The essential effector SCRE1 in Ustilaginoidea virens suppresses rice immunity via a small peptide region.
Nan ZhangJiyun YangAnfei FangJiyang WangDayong LiYuejiao LiShanzhi WangFuhao CuiJunjie YuYongfeng LiuYou-Liang PengWenxian SunPublished in: Molecular plant pathology (2020)
The biotrophic fungal pathogen Ustilaginoidea virens causes rice false smut, a newly emerging plant disease that has become epidemic worldwide in recent years. The U. virens genome encodes many putative effector proteins that, based on the study of other pathosystems, could play an essential role in fungal virulence. However, few studies have been reported on virulence functions of individual U. virens effectors. Here, we report our identification and characterization of the secreted cysteine-rich protein SCRE1, which is an essential virulence effector in U. virens. When SCRE1 was heterologously expressed in Magnaporthe oryzae, the protein was secreted and translocated into plant cells during infection. SCRE1 suppresses the immunity-associated hypersensitive response in the nonhost plant Nicotiana benthamiana. Induced expression of SCRE1 in rice also inhibits pattern-triggered immunity and enhances disease susceptibility to rice bacterial and fungal pathogens. The immunosuppressive activity is localized to a small peptide region that contains an important 'cysteine-proline-alanine-arginine-serine' motif. Furthermore, the scre1 knockout mutant generated using the CRISPR/Cas9 system is attenuated in U. virens virulence to rice, which is greatly complemented by the full-length SCRE1 gene. Collectively, this study indicates that the effector SCRE1 is able to inhibit host immunity and is required for full virulence of U. virens.
Keyphrases
- pseudomonas aeruginosa
- antimicrobial resistance
- escherichia coli
- staphylococcus aureus
- biofilm formation
- regulatory t cells
- crispr cas
- type iii
- dendritic cells
- cell wall
- signaling pathway
- poor prognosis
- cystic fibrosis
- induced apoptosis
- binding protein
- candida albicans
- genome wide
- amino acid
- genome editing
- immune response
- gene expression
- transcription factor
- dna methylation
- cell death
- genome wide identification