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

## TL;DR

This study explores the role of the Bax inhibitor MoBi-1 in the rice pathogen Magnaporthe oryzae, revealing its importance in fungal development, stress response, and disease.

## Contribution

The study reveals that MoBi-1 lacks Bax inhibitory function but is crucial for conidiation, pathogenicity, and mitochondrial energy metabolism in M. oryzae.

## Key findings

- MoBi-1 is essential for conidiation and pathogenicity in M. oryzae.
- MoBi-1 plays a role in stress adaptation and mitochondrial energy metabolism.
- MoBi-1 does not inhibit Bax-induced programmed cell death in this species.

## Abstract

Magnaporthe oryzae 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 MoBI-1, a putative Bax-inhibitor protein in M. oryzae, 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 M. oryzae.