The SWI/SNF complex subunit CgSwi1 is indispensable for host-derived ROS scavenging and infectious growth in Colletotrichum gloeosporioides.

Abstract

The SWI/SNF chromatin-remodelling complex in eukaryotic organisms plays a critical role in manipulating DNA transcription. The key subunit of the SWI/SNF complex, Swi1, participates in a range of chromatin-associated events, such as transcriptional regulation, DNA damage repair, and homologous recombination. However, the role of Swi1 in regulating the virulence of phytopathogenic fungi remains unclear. In our study, we found that Colletotrichum gloeosporioides CgSwi1, homologous to Swi1 of Saccharomyces cerevisiae, was localized in the nuclei and highly expressed during the plant infection of C. gloeosporioides. Disruption of CgSWI1 impairs vegetative growth, conidial morphology, development of invasive structures, and plant infection. Furthermore, the ΔCgswi1 mutant showed increased sensitivity to various stressors, including ion stress, cell wall perturbations, and oxidative stress from reactive oxygen species (ROS). Notably, the ability of the ΔCgswi1 mutant to detoxify excessive ROS in host cells was attenuated relative to the WT. Furthermore, the transcription levels of antioxidant genes were reduced in the ΔCgswi1 mutant during plant infection. Deletion of CgSWI1 led to ROS accumulation, which triggered the expression of host resistance genes to defence against the pathogen. Consistent with these results, it suggests that the SWI/SNF complex subunit, CgSwi1, synergistically regulates pathogenicity by maintaining ROS homoeostasis in C. gloeosporioides. This study provides a deeper insight into roles of Swi1 in fungal virulence and responses to environmental stresses.