While auditing the existing review, found that both the top-level description
and the core_functions entry for GO:0010484 (histone H3 acetyltransferase
activity) already asserted that RTT109 "prevents DNA-RNA hybrid accumulation" /
contributes to "R-loop suppression" through H3K14/H3K23 acetylation, but no
reference anywhere in the file actually cited or quoted the paper establishing
this. The gene's own working file RTT109-CURATION-REVIEW.md (an untracked
scratch document in this folder) explicitly flagged this: "R-loop/DNA-RNA
hybrid prevention not explicitly annotated but supported (NEW annotation
should be added)" -- but that follow-up was never done in the actual
RTT109-ai-review.yaml.
Identified and fetched the source paper: PMID:35866610, Cañas et al. 2022,
Genetics, "A role for the Saccharomyces cerevisiae Rtt109 histone
acetyltransferase in R-loop homeostasis and associated genome instability"
PMID:35866610. Full text now cached at
publications/PMID_35866610.md via ai-gene-review fetch-pmid.
Checked whether an existing GO term could be used for a direct NEW
existing_annotations entry (as done for e.g. ROF1's filamentous-growth
annotation). Searched QuickGO for "R-loop" and "DNA-RNA hybrid": the only
R-loop process term is GO:0062176 (R-loop processing), whose definition is
explicitly R-loop disassembly -- the opposite direction from what RTT109
does (RTT109 loss increases R-loop levels; RTT109 activity prevents their
formation). No term for "negative regulation of R-loop formation" exists in
GO. Per project convention (never force a mismatched id onto a real finding),
recorded this as a proposed_new_terms entry instead, with PMID:35866610 as
support and GO:0006325 (chromatin organization, already used elsewhere in
this review) as a defensible proposed_parent.
Also added PMID:35866610 to references: with a reference_review (HIGH
relevance, VERIFIED -- PubMed/PMC-verified, full text cached) and attached
supported_by provenance to the GO:0010484 core-function block that was
making the previously-uncited claim.
No other issues found in this review during this audit pass. The bulk of the
70 existing_annotations entries (H3K56/K9/K27/K14/K23 acetyltransferase
activity, chromatin assembly, DNA damage response, etc.) are well-supported
by the cited literature and internally consistent.
Rechecked the three RTT109 IBA rows against the cached PAINT export for
PTHR31571. All three propagate from the same fungal RTT109 ancestor,
PANTHER:PTN001586545: GO:0032931 is seeded by budding yeast RTT109, fission
yeast SPBC342.06c, and Candida CAL0000176178; GO:0006974 is seeded by budding
and fission yeast; GO:0005634 is seeded by budding yeast. The target appearing
among the descendant seeds is expected for PAINT and is positive support, not a
circular donor. The H3K56 acetyltransferase activity, nuclear localization, and
DNA damage response annotations are therefore all retained with
NO_FAILURE_CORE.
Updated the legacy generic GO:0005515 protein binding calls during the same
pass. The cited Vps75 and Asf1 interactions are real and mechanistically
important, but protein binding is not an informative molecular-function
annotation for the Rtt109 histone-chaperone acetyltransferase system. Those
rows now use REMOVE, while the catalytic and H3 histone acetyltransferase
complex rows continue to capture the relevant biology.
Searched PubMed and the web for 2023-2026 RTT109/Rtt109 papers in budding
yeast. Three new PMIDs were worth caching:
These newer papers extend the transcription and replication-associated repair
contexts but do not require new GO actions beyond the existing accepted
chromatin organization, DNA damage response, and H3 acetyltransferase activity
annotations.
Rebased the RTT109 review onto current GOA/UniProt with just fetch-gene yeast RTT109
--force; current GOA has 79 rows and the fetch seeded 15 new source assertions.
The additions were broad experimental GO:0004402 histone acetyltransferase
activity parents for the older Rtt109 HAT literature, one current RHEA/EC IEA
for the same broad activity, two generic Vps75 GO:0005515 protein binding
rows, two broad GO:0061733 protein-lysine-acetyltransferase activity rows, and
one Vps75-sourced GO:0070775 H3 histone acetyltransferase complex row. The
catalytic parents and complex row were accepted; the Vps75 protein-binding rows
were removed as generic duplicates of the specific Rtt109-Vps75 H3
acetyltransferase complex mechanism.
No PAINT topology changed in the refreshed PTHR31571 export: GO:0005634,
GO:0032931, and GO:0006974 still all propagate from the fungal node
PANTHER:PTN001586545. The prior PTN-only propagation_review entries remain
valid; SGD RTT109 appearing among the node seeds is target-supported PAINT
evidence, not circular evidence.
Checked PubMed for 2025-2026 Rtt109/RTT109/KAT11 hits. The direct budding
yeast replication-repair paper PMID:39631395 was already cached in the prior
pass; newer PubMed hits were either non-Saccharomyces, human EP300, model
systems that only mention yeast RTT109, or a 2026 bioRxiv Candida albicans
Rtt109 preprint, and did not require new RTT109 curation.
KEEP_AS_NON_CORE and changed the retiredGO:0006351 keyword row to MODIFY toward regulation of transcription.core_functions ancestor chain by dropping the broadGO:0061733 parent activity, retaining the H3K56-specific activity and the