ChIP-Seq Analysis of AtfA Interactions in Reveals Its Involvement in Aflatoxin Metabolism and Virulence Under Oxidative Stress.

The risk of contamination is expanding with global warming. Targeting the pathogenicity of at its source and diminishing its colonization within the host may be a potential control strategy. Oxidative stress transcription factor AtfA plays a pivotal role in pathogenicity by combating reactive oxygen species (ROS) generated by host immune cells. This study employed chromatin immunoprecipitation sequencing to elucidate the binding sites and epigenetic mechanisms of AtfA under oxidative stress. Among the total 1022 identified potential AtfA-binding peaks, a 10-bp region predominated by 5'-DRTGTTGCAA-3', which is highly similar to the AP-1 binding motif was predicted. The significantly regulated genes exhibited a variety of biological functions, including regulation of filamentous growth, response to extracellular stimulus, and regulation of gene expression. Moreover, AtfA indirectly influenced these processes via the MAPK signaling pathway, carbon metabolism, and fatty acid metabolism in response to oxidative stress. The absence of contributed to the decrease in the growth and development, sporulation, AFB biosynthesis, and invasion ability of under oxidative stress. These findings suggest that AtfA is critical to overcome oxidative stress induced by the host immune cells during the infection, providing a novel target for early prevention of contamination.