Coat protein of TCV suppresses RNA decay via ubiquitination and autophagy pathways to facilitate viral infection

Abstract

Highlight statementThe findings highlight that TCV manipulates 26S proteasome and autophagy pathways to obstruct antiviral RNA decay defenses and ultimately enhance its ability to infect host cells. RNA decay is a pervasive process in eukaryotic cells. Viruses utilize the host cells intracellular machinery to gain access to essential molecules and subcellular structures required for infection during the pathogenesis process. The study demonstrates that turnip crinkle virus (TCV) infection enhances the expression of Arabidopsis Dcp1 (AtDcp1), which negatively regulates the accumulation of TCV RNA, indicating its involvement in antiviral defense. Nevertheless, TCV circumvents the antiviral defense based on RNA decay, as indicated by the capsid protein (CP) of TCV stabilizing the known nonsense-mediated RNA decay targeted transcripts. In vivo, CP physically interacts with AtDcp1, promoting AtDcp1 degradation via ubiquitination and autophagy pathways. This is evidenced by the observation that the degradation is inhibited by both 26S proteasome and autophagy inhibitors. Furthermore, CP elevates the polyubiquitination of Dcp1-Flag and the quantity of pre-autophagosome or autophagosome structures. These data indicate that CP suppresses RNA decay by interacting with AtDcp1 and mediating its degradation through the 26S proteasome and autophagy pathways, effectively subduing antiviral RNA decay. This study uncovers a previously unidentified virulence strategy in the ongoing conflict between plants and viruses.