The Transcription Factor CsAtf1 Negatively Regulates the Cytochrome P450 Gene to Increase Fludioxonil Sensitivity in .

Previous studies have shown that the high-osmolarity glycerol mitogen-activated protein kinase (HOG MAPK) signaling pathway and its downstream transcription factor CsAtf1 are involved in the regulation of fludioxonil sensitivity in . However, the downstream target genes of CsAtf1 related to the fludioxonil stress response remain unclear. Here, we performed chromatin immunoprecipitation sequencing (ChIP-Seq) and high-throughput RNA-sequencing (RNA-Seq) to identify genome-wide potential CsAtf1 target genes. A total of 3809 significantly differentially expressed genes were predicted to be directly regulated by CsAtf1, including 24 cytochrome oxidase-related genes. Among them, a cytochrome P450-encoding gene, designated , was confirmed to be a target gene, and its transcriptional expression was negatively regulated by CsAtf1, as determined using an electrophoretic mobility shift assay (EMSA), a yeast one-hybrid (Y1H) assay, and quantitative real-time PCR (qRT-PCR). Moreover, the overexpression mutant of exhibited increased fludioxonil tolerance, and the deletion mutant exhibited decreased fludioxonil resistance, which revealed that is involved in fludioxonil sensitivity regulation in . However, the cellular ergosterol content of the mutants was not consistent with the phenotype of fludioxonil sensitivity, which indicated that regulates fludioxonil sensitivity by affecting factors other than the ergosterol level in . In conclusion, our data indicate that the transcription factor CsAtf1 negatively regulates the cytochrome P450 gene to increase fludioxonil sensitivity in .