Selective autophagic receptor NbNBR1 prevents NbRFP1-mediated UPS-dependent degradation of beta C1 to promote geminivirus infection

文献类型： 外文期刊

第一作者： Zhou, Tingting

作者： Zhou, Tingting;Zhou, Xueping;Zhou, Tingting;Zhang, Mingzhen;Gong, Pan;Li, Fangfang;Zhou, Xueping

作者机构：

期刊名称：PLOS PATHOGENS （ 影响因子：6.823； 五年影响因子：7.455 ）

ISSN： 1553-7366

年卷期： 2021 年 17 卷 9 期

页码：

收录情况： SCI

摘要： Autophagy is an evolutionarily conserved, lysosomal/vacuolar degradation mechanism that targets cell organelles and macromolecules. Autophagy and autophagy-related genes have been studied for their antiviral and pro-viral roles in virus-infected plants. Here, we demonstrate the pro-viral role of a selective autophagic receptor NbNBR1 in geminivirus-infected Nicotiana benthamiana plants. The beta C1 protein encoded by tomato yellow leaf curl China betasatellite (TYLCCNB) that is associated with tomato yellow leaf curl China virus (TYLCCNV) enhanced the expression level of NbNBR1. Then NbNBR1 interacted with beta C1 to form cytoplasmic granules. Interaction of NbNBR1 with beta C1 could prevent degradation of beta C1 by the NbRFP1, an E3 ligase. Overexpression of NbNBR1 in N. benthamiana plants increased beta C1 accumulation and promoted virus infection. In contrast, silencing or knocking out NbNBR1 expression in N. benthamiana suppressed beta C1 accumulation and inhibited virus infection. A single amino acid substitution in beta C1 (beta C1(K4A)) abolished its interaction with NbNBR1, leading to a reduced level of beta C1(K4A). The TYLCCNV/TYLCCNBK4A mutant virus caused milder disease symptoms and accumulated much less viral genomic DNAs in the infected plants. Collectively, the results presented here show how a viral satellite-encoded protein hijacks host autophagic receptor NbNBR1 to form cytoplasmic granules to protect itself from NbRFP1-mediated degradation and facilitate viral infection.

Author summary We provide new evidence to show that beta C1 encoded by tomato yellow leaf curl China betasatellite (TYLCCNB) that is associated with tomato yellow leaf curl China virus (TYLCCNV) can modulate plant defense against geminivirus infection. The beta C1 protein could increase the expression level of NbNBR1, known as a selective autophagic receptor protein, and interact with it to form cytoplasmic granules in planta. Interaction between NbNBR1 and beta C1 restrains interaction between NbRFP1, an E3 ligase, and beta C1, thus to stabilize beta C1 away from NbRFP1-mediated degradation. Hijacking of an autophagic receptor NbNBR1 by beta C1 to benefit geminivirus infection has not been reported previously. This study demonstrates a distinct mechanism of a viral satellite-encoded protein exploits the autophagy protein NbNBR1 to the cytoplasmic granules, thus, to prevent the NbRFP1-mediated degradation and highlight an important role for NbNBR1 in geminivirus infection.

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