期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 25, 期 21, 页码 9724-9733出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.25.21.9724-9733.2005
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资金
- Medical Research Council [G0200452] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
- Medical Research Council [G0200452] Funding Source: researchfish
- MRC [G0200452] Funding Source: UKRI
The widespread occurrence of intergenic transcription in eukaryotes is increasingly evident. Intergenic transcription in the P-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 P-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 P-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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