A NAC transcription factor MNAC3-centered regulatory network negatively modulates rice immunity against blast disease.

Abstract

NAC transcription factors (TFs) are pivotal in plant immunity against diverse pathogens. Here, we report the functional and regulatory network of MNAC3, a novel NAC TF, in rice immunity. MNAC3, a transcriptional activator, negatively modulates rice immunity against blast and bacterial leaf blight diseases and pathogen-associated molecular pattern (PAMP)-triggered immune responses. MNAC3 binds to a CACG cis-element and activates the transcription of immune-negative target genes OsINO80, OsJAZ10, and OsJAZ11. The negative function of MNAC3 in rice immunity depends on its transcription of downstream genes such as OsINO80 and OsJAZ10. MNAC3 interacts with immunity-related OsPP2C41 (a protein phosphatase), ONAC066 (a NAC TF), and OsDjA6 (a DnaJ chaperone). ONAC066 and OsPP2C41 attenuate MNAC3 transcriptional activity, while OsDjA6 promotes it. Phosphorylation of MNAC3 at S163 is critical for its negative functions in rice immunity. OsPP2C41, which plays positive roles in rice blast resistance and chitin-triggered immune responses, dephosphorylates MNAC3, suppressing its transcriptional activity on the target genes OsINO80, OsJAZ10, and OsJAZ11 and promoting the translocation of MNAC3 from nucleus to cytoplasm. These results establish a MNAC3-centered regulatory network in which OsPP2C41 dephosphorylates MNAC3, attenuating its transcriptional activity on downstream immune-negative target genes in rice. Together, these findings deepen our understanding of molecular mechanisms in rice immunity and offer a novel strategy for genetic improvement of rice disease resistance.