A calmodulin-like protein suppresses RNA silencing and promotes geminivirus infection by degrading SGS3 via the autophagy pathway in Nicotiana benthamiana

A recently characterized calmodulin-like protein is an endogenous RNA silencing suppressor that suppresses sense-RNA induced post-transcriptional gene silencing (S-PTGS) and enhances virus infection, but the mechanism underlying calmodulin-like protein-mediated S-PTGS suppression is obscure. Here, w...

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Bibliographic Details
Published in:PLoS pathogens 2017-02, Vol.13 (2), p.e1006213-e1006213
Main Authors: Li, Fangfang, Zhao, Nan, Li, Zhenghe, Xu, Xiongbiao, Wang, Yaqin, Yang, Xiuling, Liu, Shu-Sheng, Wang, Aiming, Zhou, Xueping
Format: Article
Language:English
Subjects:
Agriculture
Autophagy
Autophagy (Cytology)
Biology
Biology and Life Sciences
Biotechnology
Calmodulin - metabolism
Cloning
Deoxyribonucleic acid
Diseases and pests
DNA
Flowers & plants
Funding
Geminiviridae
Geminivirus
Gene Expression Regulation, Plant - physiology
Genes
Genetic aspects
Immunoblotting
Infections
Kinases
Laboratories
Localization
Nicotiana
Nicotiana - virology
Nicotiana benthamiana
Physiological aspects
Plant diseases
Plant Diseases - genetics
Plant Diseases - virology
Plant Proteins - metabolism
Plant viruses
Polymerase Chain Reaction
Proteins
R&D
Research & development
Rice
RNA interference
RNA Interference - physiology
Viruses
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Summary:A recently characterized calmodulin-like protein is an endogenous RNA silencing suppressor that suppresses sense-RNA induced post-transcriptional gene silencing (S-PTGS) and enhances virus infection, but the mechanism underlying calmodulin-like protein-mediated S-PTGS suppression is obscure. Here, we show that a calmodulin-like protein from Nicotiana benthamiana (NbCaM) interacts with 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. Overexpression of NbCaM reduced the number of NbSGS3-associated granules by degrading NbSGS3 protein accumulation in the cytoplasm. This NbCaM-mediated NbSGS3 degradation was sensitive to the autophagy inhibitors 3-methyladenine and E64d, and was compromised when key autophagy genes of the phosphatidylinositol 3-kinase (PI3K) complex were knocked down. Meanwhile, silencing of key autophagy genes within the PI3K complex inhibited geminivirus infection. Taken together these data suggest that NbCaM acts as a suppressor of RNA silencing by degrading NbSGS3 through the autophagy pathway.
ISSN:1553-7374
1553-7366
1553-7374
DOI:10.1371/journal.ppat.1006213