Oocytezero

OocyteZero asks a concrete question behind a disease that affects up to 1 in 8 women: can today's DNA-reading AI models name the single causal base at an unsolved PMOS (polycystic ovary syndrome) genetic locus? It's personal — someone I love lives with PMOS — and it's genuinely unsolved: most of the disease's heritable signal sits in non-coding DNA no one has decoded. Working solo with Claude Code and Claude Science, I built an in-silico saturation-mutagenesis benchmark on 589 measured variants at the DENND1A locus and ran an escalating ladder of 12 model classes — from frozen Enformer/Borzoi to AlphaGenome to the reporter-allele model Malinois. Every one reads regulatory activity, but none resolves the causal allele. Two positive controls prove the pipeline works and the negative is real; a mechanistic diagnosis — tissue gap + data gap + an eQTL-silent locus — explains why. Claude Science independently recomputed every number and caught my own overclaims. It's a rigorous, reproducible NO — and a finding others can build on: a reusable, model- and locus-agnostic benchmark, a bound that stops the field from over-calling causal variants, and the exact wet-lab experiment (a matched-tissue steroidogenic MPRA) that could flip it. Come travel the DNA strand with me → oocytezero.vercel.app