Abstract
Fusarium oxysporum is one of the main pathogens causing rice seedling blight disease. Revealing its pathogenic mechanism is of great significance for formulating prevention and control strategies for rice seedling blight disease. Copper transporting P-type ATPases (Cu-ATPase) is a large class of proteins located on the plasma membrane that utilize the energy provided by ATP hydrolysis phosphorylation to transport substrates across the membrane. It plays a crucial role in signal transduction, the maintenance of cell membrane stability, and material transport. The main function of Cu-ATPase is to maintain the homeostasis of copper in cells, which is essential for the normal growth and development of organisms. This study utilized the ATMT-mediated gene knockout method to obtain the knockout mutant ∆FoCrpA and the complementation strain ∆FoCrpA-C, which are highly homologous to the P-type heavy metal transport ATPase family in F. oxysporum. The results showed that, compared with the wild-type strain, the knockout mutant ∆FoCrpA had a lighter colony color; a reduced tolerance to copper ion, osmotic, and oxidative stress; a weakened ability to penetrate glass paper; and decreased pathogenicity. However, there was no significant difference in pathogenicity and other biological phenotypes between the complementation strain ∆FoCrpA-C and the wild-type strain. In summary, the FoCrpA gene is involved in osmotic and oxidative stress, affecting the invasion and penetration ability and pathogenicity of F. oxysporum, laying a theoretical foundation for understanding the development and pathogenic mechanism of F. oxysporum.