Letter abstract


Nature Genetics 39, 1512 - 1516 (2007)
Published online: 11 November 2007 | doi:10.1038/ng.2007.26

RNA polymerase stalling at developmental control genes in the Drosophila melanogaster embryo

Julia Zeitlinger1,7, Alexander Stark2,3, Manolis Kellis2,3, Joung-Woo Hong4, Sergei Nechaev5, Karen Adelman5, Michael Levine4 & Richard A Young1,6

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It is widely assumed that the key rate-limiting step in gene activation is the recruitment of RNA polymerase II (Pol II) to the core promoter1. Although there are well-documented examples in which Pol II is recruited to a gene but stalls2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, a general role for Pol II stalling in development has not been established. We have carried out comprehensive Pol II chromatin immunoprecipitation microarray (ChIP-chip) assays in Drosophila embryos and identified three distinct Pol II binding behaviors: active (uniform binding across the entire transcription unit), no binding, and stalled (binding at the transcription start site). The notable feature of the approx10% genes that are stalled is that they are highly enriched for developmental control genes, which are either repressed or poised for activation during later stages of embryogenesis. We propose that Pol II stalling facilitates rapid temporal and spatial changes in gene activity during development.

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  1. Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA.
  2. Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts 02141, USA.
  3. Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
  4. Department of Molecular Cell Biology, Center for Integrative Genomics, University of California, Berkeley, California 94720, USA.
  5. Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA.
  6. Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
  7. Present address: Stowers Institute for Medical Research, 1000 East 50th St., Kansas City, Missouri 64110, USA.

Correspondence to: Michael Levine4 e-mail: mlevine@berkeley.edu

Correspondence to: Richard A Young1,6 e-mail: young@wi.mit.edu



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