Abstract
Rice stripe virus (RSV) causes severe disease symptoms in leaves of Oryza sativa (rice). Movement protein (MP) of RSV has been implicated in complementation of a movement-deficient PVX and symptom development in model organism Nicotiana benthamianais. However, in rice plants, whether and how RSV MP functions as a symptom determinant remains poorly understood. Symptom development of a plant viral disease is a result of molecular interactions between the virus and its host plant; thus, the elucidation of specific interactions is a prerequisite to reveal the mechanism of viral pathogenesis. Here, we provide evidences showing that RSV targeted to the chloroplast and further disturbed the structure and the photosynthesis function of chloroplast in rice plants through immunoelectron microscopy. We also provide evidences to speculate that this deficiency of chloroplast function might be caused by interaction of RSV MP with chaperonin-60-β (CPN-60-β), a Rubisco binding protein in chloroplast as shown by yeast two-hybrid and immunoprecipitation assays, and this interaction further modulated the accumulation of CPN-60-β. Our findings shed light on the molecular mechanism underlying RSV disease symptom development in natural host, the rice.