Complex exon-intron marking by histone modifications is not determined solely by nucleosome distribution.

It has recently been shown that nucleosome distribution, histone modifications and RNA polymerase II (Pol II) occupancy show preferential association with exons ("exon-intron marking"), linking chromatin structure and function to co-transcriptional splicing in a variety of eukaryotes. Prev...

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Main Authors: Pawandeep Dhami, Peter Saffrey, Alexander W Bruce, Shane C Dillon, Kelly Chiang, Nicolas Bonhoure, Christoph M Koch, Jackie Bye, Keith James, Nicola S Foad, Peter Ellis, Nicholas A Watkins, Willem H Ouwehand, Cordelia Langford, Robert M Andrews, Ian Dunham, David Vetrie
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2010-08-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC2925886?pdf=render
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author Pawandeep Dhami
Peter Saffrey
Alexander W Bruce
Shane C Dillon
Kelly Chiang
Nicolas Bonhoure
Christoph M Koch
Jackie Bye
Keith James
Nicola S Foad
Peter Ellis
Nicholas A Watkins
Willem H Ouwehand
Cordelia Langford
Robert M Andrews
Ian Dunham
David Vetrie
author_facet Pawandeep Dhami
Peter Saffrey
Alexander W Bruce
Shane C Dillon
Kelly Chiang
Nicolas Bonhoure
Christoph M Koch
Jackie Bye
Keith James
Nicola S Foad
Peter Ellis
Nicholas A Watkins
Willem H Ouwehand
Cordelia Langford
Robert M Andrews
Ian Dunham
David Vetrie
author_sort Pawandeep Dhami
collection DOAJ
description It has recently been shown that nucleosome distribution, histone modifications and RNA polymerase II (Pol II) occupancy show preferential association with exons ("exon-intron marking"), linking chromatin structure and function to co-transcriptional splicing in a variety of eukaryotes. Previous ChIP-sequencing studies suggested that these marking patterns reflect the nucleosomal landscape. By analyzing ChIP-chip datasets across the human genome in three cell types, we have found that this marking system is far more complex than previously observed. We show here that a range of histone modifications and Pol II are preferentially associated with exons. However, there is noticeable cell-type specificity in the degree of exon marking by histone modifications and, surprisingly, this is also reflected in some histone modifications patterns showing biases towards introns. Exon-intron marking is laid down in the absence of transcription on silent genes, with some marking biases changing or becoming reversed for genes expressed at different levels. Furthermore, the relationship of this marking system with splicing is not simple, with only some histone modifications reflecting exon usage/inclusion, while others mirror patterns of exon exclusion. By examining nucleosomal distributions in all three cell types, we demonstrate that these histone modification patterns cannot solely be accounted for by differences in nucleosome levels between exons and introns. In addition, because of inherent differences between ChIP-chip array and ChIP-sequencing approaches, these platforms report different nucleosome distribution patterns across the human genome. Our findings confound existing views and point to active cellular mechanisms which dynamically regulate histone modification levels and account for exon-intron marking. We believe that these histone modification patterns provide links between chromatin accessibility, Pol II movement and co-transcriptional splicing.
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spelling doaj.art-be39a3655b4b44df83e077c95434cef82022-12-22T00:09:40ZengPublic Library of Science (PLoS)PLoS ONE1932-62032010-08-0158e1233910.1371/journal.pone.0012339Complex exon-intron marking by histone modifications is not determined solely by nucleosome distribution.Pawandeep DhamiPeter SaffreyAlexander W BruceShane C DillonKelly ChiangNicolas BonhoureChristoph M KochJackie ByeKeith JamesNicola S FoadPeter EllisNicholas A WatkinsWillem H OuwehandCordelia LangfordRobert M AndrewsIan DunhamDavid VetrieIt has recently been shown that nucleosome distribution, histone modifications and RNA polymerase II (Pol II) occupancy show preferential association with exons ("exon-intron marking"), linking chromatin structure and function to co-transcriptional splicing in a variety of eukaryotes. Previous ChIP-sequencing studies suggested that these marking patterns reflect the nucleosomal landscape. By analyzing ChIP-chip datasets across the human genome in three cell types, we have found that this marking system is far more complex than previously observed. We show here that a range of histone modifications and Pol II are preferentially associated with exons. However, there is noticeable cell-type specificity in the degree of exon marking by histone modifications and, surprisingly, this is also reflected in some histone modifications patterns showing biases towards introns. Exon-intron marking is laid down in the absence of transcription on silent genes, with some marking biases changing or becoming reversed for genes expressed at different levels. Furthermore, the relationship of this marking system with splicing is not simple, with only some histone modifications reflecting exon usage/inclusion, while others mirror patterns of exon exclusion. By examining nucleosomal distributions in all three cell types, we demonstrate that these histone modification patterns cannot solely be accounted for by differences in nucleosome levels between exons and introns. In addition, because of inherent differences between ChIP-chip array and ChIP-sequencing approaches, these platforms report different nucleosome distribution patterns across the human genome. Our findings confound existing views and point to active cellular mechanisms which dynamically regulate histone modification levels and account for exon-intron marking. We believe that these histone modification patterns provide links between chromatin accessibility, Pol II movement and co-transcriptional splicing.http://europepmc.org/articles/PMC2925886?pdf=render
spellingShingle Pawandeep Dhami
Peter Saffrey
Alexander W Bruce
Shane C Dillon
Kelly Chiang
Nicolas Bonhoure
Christoph M Koch
Jackie Bye
Keith James
Nicola S Foad
Peter Ellis
Nicholas A Watkins
Willem H Ouwehand
Cordelia Langford
Robert M Andrews
Ian Dunham
David Vetrie
Complex exon-intron marking by histone modifications is not determined solely by nucleosome distribution.
PLoS ONE
title Complex exon-intron marking by histone modifications is not determined solely by nucleosome distribution.
title_full Complex exon-intron marking by histone modifications is not determined solely by nucleosome distribution.
title_fullStr Complex exon-intron marking by histone modifications is not determined solely by nucleosome distribution.
title_full_unstemmed Complex exon-intron marking by histone modifications is not determined solely by nucleosome distribution.
title_short Complex exon-intron marking by histone modifications is not determined solely by nucleosome distribution.
title_sort complex exon intron marking by histone modifications is not determined solely by nucleosome distribution
url http://europepmc.org/articles/PMC2925886?pdf=render
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