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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Autores principales: Shihao Chen, Ruihan Zhao, Ting Wu, Dedong Wang, Biao Wang, Shiyu Pan, Xuming Hu, Zhiming Pan, Hengmi Cui
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Publicado: Frontiers Media S.A. 2021
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spelling 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)
institution DOAJ
collection DOAJ
language EN
topic ALV-J
lncRNA
lnc-LTR5B
BiP
interaction
Microbiology
QR1-502
spellingShingle 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
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