fleS / PA1098 (Q9I4N4) review notes

Summary of the literature

FleS is a 402-residue sensor histidine kinase (UniProt FLES_PSEAE, reviewed). The record
places a PAS_8 domain in the N-terminal half, a histidine-kinase domain at 188-393 and the
autophosphorylated histidine at position 191 (FT MOD_RES 191 /note="Phosphohistidine; by autocatalysis", PROSITE rule evidence). The gene lies in the fleSR operon upstream of fliE.

Primary data, Ritchings et al. 1995 PMID:7591148, abstract only — PMC173697 is a scanned
article and the PubMed MCP returns no body text:

FleS was identified by sequence: PMID:7591148.
All experiments listed in the abstract are on fleR: a gentamicin-cassette insertion
PMID:7591148, its complementation, a flagellin Western blot and EM of
the fleR mutant.
The system-level conclusion is stated as a belief: PMID:7591148.

UniProt cites PubMed:30877999 (not cached) for a fleS mutant with a severe swimming defect and
for FleS/FleR control of flagellar synthesis, adhesion, swarming, motility and antibiotic
resistance, and gives the EC 2.7.13.3 catalytic activity by similarity to E. coli AtoS
(ECO:0000250|UniProtKB:Q06067) rather than from direct assay. So no direct kinase assay on FleS
is available to me; the MF rests on the domain architecture plus the IBA.

Related cached material: FleQ (PA1097) is reviewed in genes/PSEAE/fleQ and is the master
regulator above FleSR; FleN/PMID:11673434 concerns FleQ, not FleS.

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?
PTN009166588	GO:0007165 signal transduction	7	268 (41 taxa)	GO:0000160, IDA, PMID:7591148 (PseudoCAP)	INDIRECT-PHENOTYPE (process right, evidence code wrong)	The claim is correct — FleS is the kinase of the FleS-FleR pair — but the cited paper, as far as its abstract shows, characterises FleS only by homology and takes all of its data from a fleR mutant. An IDA on FleS is not what those experiments give. Confidence PROBABLE: the abstract positively states that FleS was identified by homology and lists only fleR genetics, but the full text is unavailable and could contain a phosphorylation assay.	E. coli NtrB (P0AFB5, IDA GO:0004673/GO:0006470), E. coli ZraS (P14377, IDA GO:0004673 and IDA GO:0007165), S. pombe Mak3 (O74539, IGI GO:0000160), P. aeruginosa CbrA (Q9HV74), E. coli AtoS (Q06067, IDA GO:0007165), M. tuberculosis PdtaS (P9WGL5, IDA GO:0000160) — verified by live QuickGO query 2026-11-05	Yes. AtoS, ZraS, NtrB and PdtaS carry independent experimental signalling/kinase annotations, and signal transduction suits a histidine-kinase clade. No GO_CENTRAL defect; the defect is on the PseudoCAP row only (evidence code).

FleS also receives the GO:0000155 IBA from the same node (it is not a seed of that IBD; its
seeds are PprA, Mak3, AtoS and PdtaS — see genes/PSEAE/pprA/pprA-notes.md, where the
node-level assessment for PTN009166588 is recorded once for this batch).

Annotation decisions

GO:0000155 (IEA, IBA): ACCEPT. Complete kinase core with His191, cognate sigma-54 activator
FleR, well-seeded IBA node.
GO:0000160 (IDA, PMID:7591148): ACCEPT the claim, with a PSEUDOCAP WRONG_EVIDENCE_CODE
defect (PROBABLE) asking for the code to be checked (ISS, or IMP/IGI if a fleS mutant is in
the full text).
GO:0004673 (ISS, IEA), GO:0016772 (IEA), GO:0007165 (IEA, IBA): TOO_GENERAL — entailed by
GO:0000155 / GO:0000160, matching the treatment in genes/PSEAE/parS, genes/PSEAE/PA5484
and pprA.