One issue that seems to come up a lot here is that a lot of people are just not familiar with the basic models of how alleles respond to selection pressure. This means that for example people don't appreciate that highly deleterious alleles can stay in a population when they are recessive because evolution has a lot more trouble acting on them when their frequence becomes very low. Moreover, the weakening of selection occurs at a rate which is proportional to the square of the fraction of how common the allele is in the population.
What determines whether an allele is recessive or dominant?
Through reading Wikipedia I have encountered one theory: gene A has two alleles which actually determine something important, like Parkinson's disease. In addition, gene M has two alleles which don't really do anything on their own, but they determine which allele of gene A is recessive and which is dominant (this mechanic is easy to model: you have two copies of each gene, making four total, and you need any two of the four to be flipped to "Parkinson").
The evolution fairy then makes one version of gene M universal in the population. This seems iffier to me: gene M and gene A act symmetrically, so why would one become universal and the other not? But maybe gene M is responsible for the dominance or recessiveness (?) of multiple genes, so there's greater selection pressure because it's relevant more often. After this, the dominance or recessiveness of gene A becomes essentially fixed, and we talk about one allele being dominant and the other recessive.
However, the other thing that the (very short) Wikipedia article on evolution of dominance says is that this hypothesis has been discredited, and is no longer generally believed. It's unclear to me why not to believe it, and what the alternative is, but there you have it.
Ok. There are a variety of different issues going on here. (With the disclaimer that I'm not a biologist).
First keep in mind that genes are discrete units and population sizes are finite. This allows for genetic drift which is when random sampling allows the frequency of a gene to change in the population as a random walk. This is especially easy to occur in small populations (since the sample sizes are then smaller). So two alleles can behave completely symmetrically and still have one go to fixation in a population, and similar remarks apply to symmetricly behaving genes.
Whether a given allele is recessive or dominant can be a function of a variety of different things. Keep in mind that a lot of the traits we care about have behavior more complicated than just dominance or recessiveness. There are some examples where the heterozygous case has a middle phenotype. Another example is how many of the alleles for six fingers are dominant over alleles for five, but the alleles display variable penetrance, which is a fancy way of saying that not everyone who has the allele ends up getting the phenotype due to essentially stochastic considerations.
What makes an allele recessive or dominant can depend on what it is doing. So for example, if an allele is producing a bad protein that gets in the way of something else, then it is likely to be dominant. If an allele is just needed to at the right time in development trigger a certain pathway it is likely to be recessive. Some alleles don't code for the production of a different protein but simply don't code for a protein at all (if they are say missing a functional start codon or some other bit of instructional code). In those cases, whether the allele is recessive or dominant depends on what the allele does. So for example, if the allele calls for the production of a protein that has its level normally regulated to stay in some level of stasis (as many proteins in cells are) then the body will simply ramp up production and so it will be recessive. Similarly, the A and B alleles in bloodtypes are dominant because what matters is whether the display occurs on the outside of the cells. So as long as there's enough protein for any display, a recipients immune system will recognize it as foreign.
In general, the biochemistry can be really complicated. Huntington's disease for example is caused by mutations in the Huntingtin gene. This is one of the most studied of any single human gene but what it is causing to go wrong is still not well-understood.
This means that for example people don't appreciate that highly deleterious alleles can stay in a population when they are recessive because evolution has a lot more trouble acting on them when their frequence becomes very low.
I have no background in science and I understood this when I was ten (?) and my mother told me about Christopher Nance and answered my followup questions. I suspect people here largely do understand this.
Can you please explain more difficult things? I made this thread to try and pinpoint my confusion and ignorance.
Does this thread cause you to update at all on the level here for understanding these sorts of issues?
I for one do not understand these issues and would be interested in hearing more. Though it doesn't strike me as obviously important (counterevidence appreciated).
That's not a real thread, it's a test to see whether people think critically about what they read on LW in general and about biology in particular.
Possibly.
In any case, it was the inspiration for this post as I said about that thread:
I think it is basically storytelling with truth constrained according to rules of Aristotelian inference...Nothing useful about biology can be learned from this sort of thing...conjoins mundane observations to each other according to an entertaining narrative until a logically true and subjectively interesting influence in biology is discovered - regardless of the fact that the method used to reach the random-vectored conclusion, minus the constraint of having to be entertaining, would endorse countless other truths of similar magnitude and random vector...
Privileging the hypothesis, reversed stupidity is not intelligence, cultish countercultishness, the tragedy of group selectionism...
I'm not sure what it is that is (or is not) being explained. Phlogiston had fire, for example. There needs to be an unexplained phenomenon, or one has a fake fake explanation...
The blog post is a random story crafted to appeal to humans and not be logically false. It can be defended by saying that all that is meant is logical truth of its stories being factors, but by Gricean implication, if one writes a blog post about an effect being real, one is claiming that this could be used to make a prediction and has more of an effect than the influence of Pluto's gravity on mating patterns of the Buffy-Tufted Marmoset...
The OP seems to me like a fixation on a very small thing, a story of why a factor should have an effect, totally ignoring most other factors on the effect and most other effects of the factor...
So. I was downvoted for saying such things there, and so I made this thread to cure my misunderstanding of biology, since that post was so well received. I gave my best shot at explaining evolution in a handful of sentences, and wait for it to be corrected by a better short explanation or added to.
I would suggest that in this context the problem is not that you need more correction but that other people in the thread or the people downvoting you need such correction.
Genes, units of heredity, exist in environments that determine their immediate futures. The most important influences in such environments are often host individuals' traits and other genes. Individuals have traits according to their genes and histories. Instances of genes arise based on (usually identical) ancestor genes and their environments, and future individuals will also have traits based on their genes and histories.
Let's refine each other's understanding of biological evolution, as encapsulated as best we can manage in a short comment.
It's time to be lesswrong. Starting with me.