Millipore Home

• Home
• Products
• Services
• Learning Center
• Tech Library
• Support
• Company

Product Reference

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

Author	Dirk Haussecker, Nicholas J Proudfoot
Citation Information	Molecular and cellular biology, 25:9724-33 (2005)
Keywords	Centromere, Chromatin, DNA, Intergenic, Globins, Hela Cells, Histones, Humans, Multigene Family, RNA Interference, Ribonuclease III, Transcription, Genetic
Related Products	07-030
Pub Med ID	16227618

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.