Type 2C protein phosphatase is a key regulator of antiviral extreme resistance limiting virus spread.

Abstract

Effector-triggered immunity (ETI) is an active immune response triggered by interactions between host resistance proteins and their cognate effectors. Although ETI is often associated with the hypersensitive response (HR), various R genes mediate an HR-independent process known as extreme resistance (ER). In the soybean-Soybean mosaic virus (SMV) pathosystem, the strain-specific CI protein of SMV functions as an effector of Rsv3-mediated ER. In this study, we used the soybean (Rsv3)-SMV (CI) pathosystem to gain insight into the molecular signaling pathway involved in ER. We used genome-wide transcriptome analysis to identify a subset of the type 2C protein phophatase (PP2C) genes that are specifically up-regulated in Rsv3-mediated ER. Gain-of-function analysis of the most significantly expressed soybean PP2C gene, GmPP2C3a, showed that ABA-induced GmPP2C3a functions as a key regulator of Rsv3-mediated ER. Our results further suggest that the primary mechanism of ER against viruses is the inhibition of viral cell-to-cell movement by callose deposition in an ABA signaling-dependent manner.