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, Kristen M. Johansen

Research output: Contribution to journalArticlepeer-review

92 Scopus citations

Abstract

In this study, we show that a reduction in the levels of the JIL-1 histone H3S10 kinase results in the spreading of the major heterochromatin markers dimethyl H3K9 and HP1 to ectopic locations on the chromosome arms, with the most pronounced increase on the X chromosomes. Genetic interaction assays demonstrated that JIL-1 functions in vivo in a pathway that includes Su(var)3-9, which is a major catalyst for dimethylation of the histone H3K9 residue, HP1 recruitment, and the formation of silenced heterochromatin. We further provide evidence that JIL-1 activity and localization are not affected by the absence of Su(var)3-9 activity, suggesting that JIL-1 is upstream of Su(var)3-9 in the pathway. Based on these findings, we propose a model where JIL-1 kinase activity functions to maintain euchromatic regions by antagonizing Su(var)3-9-mediated heterochromatization.

Original languageEnglish (US)
Pages (from-to)229-235
Number of pages7
JournalDevelopment
Volume133
Issue number2
DOIs
StatePublished - Jan 2006

Keywords

  • Chromatin
  • Drosophila
  • HP1
  • Histone modifications
  • JIL-1 kinase

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