Enterovirus-induced miR-141 contributes to shutoff of host protein translation by targeting the translation initiation factor eIF4E

Bing Ching Ho, Sung Liang Yu, Jeremy J.W. Chen, Sui Yuan Chang, Bo Shiun Yan, Qi Sheng Hong, Sher Singh, Chuan Liang Kao, Hsuan Yu Chen, Kang Yi Su, Ker Chau Li, Chiou Ling Cheng, Hao Wei Cheng, Jen Yi Lee, Chun Nan Lee, Pan Chyr Yang

Research output: Contribution to journalArticle

105 Citations (Scopus)

Abstract

Viruses rely on the host translation machinery to complete their life cycles. Picornaviruses use an internal ribosome entry site to initiate cap-independent protein translation and in parallel host cap-dependent translation is shut off. This process is thought to occur primarily via cleavage of host translation initiation factors eIF4GI and eIF4GII by viral proteases. Here we describe another mechanism whereby miR-141 induced upon enterovirus infection targets the cap-dependent translation initiation factor, eIF4E, for shutoff of host protein synthesis. Knockdown of miR-141 reduces viral propagation, and silencing of eIF4E can completely reverse the inhibitory effect of the miR-141 antagomiR on viral propagation. Ectopic expression of miR-141 promotes the switch from cap-dependent to cap-independent translation. Moreover, we identified a transcription factor, EGR1, which is partly responsible for miR-141 induction in response to enterovirus infection. Our results suggest that upregulation of miR-141 upon enterovirus infection can facilitate viral propagation by expediting the translational switch.

Original languageEnglish
Pages (from-to)58-69
Number of pages12
JournalCell Host and Microbe
Volume9
Issue number1
DOIs
Publication statusPublished - 2011 Jan 20

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Virology

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