Draft skeleton. Stage scenarios and anchor quotes are in place; the simulator and code panels are not yet wired.
Meiotic drive is a subversion of meiosis. Particular alleles ensure they make it into more than 50% of the gametes — sometimes 100%. Meiosis evolved. It's coded by genes that themselves evolve. So the rules of meiosis can be cheated. There's no external rulebook keeping things fair. Strategies that work well increase in frequency. Even the rules.
— 461_lec29_04
A — Fair meiosis as the null
Build a diploid simulation where meiosis is perfectly fair: each parental allele has exactly a 50% chance of making it into a gamete. Run for many generations. No cheating. Allele frequencies follow Hardy-Weinberg.
What controls how meiosis works? Proteins. What do proteins come from? Genes. What gets copied and transmitted? Genes. So genes make the rules about how this works. Do genes want to end up in the polar bodies? They sure as hell do not. They're in constant war with each other.
— 145_lec24_03
TODO: fair-meiosis sim. Standard Wright-Fisher; verify Mendelian segregation as a baseline.
B — Introduce a driver
Add an allele that gets into 70% of gametes instead of 50%. Watch it sweep to fixation. The driver wins at the gene level — and on its way to fixation, it can drag bad genome-level consequences (mutational load, fertility cost) along with it.
As long as the battle is equal, it stays random. But if one gene develops a sword, it ends up in the egg every single time. That's meiotic drive.
— 145_lec24_03
TODO: meiotic-drive sim. Driver strength slider; trajectory; show genome-level fitness cost emerging.
C — Genome-level policing — when the genome wins
Add a suppressor at another locus. Suppressors evolve because the genome as a whole has lower fitness when one of its components cheats. Run the Price ratio at the genome vs gene level. When suppression succeeds, the between-genome cov dominates the within-genome (gene-level) cov.
It's happening in all your cells, all the time, super commonly, in a class of genes called transposons — jumping genes. They are genomic parasites: stretches of parasitic nucleic acids that copy themselves inside your own genome. They have heritability, they have differential reproduction, and they vary — so they evolve. They are not alive, but they definitely evolve.
— 202_lec12_03
TODO: driver-suppressor sim. Two-locus dynamics; Price ratio at genome vs gene level; show the suppressor evolving to restore the genome as the unit.
D — The Alu transposon that took our tail
A specific transposon insertion broke a Hox regulator and erased the long tail of our ape ancestors. At the gene/transposon level, the Alu won (it copied itself, landed somewhere new, persisted). At the genome level, the insertion was tolerable — and may even have helped. The same event reads differently at two levels.
At some point in the past, an Alu transposon jumped into a regulator of a Hox gene that activates the posterior region of the trunk. That region got broken because an Alu jumped into it. It took our tail. That is why apes don't have tails. The Alu jumped into a transcription factor binding site on the T-locus — that's the causal mechanism by which we lost the long tail. It turns out that was advantageous, or at least not bad enough that drift didn't fix it.
— 202_lec15_02
TODO: Alu-in-Hox case study. Frame as gene-level vs genome-level cov(w, z); .R export. Non-trivial code mod: model a Wolbachia symbiont as a chromosome-level driver in arthropod sex determination.