An Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells
Infection with the avian leukosis virus subgroup J (ALV-J) impairs host genes and facilitates the establishment of chronic infection and the viral life cycle. However, the involvement of long noncoding RNAs (lncRNAs) in ALV-J infection remains largely unknown. In this study, we identified a novel ch...
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2021
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oai:doaj.org-article:2f5c0643aa4d44e9b575d323c6bf30372021-12-01T13:46:45ZAn Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells1664-302X10.3389/fmicb.2021.788317https://doaj.org/article/2f5c0643aa4d44e9b575d323c6bf30372021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fmicb.2021.788317/fullhttps://doaj.org/toc/1664-302XInfection with the avian leukosis virus subgroup J (ALV-J) impairs host genes and facilitates the establishment of chronic infection and the viral life cycle. However, the involvement of long noncoding RNAs (lncRNAs) in ALV-J infection remains largely unknown. In this study, we identified a novel chicken lncRNA derived from LTR5B of the ERV-L family (namely lnc-LTR5B), which is significantly downregulated in ALV-J infected cells. lnc-LTR5B was localized in the cytoplasm and was relatively high expressed in the chicken lung and liver. Notably, the replication of ALV-J was inhibited by the overexpression of lnc-LTR5B but enhanced when lnc-LTR5B expression was knocked down. We further confirmed that lnc-LTR5B could bind to the binding immunoglobulin protein (BiP), a master regulator of endoplasmic reticulum (ER) function. Mechanistically, lnc-LTR5B serves as a competing endogenous RNA for BiP, restricting its physical availability. Upon ALV-J infection, the reduction of lnc-LTR5B released BiP, which facilitated its translocation to the cell surface. This is crucial for ALV-J entry as well as pro-survival signaling. In conclusion, we identified an endogenous retroviral LTR-activated lnc-LTR5B that is involved in regulating the cell surface translocation of BiP, and such regulatory machinery can be exploited by ALV-J to complete its life cycle and propagate.Shihao ChenShihao ChenShihao ChenRuihan ZhaoRuihan ZhaoTing WuTing WuDedong WangDedong WangBiao WangBiao WangShiyu PanShiyu PanXuming HuXuming HuZhiming PanHengmi CuiHengmi CuiHengmi CuiFrontiers Media S.A.articleALV-JlncRNAlnc-LTR5BBiPinteractionMicrobiologyQR1-502ENFrontiers in Microbiology, Vol 12 (2021) |
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ALV-J lncRNA lnc-LTR5B BiP interaction Microbiology QR1-502 |
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ALV-J lncRNA lnc-LTR5B BiP interaction Microbiology QR1-502 Shihao Chen Shihao Chen Shihao Chen Ruihan Zhao Ruihan Zhao Ting Wu Ting Wu Dedong Wang Dedong Wang Biao Wang Biao Wang Shiyu Pan Shiyu Pan Xuming Hu Xuming Hu Zhiming Pan Hengmi Cui Hengmi Cui Hengmi Cui An Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells |
description |
Infection with the avian leukosis virus subgroup J (ALV-J) impairs host genes and facilitates the establishment of chronic infection and the viral life cycle. However, the involvement of long noncoding RNAs (lncRNAs) in ALV-J infection remains largely unknown. In this study, we identified a novel chicken lncRNA derived from LTR5B of the ERV-L family (namely lnc-LTR5B), which is significantly downregulated in ALV-J infected cells. lnc-LTR5B was localized in the cytoplasm and was relatively high expressed in the chicken lung and liver. Notably, the replication of ALV-J was inhibited by the overexpression of lnc-LTR5B but enhanced when lnc-LTR5B expression was knocked down. We further confirmed that lnc-LTR5B could bind to the binding immunoglobulin protein (BiP), a master regulator of endoplasmic reticulum (ER) function. Mechanistically, lnc-LTR5B serves as a competing endogenous RNA for BiP, restricting its physical availability. Upon ALV-J infection, the reduction of lnc-LTR5B released BiP, which facilitated its translocation to the cell surface. This is crucial for ALV-J entry as well as pro-survival signaling. In conclusion, we identified an endogenous retroviral LTR-activated lnc-LTR5B that is involved in regulating the cell surface translocation of BiP, and such regulatory machinery can be exploited by ALV-J to complete its life cycle and propagate. |
format |
article |
author |
Shihao Chen Shihao Chen Shihao Chen Ruihan Zhao Ruihan Zhao Ting Wu Ting Wu Dedong Wang Dedong Wang Biao Wang Biao Wang Shiyu Pan Shiyu Pan Xuming Hu Xuming Hu Zhiming Pan Hengmi Cui Hengmi Cui Hengmi Cui |
author_facet |
Shihao Chen Shihao Chen Shihao Chen Ruihan Zhao Ruihan Zhao Ting Wu Ting Wu Dedong Wang Dedong Wang Biao Wang Biao Wang Shiyu Pan Shiyu Pan Xuming Hu Xuming Hu Zhiming Pan Hengmi Cui Hengmi Cui Hengmi Cui |
author_sort |
Shihao Chen |
title |
An Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells |
title_short |
An Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells |
title_full |
An Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells |
title_fullStr |
An Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells |
title_full_unstemmed |
An Endogenous Retroviral LTR-Derived Long Noncoding RNA lnc-LTR5B Interacts With BiP to Modulate ALV-J Replication in Chicken Cells |
title_sort |
endogenous retroviral ltr-derived long noncoding rna lnc-ltr5b interacts with bip to modulate alv-j replication in chicken cells |
publisher |
Frontiers Media S.A. |
publishDate |
2021 |
url |
https://doaj.org/article/2f5c0643aa4d44e9b575d323c6bf3037 |
work_keys_str_mv |
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