期刊
VIRUSES-BASEL
卷 13, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/v13112189
关键词
autophagy; antiviral machinery; citrus leaf blotch virus; protein degradation; virus movement
类别
资金
- National Natural Science Foundation of China [32000123, 3217010713]
- Basic Scientific Research Foundation
- Ministry of education of China [Z109021801, 2016KW-069]
This study showed that the infection of CLBV activated autophagy in Nicotiana benthamiana plants, leading to inhibition of viral spread in plants by targeting the viral movement protein.
Autophagy is an evolutionarily conserved cellular-degradation mechanism implicated in antiviral defense in plants. Studies have shown that autophagy suppresses virus accumulation in cells; however, it has not been reported to specifically inhibit viral spread in plants. This study demonstrated that infection with citrus leaf blotch virus (CLBV; genus Citrivirus, family Betaflexiviridae) activated autophagy in Nicotiana benthamiana plants as indicated by the increase of autophagosome formation. Impairment of autophagy through silencing of N. benthamiana autophagy-related gene 5 (NbATG5) and NbATG7 enhanced cell-to-cell and systemic movement of CLBV; however, it did not affect CLBV accumulation when the systemic infection had been fully established. Treatment using an autophagy inhibitor or silencing of NbATG5 and NbATG7 revealed that transiently expressed movement protein (MP), but not coat protein, of CLBV was targeted by selective autophagy for degradation. Moreover, we identified that CLBV MP directly interacted with NbATG8C1 and NbATG8i, the isoforms of autophagy-related protein 8 (ATG8), which are key factors that usually bind cargo receptors for selective autophagy. Our results present a novel example in which autophagy specifically targets a viral MP to limit the intercellular spread of the virus in plants.
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