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Elife. 2017 Dec 12;6. pii: e30590. doi: 10.7554/eLife.30590.

A picorna-like virus suppresses the N-end rule pathway to inhibit apoptosis.

Wang Z#1,2, Xia X#1,2,3, Yang X1, Zhang X1,2, Liu Y1,2, Wu D1,2, Fang Y1,2, Liu Y1,2, Xu J2, Qiu Y2, Zhou X1,2.

Author information

State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, China.
State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Guangzhou Key Laboratory of Insect Development Regulation and Application Research, Institute of Insect Science and Technology & School of Life Sciences, South China Normal University, Guangzhou, China.
Contributed equally


The N-end rule pathway is an evolutionarily conserved proteolytic system that degrades proteins containing N-terminal degradation signals called N-degrons, and has emerged as a key regulator of various processes. Viruses manipulate diverse host pathways to facilitate viral replication and evade antiviral defenses. However, it remains unclear if viral infection has any impact on the N-end rule pathway. Here, using a picorna-like virus as a model, we found that viral infection promoted the accumulation of caspase-cleaved Drosophila inhibitor of apoptosis 1 (DIAP1) by inducing the degradation of N-terminal amidohydrolase 1 (NTAN1), a key N-end rule component that identifies N-degron to initiate the process. The virus-induced NTAN1 degradation is independent of polyubiquitylation but dependent on proteasome. Furthermore, the virus-induced N-end rule pathway suppression inhibits apoptosis and benefits viral replication. Thus, our findings demonstrate that a virus can suppress the N-end rule pathway, and uncover a new mechanism for virus to evade apoptosis.


D. melanogaster; Drosophila C virus; N-end rule pathway; apoptosis; immunology; infectious disease; microbiology

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