Dicer-dependent turnover of intergenic transcripts from the human beta-globin gene cluster.

The widespread occurrence of intergenic transcription in eukaryotes is increasingly evident. Intergenic transcription in the beta-globin gene cluster has been described in murine and human cells, and models for a role in gene and chromatin activation have been proposed. In this study, we analyze int...

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Autori principali: Haussecker, D, Proudfoot, N
Natura: Journal article
Lingua:English
Pubblicazione: 2005
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author Haussecker, D
Proudfoot, N
author_facet Haussecker, D
Proudfoot, N
author_sort Haussecker, D
collection OXFORD
description The widespread occurrence of intergenic transcription in eukaryotes is increasingly evident. Intergenic transcription in the beta-globin gene cluster has been described in murine and human cells, and models for a role in gene and chromatin activation have been proposed. In this study, we analyze intergenic transcription and the chromatin state throughout the human beta-globin gene cluster and find that the data are not consistent with such activation-linked models. Thus, intergenic transcript levels correlate with neither chromatin activation nor globin gene expression. Instead, we find that intergenic transcripts of the beta-globin gene cluster are specifically upregulated in Dicer-deficient cells. This is accompanied by a shift towards more activated chromatin as indicated by changes in histone tail modifications. Our results strongly implicate RNA interference (RNAi)-related mechanisms in regulating intergenic transcription in the human beta-globin gene cluster and further suggest that RNAi-dependent chromatin silencing in vertebrates is not restricted to the centromeres.
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spelling oxford-uuid:443649b4-7511-4a36-baf4-bd040fb8d2232022-03-26T15:00:11ZDicer-dependent turnover of intergenic transcripts from the human beta-globin gene cluster.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:443649b4-7511-4a36-baf4-bd040fb8d223EnglishSymplectic Elements at Oxford2005Haussecker, DProudfoot, NThe widespread occurrence of intergenic transcription in eukaryotes is increasingly evident. Intergenic transcription in the beta-globin gene cluster has been described in murine and human cells, and models for a role in gene and chromatin activation have been proposed. In this study, we analyze intergenic transcription and the chromatin state throughout the human beta-globin gene cluster and find that the data are not consistent with such activation-linked models. Thus, intergenic transcript levels correlate with neither chromatin activation nor globin gene expression. Instead, we find that intergenic transcripts of the beta-globin gene cluster are specifically upregulated in Dicer-deficient cells. This is accompanied by a shift towards more activated chromatin as indicated by changes in histone tail modifications. Our results strongly implicate RNA interference (RNAi)-related mechanisms in regulating intergenic transcription in the human beta-globin gene cluster and further suggest that RNAi-dependent chromatin silencing in vertebrates is not restricted to the centromeres.
spellingShingle Haussecker, D
Proudfoot, N
Dicer-dependent turnover of intergenic transcripts from the human beta-globin gene cluster.
title Dicer-dependent turnover of intergenic transcripts from the human beta-globin gene cluster.
title_full Dicer-dependent turnover of intergenic transcripts from the human beta-globin gene cluster.
title_fullStr Dicer-dependent turnover of intergenic transcripts from the human beta-globin gene cluster.
title_full_unstemmed Dicer-dependent turnover of intergenic transcripts from the human beta-globin gene cluster.
title_short Dicer-dependent turnover of intergenic transcripts from the human beta-globin gene cluster.
title_sort dicer dependent turnover of intergenic transcripts from the human beta globin gene cluster
work_keys_str_mv AT hausseckerd dicerdependentturnoverofintergenictranscriptsfromthehumanbetaglobingenecluster
AT proudfootn dicerdependentturnoverofintergenictranscriptsfromthehumanbetaglobingenecluster