Abstract
Ustilaginoidea virens, which causes rice false smut (RFS), is one of the most detrimental rice fungal diseases and poses a severe threat to rice production and quality. Effectors in U. virens often act as a group of essential virulence factors that play crucial roles in the interaction between host and the pathogen. Thus, the functions of individual effectors in U. virens need to be further explored. Here, we demonstrated a small secreted hypersensitive response-inducing protein (hrip), named UvHrip1, which was highly conserved in U. virens isolates. UvHrip1 was also proven to suppress necrosis-like defense symptoms in N. benthamiana induced by the oomycete elicitor INF1. The localization of UvHrip1 was mainly in the nuclei and cytoplasm via monitoring the UvHrip1-GFP fusion protein in rice cells. Furthermore, Y2H and BiFC assay demonstrated that UvHrip1 interacted with OsHGW, which is a critical regulator in heading date and grain weight signaling pathways in rice. Expression patterns of defense- and heading date-related genes, OsPR1#051 and OsMYB21, were down-regulated over U. virens infection in rice. Collectively, our data provide a theory for gaining an insight into the molecular mechanisms underlying the UvHrip1 virulence function.
Highlights
Rice false smut (RFS) caused by the ascomycetous fungus Ustilaginoidea virens (Cooke) Takah is one of the most important fungal diseases in rice [1,2,3]
The cell death inhibition assays in N. benthamiana leaves and transcriptome analysis at different periods after pathogen infection suggest that most effectors could manipulate the plant immune responses and promote the successful colonization of pathogens in the host [2]
Core effector proteins are highly conserved in many plant pathogens [28]
Summary
Rice false smut (RFS) caused by the ascomycetous fungus Ustilaginoidea virens (Cooke) Takah (teleomorph Villosiclava virens) is one of the most important fungal diseases in rice [1,2,3]. Plant cells develop resistance (R) proteins, which detects and recognizes pathogen effectors Such interaction triggers rapid and robust defense responses, usually accompanied by the hypersensitive response (HR), called effector-triggered immunity (ETI) [16,17,18]. Tritici significantly suppresses INF1-triggered cell death in N. benthamiana, and play an essential role to the pathogen virulence [20,34,35]. The cell death inhibition assays in N. benthamiana leaves and transcriptome analysis at different periods after pathogen infection suggest that most effectors could manipulate the plant immune responses and promote the successful colonization of pathogens in the host [2]. Many putative effectors induce cell death or defense responses in rice and N. benthamiana. UvHrip suppressed INF1-triggered cell death in N. benthamiana leaves, and interacted with a heading date- and grain weight-related protein, OsHGW. Our study suggests UvHrip is a functional effector and is involved in affecting host plant immunity
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