Phytophthora cinnamomi causes significant root rot in hickory, leading to substantial yield losses. While Bacillus spp. are recognized as beneficial rhizosphere microorganisms, their application against hickory root rot and their impact on rhizosphere microbial communities remain under-investigated. This study demonstrated that Bacillus velezensis TCS001 significantly inhibited P. cinnamomi ST402 growth in vitro, and achieved 71% efficacy in root rot disease management. Scanning electron microscopy (SEM) revealed that TCS001 fermentation filtrate induced mycelial deformities in P. cinnamomi. An analysis of α and β diversity indicated a significant impact of TCS001 on rhizosphere bacterial community richness and diversity, with minimal effects on the fungal community. Moreover, TCS001 altered the hickory rhizosphere microbiome co-occurrence network. The differential abundance analysis suggests that TCS001 promotes the recruitment of beneficial microbes associated with disease resistance, thereby suppressing disease development. These findings underscore the influence of TCS001 on the hickory rhizosphere microbiome in the presence of pathogens, providing valuable data for future research and the development of effective biocontrol strategies for hickory root rot.

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.