UPF2 is a critical regulator of liver development, function and regeneration.

<h4>Background</h4>Nonsense-mediated mRNA decay (NMD) is a post-transcriptional RNA surveillance process that facilitates the recognition and destruction of mRNAs bearing premature terminations codons (PTCs). Such PTC-containing (PTC+) mRNAs may arise from different processes, including...

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Autores principales:	Lina A Thoren, Gitte A Nørgaard, Joachim Weischenfeldt, Johannes Waage, Janus S Jakobsen, Inge Damgaard, Frida C Bergström, Anna M Blom, Rehannah Borup, Hanne Cathrine Bisgaard, Bo T Porse
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ebbde6b63c394befb3c39ee3b7590405
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spelling	oai:doaj.org-article:ebbde6b63c394befb3c39ee3b75904052021-12-02T20:19:58ZUPF2 is a critical regulator of liver development, function and regeneration.1932-620310.1371/journal.pone.0011650https://doaj.org/article/ebbde6b63c394befb3c39ee3b75904052010-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20657840/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Nonsense-mediated mRNA decay (NMD) is a post-transcriptional RNA surveillance process that facilitates the recognition and destruction of mRNAs bearing premature terminations codons (PTCs). Such PTC-containing (PTC+) mRNAs may arise from different processes, including erroneous processing and expression of pseudogenes, but also from more regulated events such as alternative splicing coupled NMD (AS-NMD). Thus, the NMD pathway serves both as a silencer of genomic noise and a regulator of gene expression. Given the early embryonic lethality in NMD deficient mice, uncovering the full regulatory potential of the NMD pathway in mammals will require the functional assessment of NMD in different tissues.<h4>Methodology/principal findings</h4>Here we use mouse genetics to address the role of UPF2, a core NMD component, in the development, function and regeneration of the liver. We find that loss of NMD during fetal liver development is incompatible with postnatal life due to failure of terminal differentiation. Moreover, deletion of Upf2 in the adult liver results in hepatosteatosis and disruption of liver homeostasis. Finally, NMD was found to be absolutely required for liver regeneration.<h4>Conclusion/significance</h4>Collectively, our data demonstrate the critical role of the NMD pathway in liver development, function and regeneration and highlights the importance of NMD for mammalian biology.Lina A ThorenGitte A NørgaardJoachim WeischenfeldtJohannes WaageJanus S JakobsenInge DamgaardFrida C BergströmAnna M BlomRehannah BorupHanne Cathrine BisgaardBo T PorsePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 7, p e11650 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Lina A Thoren Gitte A Nørgaard Joachim Weischenfeldt Johannes Waage Janus S Jakobsen Inge Damgaard Frida C Bergström Anna M Blom Rehannah Borup Hanne Cathrine Bisgaard Bo T Porse UPF2 is a critical regulator of liver development, function and regeneration.
description	<h4>Background</h4>Nonsense-mediated mRNA decay (NMD) is a post-transcriptional RNA surveillance process that facilitates the recognition and destruction of mRNAs bearing premature terminations codons (PTCs). Such PTC-containing (PTC+) mRNAs may arise from different processes, including erroneous processing and expression of pseudogenes, but also from more regulated events such as alternative splicing coupled NMD (AS-NMD). Thus, the NMD pathway serves both as a silencer of genomic noise and a regulator of gene expression. Given the early embryonic lethality in NMD deficient mice, uncovering the full regulatory potential of the NMD pathway in mammals will require the functional assessment of NMD in different tissues.<h4>Methodology/principal findings</h4>Here we use mouse genetics to address the role of UPF2, a core NMD component, in the development, function and regeneration of the liver. We find that loss of NMD during fetal liver development is incompatible with postnatal life due to failure of terminal differentiation. Moreover, deletion of Upf2 in the adult liver results in hepatosteatosis and disruption of liver homeostasis. Finally, NMD was found to be absolutely required for liver regeneration.<h4>Conclusion/significance</h4>Collectively, our data demonstrate the critical role of the NMD pathway in liver development, function and regeneration and highlights the importance of NMD for mammalian biology.
format	article
author	Lina A Thoren Gitte A Nørgaard Joachim Weischenfeldt Johannes Waage Janus S Jakobsen Inge Damgaard Frida C Bergström Anna M Blom Rehannah Borup Hanne Cathrine Bisgaard Bo T Porse
author_facet	Lina A Thoren Gitte A Nørgaard Joachim Weischenfeldt Johannes Waage Janus S Jakobsen Inge Damgaard Frida C Bergström Anna M Blom Rehannah Borup Hanne Cathrine Bisgaard Bo T Porse
author_sort	Lina A Thoren
title	UPF2 is a critical regulator of liver development, function and regeneration.
title_short	UPF2 is a critical regulator of liver development, function and regeneration.
title_full	UPF2 is a critical regulator of liver development, function and regeneration.
title_fullStr	UPF2 is a critical regulator of liver development, function and regeneration.
title_full_unstemmed	UPF2 is a critical regulator of liver development, function and regeneration.
title_sort	upf2 is a critical regulator of liver development, function and regeneration.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/ebbde6b63c394befb3c39ee3b7590405
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UPF2 is a critical regulator of liver development, function and regeneration.

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