Reviewed all 20 source rows and the Falcon report body. The actual PTHR43836 lineage (separate JSON, full response hash retained) places A0A193KX02 below all four positive IBDs at PTN000053580. Restored broad developmental and metabolic assertions: a mechanotransduction role does not establish loss of another ancestral function. PMID:28534737 full text shows that H183A is a mouse TOMT transgene, and mouse TOMT/TMC1 were co-immunoprecipitated in HEK cells. Do not transfer mammalian active-site substitutions to zebrafish or claim experimentally proven zebrafish chaperone activity. Native physiological methyl acceptor remains unknown.
Endocytosis remains UNDECIDED: PMID:10526320 is abstract-only, interprets rapid FM1-43 loading; PMID:11549711 establishes MET-channel permeation in mouse cochlear cells, and PMID:28534737 directly attributes mercury to absent MET/Tmc trafficking. Independent vesicle-uptake evidence in the original target study must be assessed. A focused parent-coordinated adjudication was requested; no duplicate report was run. Development/behavior/location positives were assessed individually and retained with assay scope. No NEW assertions were added; all source fields preserved.
Reviewed tomt-hypotheses/endocytosis-versus-met-dye-permeation/openscientist.md. The report strengthens the negative side of the assay interpretation: later work establishes rapid FM1-43 loading as MET-channel permeation, and the mercury/tomt phenotype is therefore parsimoniously downstream of Tomt-dependent Tmc trafficking rather than a direct endocytosis defect.
The report recommended removing GO:0006897 endocytosis; kept the review action at UNDECIDED instead. The original IMP source, PMID:10526320, remains abstract-only in the local cache, so the full-text curation rule still applies: do not overrule the curator until the original paper can be checked for independent vesicle-uptake evidence beyond FM1-43 loading.