Summary
Xanthomonas citri
ssp.
citri
, a polar flagellated bacterium, causes citrus canker disease worldwide. In this study, we found that the
X. citri
ssp.
citri
response regulator VemR plays a regulatory role in flagellum‐derived cell motility. Deletion of the
vemR
gene resulted in a reduction in cell motility, as well as reductions in virulence and exopolysaccharide production. Reverse transcription‐polymerase chain reaction (RT‐PCR) demonstrated that
vemR
is transcribed in an operon together with
rpoN2
and
fleQ.
In the
vemR
mutant, the flagellar distal rod gene
flgG
was significantly down‐regulated. Because
flgG
is also
rpoN2
dependent, we speculated that VemR and RpoN2 physically interact, which was confirmed by yeast two‐hybrid and maltose‐binding protein (MBP) pull‐down assays. This suggested that the transcription of
flgG
is synergistically controlled by VemR and RpoN2. To confirm this, we constructed a
vemR
and
rpoN2
double mutant. In this mutant, the reductions in cell motility and
flgG
transcription were unable to be restored by the expression of either
vemR
or
rpoN2
alone. In contrast, the expression of both
vemR
and
rpoN2
together in the double mutant restored the wild‐type phenotype. Together, our data demonstrate that the response regulator VemR functions as an RpoN2 cognate activator to positively regulate the transcription of the rod gene
flgG
in
X. citri
ssp.
citri.