March 31,2017 | Vol. 1
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A Calmodulin-like Protein Suppresses RNA Silencing and Promotes Geminivirus Infection by Degrading SGS3 via the Autophagy Pathway in Nicotiana Benthamiana

Post-transcriptional gene silencing (PTGS) is an elaborately regulated process for defense against virus infection in plants. To achieve effective infection, a betasatellite molecule associated with geminivirus induced high levels of an endogenous RNA silencing suppressor, calmodulin-like protein (CaM), to counter host defenses. However, the mechanism underlying CaM-mediated PTGS suppression is poorly understood. Recently, researchers at the State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection of CAAS have published a research paper about autophagy pathway-mediated degradation of SGS3 by CaM in Nicotiana benthamiana.

Proposed working model summarizing the roles of the endogenous suppressor NbCaM in regulation of PTGS and geminivirus infection

They have previously demonstrated that CaM is an endogenous RNA silencing suppressor that suppresses PTGS and enhances geminivirus infection. The research showed that CaM from Nicotiana benthamiana (NbCaM) interacts with and degrades Suppressor of Gene Silencing 3 (NbSGS3). Deletion analyses showed that domains essential for the interaction between NbSGS3 and NbCaM are also required for the subcellular localization of NbSGS3 and NbCaM suppressor activity. Moreover, NbCaM-mediated NbSGS3 protein degradation can be blocked using the autophagy inhibitors 3-methyladenine and E64d, and by knock-down of key autophagy-related genes within the phosphatidylinositol 3-kinase (PI3K) complex. Silencing of the PI3K complex also inhibited geminivirus infection. These data suggest that NbCaM acts as a suppressor of RNA silencing by degrading NbSGS3 through the autophagy pathway.

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