A calmodulin-like protein suppresses RNA silencing and promotes geminivirus infection by degrading SGS3 via the autophagy pathway in Nicotiana benthamiana
Fig 7
A working model summarizing the roles of the endogenous suppressor NbCaM in regulation of PTGS and geminivirus infection.
The replication intermediates produced during geminivirus infection serve as templates for bidirectional transcription, and the resulting convergent transcripts induce RNA silencing. The dsRNAs with 5’ overhangs are further recognized by SGS3 and then converted into longer dsRNAs by RDR6, which amplifies RNA silencing and processes secondary siRNAs targeted against geminivirus infection. As a cellular negative regulator of RNA silencing, NbCaM could repress expression of RDR6 by an unidentified mechanism. Alternatively, the betasatellite encoded βC1 up-regulates NbCaM expression and NbCaM interacts with NbSGS3 to mediate degradation of NbSGS3 via the autophagy pathway. This then promotes efficient viral invasion by suppression of the host anti-viral RNA silencing machinery.