Ribosomal protein L22 and ribosomal protein L32 respond to Bacillus velezensis 1 stress through interactions.

Fusarium crown rot (FCR) poses a threat to wheat yield and food safety because of the production of mycotoxins such as deoxynivalenol (DON), which has attracted significant attention in the fields of food science and agriculture. This study found that Bacillus velezensis 1 (BV1) exhibited inhibitory effects on the growth of Fusarium pseudograminearum, with an inhibition rate of 66.67 %. BV1 caused mycelial swelling, malformation, and apoptosis. The mechanism by which BV1 inhibits the growth of F. pseudograminearum was investigated. After coculturing BV1 with F. pseudograminearum for 4 h, the structure, composition, and translation process of F. pseudograminearum ribosomes were significantly affected; after 16 h of coculture, the metabolism of numerous amino acids and cell membrane functions were also significantly impacted. Further exploration was conducted on the function of the ribosomal protein L22 (RPL22) gene, which is associated primarily with pathogenicity in F. pseudograminearum. Knockout of the RPL22 gene significantly reduced pathogenicity, whereas pathogenicity was restored in the complemented strain. RPL22 serves as a stress response factor for BV1 and a pathogenic factor in wheat. Bimolecular fluorescence complementation and co-immunoprecipitation assays revealed that RPL22 interacts with ribosomal protein L32 (RPL32) to respond to BV1 stress. RPL22 is an important target gene for both stress response and pathogenicity.