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First published online August 12, 2008

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Promoter-proximal pausing model JILted

Promoter-proximal pausing, a block to elongation in which RNA polymerase II (Pol II) pauses downstream of the promoter, regulates the transcription of many eukaryotic genes. One recent model suggests that, in Drosophila, JIL-1-dependent phosphorylation of histone H3 at serine 10 (H3S10) releases Pol II from promoter-proximal pausing. But, on p. 2917, Kristen Johansen and colleagues comprehensively refute this model and suggest instead that the transcriptional defects seen in JIL-1 null fly mutants are caused by global chromatin structure alterations. Using several histone H3S10 phosphorylation antibodies and an acid-free polytene chromosome squash protocol, the researchers show that there is no redistribution or upregulation of JIL-1 or histone H3S10 phosphorylation in transcriptionally active puffs in heat-shocked Drosophila salivary glands. They also show that the elongating form of Pol II is present at heat-shock induced puffs in JIL-1 null mutants and that Hsp70 mRNA is robustly transcribed in these mutants. Thus, they conclude, JIL-1-mediated histone H3S10 phosphorylation is not required for Pol II-mediated transcription at active loci in Drosophila.

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RNA polymerase II-mediated transcription at active loci does not require histone H3S10 phosphorylation in Drosophila

Weili Cai, Xiaomin Bao, Huai Deng, Ye Jin, Jack Girton, Jørgen Johansen, and Kristen M. Johansen
Development 2008 135: 2917-2925. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?