All 26 source rows reviewed and source fields preserved. Restore broad mitochondrial membrane, GTPase and GTP metabolism annotations: specificity is not exclusivity. Full PMID:25022898 Fig. 6H directly tests zebrafish Opa1 and ventricular hypertrophy; the title foregrounding Tom70 is not a gene-misattribution argument. PMID:23516612 directly supports mitochondrial morphology and developmental phenotypes.
Mouse ISS donor P58281 resolves to PMID:36171294. The full paper distinguishes cytokine output from early differentiation: “Thus, OPA1 sustains cytokine production in TH17 cells in vitro, but not early differentiation events associated with transcription factor expression.” Retain IL-17 production as inferred noncore; modify lineage commitment to that better-supported process. Zebrafish-specific immune tests remain absent from this evidence set, which is not negative evidence.
Read the complete existing Falcon report and the shared EAT-3 OpenScientist adjudication. The latter is useful for domain/topology concerns but overstates exclusion. It supplies no executable analysis artifact or target-negative capacity assay. Its caveat that primary localization alone does not refute a conditional interaction is retained. No duplicate report requested.
Independent live PANTHER treeinfo response (v19) verifies PTN000170013 → PTN000902162 → PTN008520527 → PTN008520528 → PTN008973342 → PTN007514526 (OPA1) → … → PTN000170160 (Q5U3A7). Thus neither challenged node is restricted to its extant classical-dynamin/DRP1 donors. Current PAINT IBDs were read directly; no target-loss event was established. Peroxisome fission and microtubule binding remain UNDECIDED. Compact API provenance/ancestry is in projects/IBA_REVIEW/rereview-2026-09-20/organelle-paint-lineages.json.
Additional full-primary cross-check: PMID:20185555 Fig. 2A tests purified human OPA1-S1 liposome association with phosphatidic acid as well as cardiolipin; Fig. 4 demonstrates membrane tubulation. PMID:32228866 Fig. 1A explicitly identifies an OPA1 middle domain and C-terminal GED, so the shared report's claim that absent GED database labels prove absence of that structural machinery is unsound. Its structure demonstrates a dynamin-like power stroke and helical membrane remodeling. This supports the accepted lipid-binding/tubulation terms without proving microtubule binding or peroxisome fission. PMID:28628083 abstract independently reports human L-OPA1/cardiolipin reconstituted fusion; PMID:37612504 abstract describes the lipid-binding paddle and membrane-bending lattice. The last two were not full-text verified.
Restored readable identifiers in manual prose. Where applicable, reconciled AP3M2 reference notes with the retained contextual claim, removed unrelated PIK3C3 support from unresolved projections, separated PIK3C3 aspect-specific reasons, and documented the surviving/renamed ATG14 membrane term. Source assertion fields and verbatim quotations are unchanged.
Removed the physical-interaction quotation from the peroxisome-fission review because it concerns a different capacity. The verified ancestral placement remains documented in projects/IBA_REVIEW/rereview-2026-09-20/organelle-paint-lineages.json; the UNDECIDED call does not assert that Opa1 performs peroxisome fission. Mitochondrial topology and specialization are relevant evidence, and rejection need not await a negative experiment, but the shared report's clade-exclusion and GED-loss premises were independently contradicted. Inheritance or loss at the OPA1 branch remains the question requiring adjudication.
The same burden-of-proof clarification now applies to both disputed peroxisome-fission and microtubule-binding rows: rejection does not require a negative assay. The reasons preserve the independently verified ancestry and contradicted domain-loss premise, with inheritance/loss unresolved. Opa1 no longer uses the AI report as a supporting quotation for either capacity.
Remove the negative-assay absence clause from the disputed report reference review, aligning it with the annotation reasons. Preserve the independently verified ancestry and domain-architecture rebuttal; no action or supporting quotation changes in this gene.