A thiadiazole reduces the virulence of Xanthomonas oryzae pv. oryzae by inhibiting the histidine utilization pathway and quorum sensing.

Thiazole, isothiazole, thiadiazole and their derivatives are widely thought to induce host defences against plant pathogens. In this article, we report that bismerthiazol, a thiadiazole molecule, reduces disease by inhibiting the histidine utilization (Hut) pathway and quorum sensing (QS). Bismerthiazol provides excellent control of bacterial rice leaf blight (BLB) caused by Xanthomonas oryzae pv. oryzae (Xoo), but does not greatly inhibit Xoo growth in vitro. According to RNA-sequencing analysis, the transcription of the Hut pathway genes of Xoo ZJ173 was inhibited after 4.5 and 9.0 h of bismerthiazol treatment. Functional studies of hutG and hutU indicated that the Hut pathway had little effect on the growth and bismerthiazol sensitivity of Xoo in vitro, but significantly reduced the aggregation of Xoo cells. Deletion mutants of hutG or hutU were more motile, produced less biofilm and were less virulent than the wild-type, indicating that the Hut pathway is involved in QS and contributes to virulence. The overexpression of the hutG-U operons in ZJ173 reduced Xoo control by bismerthiazol. Bismerthiazol did not inhibit the transcription of Hut pathway genes, QS or virulence of the bismerthiazol-resistant strain 2-1-1. The results indicate that bismerthiazol reduces Xoo virulence by inhibiting the Hut pathway and QS.