Artificial coat protein variants of cucumber mosaic virus induce enhanced resistance upon recognition by an R gene

Induction of R-gene-mediated antiviral resistance results in phenotypically different responses depending on host R gene—virus combinations. The responses include a hypersensitive response (HR), in which virus infection is stopped within the initially infected tissues to form necrotic local lesions (NLLs) by induction of programmed-cell death (PCD), as well as an extreme resistance (ER), in which virus replication is suppressed at the cellular level without PCD induction. A response that causes only tiny NLLs is called a micro-HR, and a response that causes systemic death of the plant by systemic PCD induction is called a systemic HR (SHR). In this study, we used our RCY1—cucumber mosaic virus (CMV) coat protein (CP) system as a model system for R gene—virus recognition and resistance induction, and showed that artificial deletion/alanine substitutions in an arginine-rich motif in CMV CP changed the induced response from an HR to an ER and to intermediate responses between an ER and a micro-HR, where different numbers of tiny NLLs were formed. Using a micro-HR inducing variant, we showed that viral MOI (multiplicity of infection) reduced by 51.5% upon a micro-HR induction, which was much greater than the reduction observed upon an HR induction, providing the first quantitative evidence that a micro-HR is a result of enhanced resistance. Based on the obtained results, we discuss a possible molecular mechanism for the induction of enhanced resistance and the mechanisms for the induction of phenotypically different responses.