Lesson 21 — Mutation target size and the parallel evolution it produces
BIO 202, Spring 2026, draft v0. Big mutational targets evolve fast and in parallel. Small targets evolve slowly. Some genes are mothers; some are shitposts.
Draft skeleton. Stage scenarios and anchor quotes are in place; the simulator and code panels are not yet wired.
Some genes are harder to change. We'll see those — like Hox genes. They're going to vary very little across all living things, all animals. On the other hand, things like microsatellites don't matter. Microsatellites are like the shitposting memes you make. Hox genes are like the word "mother."
— 202_lec01_09
A — Two genes, two mutation rates
Simulate two loci. One has 10× the mutation rate of the other. Watch their substitution rates over time. The pattern is exactly what you'd expect when the per-base mutation rate is the same but the target size differs.
The word "mother" varies less across languages than the word "cup." Changing the word "cup" is easy — if I use a different word for cup, that's not a big deal. If, on the other hand, a lost child asks for their mother in a different way so that the person they're asking doesn't understand the kid is looking for their mother — that's a problem. Some things are important, so they change less.
— 202_lec01_10
When a phenotype can be reached by mutating any of many genes, it will be reached many times independently. When only one gene can do it, the phenotype evolves once or never. Show five traits and predict how many independent origins each has.
Vertebrate paralogs subfunctionalized: each picked up a piece of what the ancestral single Hox gene used to do. They aren't redundant. They aren't doing the same job in parallel. They're each doing a part of the job, and you need them both. That's what made the four-cluster duplication evolutionarily useful — it gave vertebrates more knobs to turn.
— 336_lec11_06
TODO: parallel-evolution drill. Five traits classified by mutational target size; predict number of independent origins.
C — The Alu in the regulator
A specific case: an Alu transposon jumped into a regulator of a Hox gene that activates the posterior region of the trunk. That one event took our tail. Specify the test that distinguishes "big-target rapid evolution" from "small-target lucky single event."
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.
— 202_lec15_02
TODO: target-size diagnostic. Count of independent origins as a function of target size; bootstrap CI.
D — Five phenotypes, five effective mutation rates
Classify webbed feet, cave eye loss, lactase persistence, the placenta, hinged jaws by their effective mutational target size (scaffold S17 already drills the intuition; this lesson formalizes it).
Your Hox genes are more than half a billion years old. As things that have made successful copies of themselves, they're doing amazing — with almost no changes. Nearly zero mutations in these genes for over half a billion years. That's impressive making more copies of yourself.
— 202_lec31_03
TODO: five-phenotype classification panel. Stretch: connect to S17 scaffold; show that the "number of independent origins" pattern follows the target-size hierarchy.