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.
Cyhalofop-butyl, a widely used acetyl-CoA carboxylase (ACCase)-inhibiting herbicide, is increasingly resisted by Echinochloa crus-galli in paddy fields. However, the physiological and molecular mechanisms of this resistance have not been fully elucidated. In this study, a highly resistant population (HL-R, resistance index [RI] = 19.05) from Hulin and a susceptible population (HL-S, RI = 1.00) were used. The results showed that HL-R population exhibited broad-spectrum resistance to five herbicides (RI = 1.98–14.53). No target-site mutations were found in the ACCase gene; instead, its overexpression contributed to target-site resistance (TSR). Metabolic inhibitor assays confirmed non-target-site metabolic resistance (NTSR). Transcriptome and qRT-PCR analyses identified two detoxification-related differentially expressed genes (DEGs; CH01.636, BH02.4557) as key regulators. The activity of the antioxidant enzyme peroxidase (POD) was also associated with resistance. Collectively, the high resistance of HL-R to cyhalofop-butyl is synergistically driven by ACCase overexpression, POD activity and P450/GST-mediated metabolic detoxification. These findings provide theoretical guidance for the management of resistant barnyard grass.
About Me
I mainly focus on the integrated management of agricultural pests and diseases.
I mainly focus on the integrated management of agricultural pests and diseases.