The type III secretion system (T3SS) of plant-pathogenic is essential for virulence. Genes encoding the T3SS are not constitutively expressed and must be induced upon infection. Plant-derived metabolites, including sugars such as fructose and sucrose, are inducers of T3SS-encoding genes, yet the molecular mechanisms underlying perception of these host signals by are unknown. Here, we report that (), predicted to encode a DeoR-type transcription factor, is required for maximal sugar-induced expression of T3SS-associated genes in DC3000. From a Tn transposon mutagenesis screen, we identified two independent mutants with insertions in . When both ::Tn mutants were cultured in minimal medium containing fructose, genes encoding the T3SS master regulator HrpL and effector AvrRpm1 were expressed at lower levels relative to that of a wild-type strain. Decreased and expression also occurred in a ::Tn mutant in response to glucose, sucrose, galactose, and mannitol, demonstrating that is genetically required for T3SS induction by many different sugars. Expression of upstream regulators / and was not altered in ::Tn, indicating that SetA positively regulates expression independently of increased transcription of these genes. In addition to decreased response to defined sugar signals, a ::Tn mutant had decreased T3SS deployment during infection and was compromised in its ability to grow in planta and cause disease. These data suggest that SetA is necessary for to effectively respond to T3SS-inducing sugar signals encountered during infection.

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http://dx.doi.org/10.1094/MPMI-10-19-0290-RDOI Listing

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