In eukaryotes, Maf1 is an essential and specific negative regulator of RNA polymerase (Pol) III. Pol III, which synthesizes transfer RNAs (tRNAs), is suppressed by Maf1 under conditions of nutrient starvation or environmental stress. Here, we identified M. oryzae MoMaf1, a homolog of ScMaf1 in budding yeast. A heterogeneous complementation assay revealed that MoMaf1 fully restored growth defects in the ΔScmaf1 mutant under SDS stress. Disrupting MoMAF1 elevated the tRNA content and increased sensitivity to cell wall agents. Moreover, the ΔMomaf1 mutant exhibited reduced vegetative growth, conidiogenesis, and pathogenicity. Interestingly, we found that MoMaf1 undergoes nuclear–cytoplasmic shuffling, through which MoMaf1 accumulates in nuclei under nutrient deficiency or upon the interaction of M. oryzae with rice. Therefore, this study helps to elucidate the pathogenic molecular mechanism of M. oryzae.

In eukaryotes, Maf1 is an essential and specific negative regulator of RNA polymerase (Pol) III. Pol III, which synthesizes 5S RNA and transfer RNAs (tRNAs), is suppressed by Maf1 under the conditions of nutrient starvation or environmental stress. Here, we identified M. oryzae MoMaf1, a homolog of ScMaf1 in budding yeast. A heterogeneous complementation assay revealed that MoMaf1 restored growth defects in the ΔScmaf1 mutant under SDS stress. Destruction of MoMAF1 elevated 5S rRNA content and increased sensitivity to cell wall agents. Moreover, the ΔMomaf1 mutant exhibited reduced vegetative growth, conidiogenesis, and pathogenicity. Interestingly, we found that MoMaf1 underwent nuclear-cytoplasmic shuffling, through which MoMaf1 accumulated in nuclei under nutrient deficiency or upon the interaction of M. oryzae with rice. Therefore, this study can help to elucidate the pathogenic molecular mechanism of M. oryzae.