The Mgv1-Rlm1 axis orchestrates SAGA and SWI/SNF complexes at target promoters.

The SWI/sucrose non-fermentable (SWI/SNF)-facilitated removal of nucleosomes and Spt-Ada-Gcn5 acetyltransferase (SAGA) complex-mediated histone acetylation are crucial for the activation of transcription initiation. However, the mechanism by which these two complexes coordinate to regulate gene expression involved in cell wall remodeling during infection process or in response to external stimuli remains largely unknown in plant pathogenic fungi. Here, we demonstrate that the cell wall integrity (CWI) pathway is activated under toxin (deoxynivalenol)-inducing conditions in the phytopathogenic fungus Fusarium graminearum. This treatment results in the phosphorylation and nuclear translocation of the mitogen-activated protein kinase FgMgv1 in the CWI signaling pathway. Once in the nucleus, the activated FgMgv1 phosphorylates the downstream transcription factor FgRlm1, which binds to a 12- or 14-bp cis-element in the promoters of target genes. Notably, FgMgv1 forms a polymer and interacts with FgRlm1 via its kinase domain. Crucially, this polymerization enables FgMgv1 to recruit both the SWI/SNF and SAGA complexes simultaneously through its C-terminal domain at the target promoters. This coordinated action among FgMgv1, FgRlm1, SWI/SNF, and SAGA ultimately facilitates the transcriptional activation of target genes. Collectively, these findings illuminate a regulatory framework in which Mgv1-Rlm1 axis serves as a key regulatory hub, integrating CWI signals with epigenetic modifications to ensure transcriptional responsiveness to external stimuli.