Bax Inhibitor MoBi-1 Is Required for Conidiation, Pathogenicity, and Stress Responses in Magnaporthe oryzae

<i>Magnaporthe oryzae</i> serves as a model organism for studying the molecular biology of filamentous fungi and the pathogenic mechanisms of fungal pathogens. It also poses a significant threat to rice production in China. Bax inhibitor-1 (Bi-1), a protein with evolutionary conservation, functions as an inhibitor of programmed cell death induced by the proapoptotic protein Bax. Despite the widespread presence of Bi-1 proteins in hyphal fungi, their biological functions have not been extensively characterized. Here, we characterized the function of <i>MoBI</i>-1, a putative Bax-inhibitor protein in <i>M. oryzae</i>, which is located in the mitochondria and participates in conidiation, stress adaptation, and pathogenicity. Further investigations revealed that MoBi-1 is also essential for the regulation of mitochondrial energy metabolism. Remarkably, experimental evidence indicates that MoBi-1 does not seem to function in inhibiting Bax-induced programmed cell death, thus lacking inherent Bax inhibitory function, which broadens the existing understanding of Bax inhibitor-1's function and provides significant new insights into the disease-causing mechanisms of <i>M. oryzae</i>.