Affiliations
- State Key Laboratory for Conservation and Utilization of Subtropical Agri-Biological Resources, Guangxi Key Laboratory of Sugarcane Biology, Guangxi University, Nanning, China.
- IRREC-IFAS, University of Florida, Fort Pierce, Florida, USA.
PMID: 38279852 PMCID: PMC10782473 DOI: 10.1111/mpp.13414
Abstract
Fusarium sacchari is one of the primary pathogens causing pokkah boeng disease, which impairs the yield and quality of sugarcane around the world. Understanding the molecular mechanisms of the F. sacchari effectors that regulate plant immunity is of great importance for the development of novel strategies for the persistent control of pokkah boeng disease. In a previous study, Fs00367 was identified to inhibit BAX-induced cell death. In this study, Fs00367nsp (without signal peptide) was found to suppress BAX-induced cell death, reactive oxygen species bursts and callose accumulation. The amino acid region 113-142 of Fs00367nsp is the functional region. Gene mutagenesis indicated that Fs00367 is important for the full virulence of F. sacchari. A yeast two-hybrid assay revealed an interaction between Fs00367nsp and sugarcane ScPi21 in yeast that was further confirmed using bimolecular fluorescence complementation, pull-down assay and co-immunoprecipitation. ScPi21 can induce plant immunity, but this effect could be blunted by Fs00367nsp. These results suggest that Fs00367 is a core pathogenicity factor that suppresses plant immunity through inhibiting ScPi21-induced cell death. The findings of this study provide new insights into the molecular mechanisms of effectors in regulating plant immunity.
Keywords: Fusarium sacchari; pathogenicity; plant immunity; pokkah boeng disease; small cysteine-rich effector protein; sugarcane.
