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First published online December 20, 2005

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Subduing Su(var)3-9

The formation of heterochromatin - tightly packed, transcriptionally inactive chromosomal DNA - involves a complex arrangement of histone modifications, including histone H3K9 methylation, which, in flies, is catalysed by the methyltransferase Su(var)3-9. Having observed that hypomorphic mutations in JIL-1 (a histone H3S10 kinase) cause heterochromatin to spread to ectopic chromosomal regions in Drosophila, Johansen and colleagues set out to explain why (see p. 229). To do so, they generated flies that carry both a null and a hypomorphic copy of JIL-1, which almost never survive to adulthood. But when these flies carry an additional copy of the Su(var)3-9 gene that has reduced function, they mostly survive, indicating that Su(var)3-9 and JIL-1 function in the same pathway and are antagonistic. From their results, the authors propose that JIL-1 kinase marks transcriptionally active euchromatin - possibly by phosphorylating histone H3S10 - to prevent Su(var)3-9 from triggering the formation of heterochromatin at ectopic locations.

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Related articles in Development:

The JIL-1 histone H3S10 kinase regulates dimethyl H3K9 modifications and heterochromatic spreading in Drosophila

Weiguo Zhang, Huai Deng, Xiaomin Bao, Stephanie Lerach, Jack Girton, Jørgen Johansen, and Kristen M. Johansen
Development 2006 133: 229-235. [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?