A putative rRNA methyltransferase Mrm1 regulates mitochondrial dynamics and pathogenicity in Magnaporthe oryzae

Le résumé fourni par la source

Rice blast disease, a major global threat to staple crops, is caused by the ascomycete fungus Magnaporthe oryzae. This pathogen has complex mechanisms to invade rice, with mitochondrial function crucial for infection energy. Our study looks at the impact of Mrm1, a putative rRNA methyltransferase, on mitochondrial dynamics and pathogenicity of M. oryzae. Mrm1 deficiency delays appressorium formation and reduces turgor pressure for host penetration and infection hypha expansion. The N-terminal sequence of Mrm1, with a mitochondrial targeting sequence (MTS), is vital for its localization and function. Deletions cause impaired growth and lower pathogenicity. Deleting MRM1 leads to abnormal mitochondrial morphology, with more filamentous mitochondria during invasive growth, disrupting the balance of fission and fusion. This imbalance reduces the fungus’s infection ability. Furthermore, loss of Mrm1 alters the steady-state protein levels of mitochondrial dynamics regulators Dnm1 and Fzo1, likely through translational regulation, while their transcript abundances remain unchanged. In the absence of Mrm1, the levels of these proteins are significantly reduced. Our findings deepen the understanding of epitranscriptomic regulation in fungal pathogenicity and represent a potential candidate for future target-based intervention strategies, pending validation through chemical or genetic approaches.

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