E. coli K-12 YbjN, "putative sensory transduction regulator" (Pfam PF10722 YbjN;
InterPro IPR019660; CDD cd17511 YbjN_AmyR-like). 158 aa, no catalytic motifs,
no transmembrane segment, no signal peptide in the UniProt record.
Deep research was unavailable for this gene. No deep-research API keys are
configured in this container, so just deep-research was not run and no
-deep-research-<provider>.md file exists. Everything below comes from the
cached publications in publications/, from PubMed searches (the complete
PubMed hit list for ybjN Escherichia coli is five papers: PMID:38822378,
PMID:28426806, PMID:23028751, PMID:21980417, PMID:16701556), and from the
UniProt flat file.
The GONUTS wiki could not be consulted. https://gowiki.tamu.edu/wiki/index.php/PMID:21980417
returns only "This site is temporarily offline while we perform upgrades"
(checked 2026-10-29), matching the note in projects/CACAO.md. The four CACAO
rows were therefore judged from the paper alone — which is sufficient here,
because the single cited paper (PMID:21980417) has full text cached.
YbjN orthologs are restricted to Enterobacteriaceae
PMID:21980417.
The gene sits immediately upstream of the potFGHI putrescine transport operon,
with rimK and nfsA upstream in E. coli
PMID:21980417.
The one structure of the family, Erwinia amylovora AmyR (the functionally
conserved YbjN ortholog), is a homodimer with a class I type III secretion
chaperone-like fold
PMID:28426806,
despite no secretion role; the authors read this as a protein–protein
interaction module rather than an enzyme
PMID:28426806.
Byrne et al. independently note the structural resemblance
PMID:25049088.
Note that the fold is from the Erwinia ortholog, not from E. coli YbjN
itself, so it is family-level evidence and is not used here to assert a
molecular function.
ybjN was isolated as a multicopy suppressor of the temperature-sensitive
coaA1 (pantothenate kinase L236F) allele
PMID:16701556,
and also suppresses coaA14, coaA15 and ilu-1, leading the authors to
propose a chaperone/stabilizer role
PMID:16701556.
This is an over-expression (multicopy) phenotype throughout, and no direct
holdase or stabilizer assay has been reported for YbjN.
Wang et al. confirmed the suppression and showed the ybjN transcript is
~10-fold lower in ts9 than in BW25113, and ~10-fold higher than BW when
supplied on a multicopy plasmid (Fig. 1).
All from Wang et al. 2011 (PMID:21980417), comparing BW25113 (BW), ΔybjN, and
BW carrying multicopy ybjN:
Fimbriae / type 1 pili (Fig. 3C, 3D). ΔybjN over-produces fimbriae by
TEM; multicopy ybjN abolishes them
PMID:21980417
PMID:21980417.
fimD (outer-membrane usher) up 8-fold in the mutant, down 12-fold on
overexpression
PMID:21980417,
with fimC, fimD, fimG confirmed by microarray
PMID:21980417.
The authors' conclusion is explicitly a negative one
PMID:21980417.
This is why the CACAO GO:0009297 pilus assembly row has the sign
inverted: YbjN suppresses pilus formation, it does not build pili.
Motility (Fig. 4A, 4B). ΔybjN spreads further on 0.25% agar
PMID:21980417,
0.84 mm (BW) vs 1.88 (ΔybjN) vs 0.41 (overexpression)
PMID:21980417.
Flagellar gene expression (Fig. 4C, Table 1). fliA and flgD up 12.5-
and 11.3-fold in the mutant
PMID:21980417,
with structural/assembly genes following
PMID:21980417
PMID:21980417.
Biofilm (Fig. 6). Crystal violet on PVC microtitre plates: ΔybjN ~3-fold
more, overexpression ~half
PMID:21980417
PMID:21980417.
Capsule / colanic acid (Fig. 5). ΔybjN is highly mucoid on 700 mM NaCl
LB; multicopy ybjN makes colonies non-mucoid and also suppresses the
mucoidy of ackA and ackA/rcsC mutants
PMID:21980417.
This phenotype is not in GOA and is the one gap worth filling
(GO:1901914 negative regulation of capsule organization). The orthologous
phenotype in E. amylovora is the same sign
PMID:23028751.
Ionizing radiation. TraDIS plus direct deletion/survival curves put
ybjN in the mildest validated group
PMID:25049088
PMID:25049088.
So the EcoCyc response to ionizing radiation row rests on real
loss-of-function data, but it is one of several stress survival phenotypes
rather than the gene's defining role.
Independent corroboration of the motility direction comes from avian
pathogenic E. coli, where loss of FdeC raises motility via YbjN
down-regulation
PMID:38822378.
GO:0030308 negative regulation of cell growth row therefore hasThe only GOA molecular-function row is a bare GO:0005515 protein binding
(IntAct IPI, PMID:24561554) with YpjF (Q46953), from the Rajagopala E. coli
binary interactome screen; the cached full text does not mention either
protein by name (the pair is in the supplementary interaction tables, and
UniProt records it as P0AAY6; Q46953: ypjF; NbExp=3). Suggestive, given that
multicopy ybjN induces toxin–antitoxin modules and YpjF is a YpjF/YfjZ-type
toxin, but a Y2H pair is not a molecular function. Removed under the
protein-binding policy (removal does not dispute the interaction).
Four of the seven GOA rows are CACAO, all IMP from PMID:21980417, all on the
right gene and the right paper with an evidence code that fits the assay. Two
are right (biofilm, flagellum assembly). Two fail:
GO:0009297 pilus assembly — sign inverted: the figure shows the mutantGO:0030308 negative regulation of cell growth — overexpression-onlyECO:0000315, mutant phenotype) code.