Figure 7.

Betasatellite‐encoded βC1 protein subverts PsbP‐mediated defence response against geminivirus infection. (a) PsbP‐mediated defence response against geminivirus infection. During the early stage of viral infection, plant innate immunity necessitates the oxygen‐evolving enhancer protein 2, PsbP to exhibit an antiviral response in the infected plant cells. PsbP binding to viral DNA possibly interferes with systemic infection and/or movement of viral DNA from the infected cells. Consequently, PsbP binding to geminivirus DNA impedes symptom induction and viral DNA accumulation, thereby hampers viral pathogenesis. In addition, the OEC of PSII facilitated defence‐related reactive oxygen species (ROS) production lead to an antiviral state and subsequently impedes the viral infection cycle. (b) βC1 attenuates the PsbP‐mediated defence response during betasatellite infection. During the later stage of viral infection, βC1 protein being pathogenicity determinant targets the OEC of PSII and disturbs the photosynthetic function and ultrastructure of chloroplasts. The damage caused by βC1 on the OEC of PSII possibly suppresses defence‐related reactive oxygen species (ROS) production, subsequently exhibit compromised cell death supporting viral pathogenesis. Betasatellite‐mediated veinal chlorosis symptom induction is associated with damage in the chloroplastic structure and function. Further, βC1 protein interacts with PsbP protein and hampers its DNA binding ability. The βC1‐PsbP interaction subverts the impediment on viral pathogenesis mediated by PsbP binding to geminivirus DNA. However, precise subcellular locations of these interactions are not known.