Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus

Prader-Willi Syndrome (PWS) is a neurogenetic disorder caused by the deletion of imprinted genes on the paternally inherited human chromosome 15q11-q13. This locus harbours a long non-protein-coding RNA (U-UBE3A-ATS) that contains six intron-encoded snoRNAs, including the SNORD116 and SNORD115 repet...

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Main Authors: Galiveti, Chenna R., Raabe, Carsten A., Konthur, Zoltán, Rozhdestvensky, Timofey S.
Format: Online
Language:English
Published: Nature Publishing Group 2014
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4171697/
id pubmed-4171697
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spelling pubmed-41716972014-09-24 Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus Galiveti, Chenna R. Raabe, Carsten A. Konthur, Zoltán Rozhdestvensky, Timofey S. Article Prader-Willi Syndrome (PWS) is a neurogenetic disorder caused by the deletion of imprinted genes on the paternally inherited human chromosome 15q11-q13. This locus harbours a long non-protein-coding RNA (U-UBE3A-ATS) that contains six intron-encoded snoRNAs, including the SNORD116 and SNORD115 repetitive clusters. The 3′-region of U-UBE3A-ATS is transcribed in the cis-antisense direction to the ubiquitin-protein ligase E3A (UBE3A) gene. Deletion of the SNORD116 region causes key characteristics of PWS. There are few indications that SNORD115 might regulate serotonin receptor (5HT2C) pre-mRNA processing. Here we performed quantitative real-time expression analyses of RNAs from the PWS locus across 20 human tissues and combined it with deep-sequencing data derived from Cap Analysis of Gene Expression (CAGE-seq) libraries. We found that the expression profiles of SNORD64, SNORD107, SNORD108 and SNORD116 are similar across analyzed tissues and correlate well with SNORD116 embedded U-UBE3A-ATS exons (IPW116). Notable differences in expressions between the aforementioned RNAs and SNORD115 together with the host IPW115 and UBE3A cis-antisense exons were observed. CAGE-seq analysis revealed the presence of potential transcriptional start sites originated from the U-UBE3A-ATS spanning region. Our findings indicate novel aspects for the expression regulation in the PWS locus. Nature Publishing Group 2014-09-23 /pmc/articles/PMC4171697/ /pubmed/25246219 http://dx.doi.org/10.1038/srep06445 Text en Copyright © 2014, Macmillan Publishers Limited. All rights reserved http://creativecommons.org/licenses/by-nc-nd/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Galiveti, Chenna R.
Raabe, Carsten A.
Konthur, Zoltán
Rozhdestvensky, Timofey S.
spellingShingle Galiveti, Chenna R.
Raabe, Carsten A.
Konthur, Zoltán
Rozhdestvensky, Timofey S.
Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus
author_facet Galiveti, Chenna R.
Raabe, Carsten A.
Konthur, Zoltán
Rozhdestvensky, Timofey S.
author_sort Galiveti, Chenna R.
title Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus
title_short Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus
title_full Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus
title_fullStr Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus
title_full_unstemmed Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus
title_sort differential regulation of non-protein coding rnas from prader-willi syndrome locus
description Prader-Willi Syndrome (PWS) is a neurogenetic disorder caused by the deletion of imprinted genes on the paternally inherited human chromosome 15q11-q13. This locus harbours a long non-protein-coding RNA (U-UBE3A-ATS) that contains six intron-encoded snoRNAs, including the SNORD116 and SNORD115 repetitive clusters. The 3′-region of U-UBE3A-ATS is transcribed in the cis-antisense direction to the ubiquitin-protein ligase E3A (UBE3A) gene. Deletion of the SNORD116 region causes key characteristics of PWS. There are few indications that SNORD115 might regulate serotonin receptor (5HT2C) pre-mRNA processing. Here we performed quantitative real-time expression analyses of RNAs from the PWS locus across 20 human tissues and combined it with deep-sequencing data derived from Cap Analysis of Gene Expression (CAGE-seq) libraries. We found that the expression profiles of SNORD64, SNORD107, SNORD108 and SNORD116 are similar across analyzed tissues and correlate well with SNORD116 embedded U-UBE3A-ATS exons (IPW116). Notable differences in expressions between the aforementioned RNAs and SNORD115 together with the host IPW115 and UBE3A cis-antisense exons were observed. CAGE-seq analysis revealed the presence of potential transcriptional start sites originated from the U-UBE3A-ATS spanning region. Our findings indicate novel aspects for the expression regulation in the PWS locus.
publisher Nature Publishing Group
publishDate 2014
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4171697/
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