Re-checked the four current ROT1 IBA annotations against GOA, the cached
PTHR28090 PAINT table, and the cached Rot1 literature:
GO:0005789 endoplasmic reticulum membrane, tracing to PANTHER:PTN001999053GO:0006458 'de novo' protein folding, tracing to PANTHER:PTN001999053GO:0007118 budding cell apical bud growth, tracing to PANTHER:PTN001999057GO:0051082 unfolded protein binding, tracing in GOA to PANTHER:PTN001999053All four rows list the S. cerevisiae target SGD:S000004813 as a descendant
evidence, which is expected for a target-supported PAINT node. The ER membrane
and de novo folding rows are core Rot1 annotations and now carry
NO_FAILURE_CORE. The apical bud-growth row is experimentally observed in
S. cerevisiae but downstream of ER proteostasis and cell-wall defects, so it now
carries NO_FAILURE_NON_CORE.
The unfolded-protein binding IBA needed a different PAINT review. GOA still
reports the row with PANTHER:PTN001999053, but the current PTHR28090 PAINT
cache no longer contains GO:0051082 at that node; it retains ER membrane and
de novo protein folding instead. The underlying biology remains Rot1's
antiaggregation and ER folding-support activity PMID:18508919, so the action
stays MODIFY to GO:0044183 protein folding chaperone, while the structured
IBA root cause is SOURCE_STALE_OR_MISSING.
The newer-paper search found a 2025 peer-reviewed version of the 2024 UPR
preprint discussed in the Falcon report. Bartolutti et al. used inducible Rot1
as a UPR-independent ER chaperone to maintain euploid UPR-deficient populations
PMID:40846641, which is consistent with the chaperone model but does not
change any of the four IBA decisions.