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v0 cycle complete. Gain is frozen here as a public-data evidence audit + substrate-gap diagnosis for the canonical lung developmental regulators (NKX2-1, SOX2, SOX9).
Read first:
notes/project_summary.md— full narrativenotes/key_findings.md— concise findingsnotes/limitations_and_next_methods.md— method-level futuresnotes/next_project_decision.md— decision memo for the successor project (CELLxGENE Census expression route picked)
What this release establishes:
- Substrate-gap diagnosis: no primary human lung tissue ChIP-seq for NKX2-1 / SOX2 / SOX9 / CTNNB1 / SMAD1 / GLI2 in ChIP-Atlas hg38 (verified via NCBI GEO + SRA E-utilities external search).
- 5 NKX2-1 chromatin-supported standing distal candidate loci (FOXA2 chr20:22,716,796 strongest; FOXA2 ×2, SCGB1A1 ×2, ABCA3 ×1).
- 18 stdlib-only audit scripts implementing a 5-class evidence model + peak intersection + sensitivity sweep + distal-candidate tiering + histone-support filter + motif + accessibility scan + quantitative refinement.
- Negative finding: bulk fetal lung motif + accessibility at v0 settings cannot discriminate canonical SOX2 targets from controls.
Standing biological output: the 5 NKX2-1 candidate loci. Candidates, not validated regulatory elements. Become testable when primary lung developmental ChIP-seq is published or when Hi-C / promoter-capture data is brought into scope.