The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122
The P body protein LSm1 stimulates translation and replication of hepatitis C virus (HCV). As the liver-specific microRNA-122 (miR-122) is required for HCV replication and is associated with P bodies, we investigated whether regulation of HCV by LSm1 involves miR-122. Here, we demonstrate that LSm1...
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| Format: | Article |
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Oxford University Press
2014
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| Online Access: | https://eprints.nottingham.ac.uk/3109/ |
| _version_ | 1848790956217729024 |
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| author | Roberts, Ashley P.E. Doidge, Rachel Tarr, Alexander W. Jopling, Catherine L. |
| author_facet | Roberts, Ashley P.E. Doidge, Rachel Tarr, Alexander W. Jopling, Catherine L. |
| author_sort | Roberts, Ashley P.E. |
| building | Nottingham Research Data Repository |
| collection | Online Access |
| description | The P body protein LSm1 stimulates translation and replication of hepatitis C virus (HCV). As the liver-specific microRNA-122 (miR-122) is required for HCV replication and is associated with P bodies, we investigated whether regulation of HCV by LSm1 involves miR-122. Here, we demonstrate that LSm1 contributes to activation of HCV internal ribosome entry site (IRES)-driven translation by miR-122. This role for LSm1 is specialized for miR-122 translation activation, as LSm1 depletion does not affect the repressive function of miR-122 at 3′ untranslated region (UTR) sites, or miR-122–mediated cleavage at a perfectly complementary site. We find that LSm1 does not influence recruitment of the microRNA (miRNA)-induced silencing complex to the HCV 5′UTR, implying that it regulates miR-122 function subsequent to target binding. In contrast to the interplay between miR-122 and LSm1 in translation, we find that LSm1 is not required for miR-122 to stimulate HCV replication, suggesting that miR-122 regulation of HCV translation and replication have different requirements. For the first time, we have identified a protein factor that specifically contributes to activation of HCV IRES-driven translation by miR-122, but not to other activities of the miRNA. Our results enhance understanding of the mechanisms by which miR-122 and LSm1 regulate HCV. |
| first_indexed | 2025-11-14T18:20:51Z |
| format | Article |
| id | nottingham-3109 |
| institution | University of Nottingham Malaysia Campus |
| institution_category | Local University |
| last_indexed | 2025-11-14T18:20:51Z |
| publishDate | 2014 |
| publisher | Oxford University Press |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | nottingham-31092020-05-04T20:15:51Z https://eprints.nottingham.ac.uk/3109/ The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122 Roberts, Ashley P.E. Doidge, Rachel Tarr, Alexander W. Jopling, Catherine L. The P body protein LSm1 stimulates translation and replication of hepatitis C virus (HCV). As the liver-specific microRNA-122 (miR-122) is required for HCV replication and is associated with P bodies, we investigated whether regulation of HCV by LSm1 involves miR-122. Here, we demonstrate that LSm1 contributes to activation of HCV internal ribosome entry site (IRES)-driven translation by miR-122. This role for LSm1 is specialized for miR-122 translation activation, as LSm1 depletion does not affect the repressive function of miR-122 at 3′ untranslated region (UTR) sites, or miR-122–mediated cleavage at a perfectly complementary site. We find that LSm1 does not influence recruitment of the microRNA (miRNA)-induced silencing complex to the HCV 5′UTR, implying that it regulates miR-122 function subsequent to target binding. In contrast to the interplay between miR-122 and LSm1 in translation, we find that LSm1 is not required for miR-122 to stimulate HCV replication, suggesting that miR-122 regulation of HCV translation and replication have different requirements. For the first time, we have identified a protein factor that specifically contributes to activation of HCV IRES-driven translation by miR-122, but not to other activities of the miRNA. Our results enhance understanding of the mechanisms by which miR-122 and LSm1 regulate HCV. Oxford University Press 2014-01 Article PeerReviewed Roberts, Ashley P.E., Doidge, Rachel, Tarr, Alexander W. and Jopling, Catherine L. (2014) The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122. Nucleic Acids Research, 42 (2). pp. 1257-1269. ISSN 0305-1048 http://nar.oxfordjournals.org/content/42/2/1257 doi:10.1093/nar/gkt941 doi:10.1093/nar/gkt941 |
| spellingShingle | Roberts, Ashley P.E. Doidge, Rachel Tarr, Alexander W. Jopling, Catherine L. The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122 |
| title | The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122 |
| title_full | The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122 |
| title_fullStr | The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122 |
| title_full_unstemmed | The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122 |
| title_short | The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122 |
| title_sort | p body protein lsm1 contributes to stimulation of hepatitis c virus translation, but not replication, by microrna-122 |
| url | https://eprints.nottingham.ac.uk/3109/ https://eprints.nottingham.ac.uk/3109/ https://eprints.nottingham.ac.uk/3109/ |