype.
But you can still lose any given hand. That's selection.
At the end of the day, if you have more money than the house, that's evolution.
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