Abstract: The necrotrophic pathogen Cochliobolus carbonum infects maize through its main virulence factor, HC-toxin (HCT), a lysin deacetylase inhibitor. The transcription factor ZmMYC2 is one of the many targets of HCT, which will be hyperacetylated upon C. carbonum infection, or HCT direct application on maize. We found that acetylation triggers ZmMYC2 downstream signaling by enhancing its dimerization and DNA binding activity. ZmMYC2 ChIP-seq data show that a large part of ZmMYC2 targets are genes belonging to multiple phytohormones, especially JA and IAA. Moreover, approximately 75% of ZmMYC2 targets show differential transcript expression in maize seedlings treated with either HCT or C. carbonum, compared to mock-treated samples. We also detected that ZmMYC2 binds to a long-distance 3’ transcriptional enhancer on C. carbonum resistance gene hm1. Binding of ZmMYC2 on this region regulates the expression of hm1 and help plant response to C. carbonum infection. Reduced hm1 transcript expression was detected on zmmyc2 loss-of-function mutant, and these showed high susceptibility to C. carbonum infection, while wild-type plants are completely resistant to it.  Overall, this study reveals an acetylation-triggered activation of the ZmMYC2 transcription factor and its downstream signaling pathway, which play an essential role in maize defense response to C. carbonum. 

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