Plant diseases caused by pathogenic fungi pose a significant threat to agricultural production. This study reports on a strain YBS22 with broad-spectrum antifungal activity that was isolated and identified, and its active metabolites were purified and systematically studied. Based on a whole genome sequence analysis, the new strain YBS22 was identified as Streptomyces melanogenes. Furthermore, eight gene clusters were predicted in YBS22 that are responsible for the synthesis of bioactive secondary metabolites. These clusters have homologous sequences in the MIBiG database with a similarity of 100%. The antifungal effects of YBS22 and its crude extract were evaluated in vivo and vitro. Our findings revealed that treatment with the strain YBS22 and its crude extract significantly reduced the size of necrotic lesions caused by Magnaporthe oryzae on rice leaves. Further analysis led to the isolation and purification of an active compound from the crude extract of the strain YBS22, identified as N-formylantimycin acid methyl ester, an analog of antimycin, characterized by NMR and MS analyses. Consistently, the active compound can significantly inhibit the germination and development of M. oryzae spores in a manner that is both dose- and time-dependent. As a result, we propose that the strain YBS22 could serve as a novel source for the development of biological agents aimed at controlling rice blast disease.

Background: Fumonisin B1 (FB1) is a toxic secondary metabolite produced by Fusarium species that commonly contaminates cereal crops, posing serious threats to crop productivity and food safety. In plants, FB1 inhibits ceramide synthase, disrupts sphingolipid metabolism, and induces growth inhibition and programmed cell death. Despite the agricultural importance of fumonisin contamination, genetic strategies to enhance FB1 tolerance or detoxification capacity in crops remain limited, largely due to an incomplete understanding of the underlying genetic determinants. Methods: To identify genetic determinants associated with FB1 tolerance, we exploited natural variation in Arabidopsis thaliana and conducted a genome-wide association study (GWAS). Candidate genes were further examined using gene expression analyses and functional characterization of overexpression and SALK mutant lines. Results: GWAS revealed a significant association locus on chromosome 1 linked to FB1 tolerance. Two adjacent genes within this locus, AT1G14750 and AT1G14755, were identified as positive regulators of FB1 tolerance. Both genes were rapidly induced upon FB1 exposure. Functional analyses demonstrated that overexpression of either gene significantly enhanced tolerance to FB1-induced damage, whereas SALK mutant lines displayed increased sensitivity, manifested by enhanced growth inhibition and necrosis. Conclusions: Our study identifies AT1G14750 and AT1G14755 as previously uncharacterized components of FB1 tolerance in Arabidopsis. These findings provide new insights into the genetic architecture of plant response to mycotoxin stress and establish a foundation for further studies on the molecular mechanisms underlying FB1 tolerance.