Abstract

ER Stress Machinery Downregulates Potyvirus and Potexvirus Infection

Jeanmarie Verchot, Professor, Oklahoma State University

In plants there are several ER embedded sensors that play key roles in UPR pathways in response to heat, cold and pathogen attach. Such sensors include IRE1a, IRE1b, BI-1, bZIP17, bZIP28, BI-1,and BAG7, which identify changes in the condition of the ER and activate signaling routes that lead to restoring ER homeostasis, or under conditions of chronic stress, activate an alternative route that leads to cell death. Recent comparative studies indicate that ER resident sensors interact with the 6 kDa protein of two potyviruses (Turnip mosaic virus (TuMV) and Potato virus Y (PVY) and two potexviruses (Plantago asiatica mosaic virus (PlaMV) and Potato virus X (PVX)). Data indicates that the viral ER resident 6K2 or TGB3 proteins acts via the IRE1a/b pathway. Experiments determined each of these viral proteins activate bZIP60 mRNA splicing producing a truncated transcription factor that upregulates expression of ER resident protein chaperones. Mutational analysis indicates that activation of IRE1a/b pathways reduce virus infection and disease. Knockdown of bZIP60 and BI-1 expression leads to enhanced systemic virus accumulation and loss of BI-1 leads to systemic necrosis. These data indicate that the ER stress machinery attenuates virus disease and may be used to develop engineer resistance that may be broad spectrum.