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The rice bacterial blight pathogen  Xanthomonas oryzae  pv. oryzae ( Xoo ) injects transcription activator-like effectors (TALEs) that bind and activate host “susceptibility” ( S ) genes important for disease. Clade III  SWEET  genes are major S genes for bacterial blight. The resistance genes  xa5 , which reduces TALE activity generally, and  xa13 , a  SWEET11  allele not recognized by the cognate TALE, have been effectively deployed. However, strains that defeat both resistance genes individually were recently reported in India and Thailand. To gain insight into the mechanism(s), we completely sequenced the genome of one such strain from each country and examined the encoded TALEs. Strikingly, the two strains are clones, sharing nearly identical TALE repertoires, including a TALE known to activate  SWEET11  strongly enough to be effective even when diminished by  xa5 . We next investigated  SWEET  gene induction by the Indian strain. The Indian strain induced no clade III  SWEET  in plants harboring  xa13 , indicating a pathogen adaptation that relieves dependence on these genes for susceptibility. The findings open a door to mechanistic understanding of the role  SWEET  genes play in susceptibility and illustrate the importance of complete genome sequence-based monitoring of  Xoo  populations in developing varieties with effective disease resistance.

frontiers in microbiology

A Strain of an Emerging Indian Xanthomonas oryzae pv. oryzae Pathotype Defeats the Rice Bacterial Blight Resistance Gene xa13 Without Inducing a Clade III SWEET Gene and Is Nearly Identical to a Recent Thai Isolate