Type 2C Protein Phosphatase Is a Key Regulator of Antiviral Extreme Resistance Limiting Virus Spread

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. P lants fight pathogen attack via a complex immune system that includes basal and highly specific defense responses 1-3 . The first line of defense against the vast majority of potential pathogens is termed pathogenassociated molecular pattern (PAMP)-triggered immunity (PTI) 1-2 . To circumvent PTI, many host-adapted pathogens produce different classes of effector molecules 1-2 . In turn, plants have evolved a second surveillance mode to recognize pathogen-derived effector proteins. This second mode or line of defense is triggered by specialized molecules such as resistance (R) proteins, which recognize the effectors and activate effector-triggered immunity (ETI) 1-2 . When R genes recognize effector proteins, the typical resistance responses include the hypersensitive response (HR) and extreme resistance (ER) HR results in localization of the pathogen at the inoculation site as a consequence of the rapid death of infected and neighboring cells 5 . In contrast, ER is characterized by the arrest of pathogens at the inoculation site without any macroscopic or microscopic cell death lesions