MoSnf5 Regulates Fungal Virulence, Growth, and Conidiation in Magnaporthe oryzae .
Xiao-Wen XuRui ZhaoXiao-Zhou XuLiu TangWei ShiDeng ChenJun-Bo PengVijai BhadauriaWen-Sheng ZhaoJun YangYou-Liang PengPublished in: Journal of fungi (Basel, Switzerland) (2022)
Snf5 (sucrose nonfermenting) is a core component of the SWI/SNF complexes and regulates diverse cellular processes in model eukaryotes. In plant pathogenic fungi, its biological function and underlying mechanisms remain unexplored. In this study, we investigated the biological roles of MoSnf5 in plant infection and fungal development in the rice blast pathogen Magnaporthe oryzae. The gene deletion mutants of MoSNF5 exhibited slower vegetative hyphal growth, severe defects in conidiogenesis, and impaired virulence and galactose utilization capacities. Domain dissection assays showed that the Snf5 domain and the N- and C-termini of MoSnf5 were all required for its full functions. Co-immunoprecipitation and yeast two-hybrid assays showed that MoSnf5 physically interacts with four proteins, including a transcription initiation factor MoTaf14. Interestingly, the ∆MoTaf14 mutants showed similar phenotypes as the ∆Mosnf5 mutants on fungal virulence and development. Moreover, assays on GFP-MoAtg8 expression and localization showed that both the ∆Mosnf5 and ∆MoTaf14 mutants were defective in autophagy. Taken together, MoSnf5 regulates fungal virulence, growth, and conidiation, possibly through regulating galactose utilization and autophagy in M. oryzae .
Keyphrases
- pseudomonas aeruginosa
- escherichia coli
- staphylococcus aureus
- biofilm formation
- cell wall
- antimicrobial resistance
- candida albicans
- high throughput
- cell death
- oxidative stress
- endoplasmic reticulum stress
- wild type
- poor prognosis
- signaling pathway
- cystic fibrosis
- genome wide
- transcription factor
- early onset
- gene expression
- copy number
- single cell
- mass spectrometry
- dna methylation
- atomic force microscopy
- single molecule
- genome wide identification