atg-16.2 (Q09406, K06A1.5) review notes

Provenance / process

• Q09406 is the Swiss-Prot entry (534 aa); used.
• Deep research failed (falcon timeout; perplexity-lite fallback killed, exit 137). No deep-research file; review based on cached publications, UniProt and PubMed. PMC full text for PMID:24185444 could not be retrieved via PubMed MCP (empty full_text), and the cache lacks Results.

Key evidence PMID:24185444

• "We showed that atg-16.2 mutants exhibit a stronger autophagic defect than atg-16.1 mutants."
• "In atg-16.2; atg-16.1 double mutants, the lipidated form of LGG-1 accumulates, but LGG-1 puncta are completely absent."
• "ATG-16.2 ectopically expressed on the plasma membrane provides novel sites of LGG-1 puncta formation."
• "the C-terminal WD repeats are dispensable for the role of atg-16.2 in aggrephagy"
• "Lipidation of LGG-1 increases rather than reduces in atg-16.2; atg-16.1 mutants." - i.e. worm ATG-16 is a site-specifier, not required for lipidation per se.
• LGG-2 (not LGG-1) binds ATG-16.1/ATG-16.2 PMID:27046254.
• Germline: "ATG-16.2/ATG16L all promote cell-cycle progression" via DAF-16 PMID:28285998.

Decisions

• Core MF: protein-membrane adaptor activity (GO:0043495, IBA accepted) in Atg12-Atg5-Atg16 complex.
• Plasma membrane EXP/IEA marked over-annotated: the visible evidence is engineered PM targeting. Not removed because Results were not visible.
• GO:0034045 (obsolete; replaced_by GO:7770114) rows MODIFY to phagophore membrane.
• Autophagosome membrane IBA kept non-core (complex acts on phagophore).
• protein binding IPI rows REMOVE; germline and S. aureus IEP rows kept non-core.