parR (PA1799) review notes

UniProt: Q9I2U3 (unreviewed, 235 aa), "Two-component response regulator, ParR".
Locus PA1799; cognate sensor kinase ParS is PA1798.

What is established

ParR-ParS is the two-component system that mediates adaptive resistance to
polymyxin B, colistin and antimicrobial peptides
PMID:20547815. The system is required for induction of the
arnBCADTEF lipid A modification operon by subinhibitory peptide concentrations
PMID:20547815.
ParR is a cytoplasmic OmpR/PhoB-family response regulator with a REC receiver
domain and a winged-helix DNA-binding domain (InterPro IPR001789, IPR001867,
IPR039420 on Q9I2U3)
PMID:24034668.
The ParS/ParR regulon is large and condition-dependent: over 100 genes in the
presence of antimicrobials, including mexEF-oprN, oprD, quorum-sensing
regulators, and arnBCADTEF-ugd only when the inducing peptide is present
PMID:24034668,
PMID:24034668.
So ParR both activates and represses transcription.

Notes on specific annotations

GO:0071073 positive regulation of phospholipid biosynthetic process (IMP,
PMID:20547815). This looks odd but is defensible: lipid A biosynthesis
(GO:0009245) is, in GO, a descendant of GO:0008654 phospholipid biosynthetic
process, and ParR positively regulates the arn operon that modifies lipid A.
No "regulation of lipid A biosynthetic process" term exists (checked against
go-basic, 2026-11-05), so the asserted term is the most specific regulation
term available in that branch and the row is kept rather than modified. Raised
as a suggested_questions entry instead.
The cited paper reports genetics (mutants fail to induce arn; resistance
phenotypes). Nothing in the cached abstract reports phosphotransfer to ParR or
ParR-DNA binding, which is why the GO:0000156 IMP row is judged
INDIRECT-PHENOTYPE below. The claim itself is not in doubt: the protein is a
canonical OmpR/PhoB response regulator.

Literature search

Europe PMC and PubMed, 2026-11-05: aeruginosa AND ParR AND ParS,
TITLE:"ParR" AND aeruginosa, aeruginosa AND (parR OR ParRS) AND mexXY.
PMC2916309 (PMID:20547815) returns an abstract only through the PubMed MCP, so
the full text of the seed paper was not read. Cached and used: PMID:20547815,
PMID:24034668. Also seen but not cached: PMID:24994873 (colistin resistance in
parR-inactivated mutants) and a 2026 report on ParR promoter architecture with
no PMID yet in Europe PMC.

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?
PTN000724188	GO:0000156 phosphorelay response regulator activity	10	475 (45 taxa)	GO:0000156, IMP, PMID:20547815 (PseudoCAP)	INDIRECT-PHENOTYPE	A molecular function asserted from a mutant phenotype: the paper shows that loss of parR abolishes peptide-induced arn expression and adaptive resistance, not that ParR accepts a phosphoryl group or acts as a response regulator in a biochemical assay. The claim is almost certainly right (receiver domain plus winged-helix DNA-binding domain, cognate kinase ParS next door), so the row is kept; only the evidence coding is questioned, and at SUSPECTED confidence because the full text of the seed paper could contain a phosphorylation experiment that the abstract does not mention.	E. coli ArcA (P0A9Q1), OmpR (P0AA16), CpxR (P0AE88), PhoP/PhoB-family members P30843 and P38684, Bacillus O07776, Streptococcus Q8DPL7 and Q8DN02, P36556	Yes. The E. coli response regulators carry direct experimental evidence for this activity, so the node assertion does not depend on ParR. No `GO_CENTRAL` defect.

Node-level consistency: PTN000724188 also carries IBDs for GO:0006355,
GO:0000976, GO:0032993 and GO:0005829, and both parR and copR in this batch are
leaves of it. The node-level judgement for all of them is the same - a broad,
well-seeded OmpR/PhoB response-regulator node whose terms suit the clade - and
is recorded once in genes/PSEAE/copR/copR-notes.md, the gene in this batch with
in-organism transcriptional data (PMID:17449606, full text). No GO_CENTRAL
defect is filed from either gene.

PseudoCAP defects from this gene: one, WRONG_EVIDENCE_CODE (SUSPECTED) on the
GO:0000156 IMP row, asking whether the row should be an IC or ISS-style
inference rather than IMP.