Rice is an important source of food for more than half the world’s population. Bacterial panicle blight (BPB) is a disease of rice characterized by grain discoloration or sheath rot caused mainly by
Burkholderia glumae
.
B. glumae
synthesizes toxoflavin, an essential virulence factor, that is required for symptoms of the disease. The products of the
tox
operons, ToxABCDE and ToxFGHI, are responsible for the synthesis and the proton motive force (PMF)-dependent secretion of toxoflavin, respectively. The DedA family is a highly conserved membrane protein family found in most bacterial genomes that likely function as membrane transporters. Our previous work has demonstrated that absence of certain DedA family members results in pleiotropic effects, impacting multiple pathways that are energized by PMF. We have demonstrated that a member of the DedA family from
Burkholderia thailandensis
, named DbcA, is required for the extreme polymyxin resistance observed in this organism.
B. glumae
encodes a homolog of DbcA with 73% amino acid identity to
Burkholderia thailandensis
DbcA. Here, we created and characterized a
B. glumae
Δ
dbcA
strain. In addition to polymyxin sensitivity,
B. glumae
Δ
dbcA
is compromised for virulence in several BPB infection models and secretes only low amounts of toxoflavin (∼15% of wild type levels). Changes in membrane potential in
B. glumae
Δ
dbcA
were reproduced in the wild type strain by the addition of sub-inhibitory concentrations of sodium bicarbonate, previously demonstrated to cause disruption of PMF. Sodium bicarbonate inhibited
B. glumae
virulence in rice suggesting a possible non-toxic chemical intervention for bacterial panicle blight.
IMPORTANCE
Bacterial panicle blight (BPB) is a disease of rice characterized by grain discoloration or sheath rot caused mainly by
Burkholderia glumae
. The DedA family is a highly conserved membrane protein family found in most bacterial genomes that likely function as membrane transporters. Here, we constructed a
B. glumae
mutant with a deletion in a DedA family member named
dbcA
and report a loss of virulence in models of BPB. Physiological analysis of the mutant shows that the proton motive force is disrupted, leading to reduction of secretion of the essential virulence factor toxoflavin. The mutant phenotypes are reproduced in the virulent wild type strain without an effect on growth using sodium bicarbonate, a nontoxic buffer that has been reported to disrupt the PMF. The results presented here suggest that bicarbonate may be an effective antivirulence agent capable of controlling BPB without imposing an undue burden on the environment.