parS (PA1798, Q9I2U4) review notes

Review session 2026-11-05 (PseudoCAP IBA-seed protocol, tier 2)

Fetched with just fetch-gene PSEAE Q9I2U4 --alias parS (symbol fetch hit
UniProt rate limits). Accession Q9I2U4 matches the worklist (rank 330).
Unreviewed TrEMBL entry, 428 aa. Checked against the existing review of its
cognate response regulator, genes/PSEAE/parR (same seed paper, same kind of
call). No deep-research provider was used.

Identity

Literature

Clade check (cached PAINT IBD/leaf GAF; QuickGO 2026-11-05)

PseudoCAP IBA-seed assessment

PTN node node term n_seeds leaf IBAs seed annotation (term, evidence, PMID) verdict rationale other seeds IBD stands without this seed?
PTN001293174 GO:0000155 phosphorelay sensor kinase activity 3 30 (13 taxa) GO:0000155, IMP, PMID:20547815 (PseudoCAP) INDIRECT-PHENOTYPE A molecular function asserted from a mutant phenotype: loss of parS abolishes peptide-induced arn expression and adaptive resistance; no kinase assay is described in the abstract. The term itself is almost certainly right (HisKA/HATPase domains with the conserved His218, cognate RR next door), so the row is kept and only the evidence code is questioned, at SUSPECTED, as for the parR GO:0000156 row. E. coli EnvZ P0AEJ4 (IDA); P. aeruginosa KinB Q9HT87 (IDA) Yes. Two seeds with direct kinase assays ground the node; no GO_CENTRAL defect.

Defects filed: PSEUDOCAP WRONG_EVIDENCE_CODE (CHECK, SUSPECTED) on the
GO:0000155 IMP row, mirroring the parR defect from the same paper.

Decisions summary