MTC7 rereview notes

2026-09-28 re-review

• MTC7 has no IBA annotations in MTC7-goa.tsv; the GOA rows are membrane IEA, two duplicate molecular-function ND rows, cellular-component ND, and biological-process ND.
• Re-read the MTC7 review, UniProt record, Falcon deep-research report, prior manual deep-research report, local bioinformatics summary, and the cached full text of Addinall et al. 2008 PMID:18845848.
• Searched newer literature for MTC7, YEL033W, and Maintenance of telomere capping. The hits were database pages, theses, older screen papers, or broad studies in which MTC7 appears only in a table; no newer primary paper establishes a molecular function or direct pathway role for Mtc7.
• Fetched Askree et al. 2004 PMID:15161972 after a search found the earlier telomere-length screen. That paper is important counterevidence: YEL033W was the one tested hit whose short-telomere phenotype did not cosegregate with the deletion marker.
• UniProt records MTC7 as PE 4 (Predicted), so the broad GO:0016020 membrane row was retained only as a sequence-prediction annotation. Follow UniProt and the local topology analysis over the Falcon statement that Mtc7 lacks predicted transmembrane segments: both the UniProt feature table and MTC7-bioinformatics/RESULTS.md support two N-terminal hydrophobic helices.
• Retracted the proposed GO:0016233 telomere capping assertion. Addinall et al. justify MTC7 as a telomere-biology candidate, but a high-throughput cdc13-1 modifier phenotype does not show that Mtc7 itself carries out chromosome-end capping or acts directly at telomeres.
• Rewrote MTC7-pathway.md to mark MTC7 as pathway-unresolved instead of modeling unproven nuclear shuttling, telomerase regulation, telomeric chromatin interaction, and short-telomere causality.