Campus Units

Biochemistry, Biophysics and Molecular Biology, Roy J. Carver Department of

Document Type

Article

Publication Version

Published Version

Publication Date

2006

Journal or Book Title

Development

Volume

133

Issue

2

First Page

229

Last Page

235

DOI

10.1242/dev.02199

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.

Comments

This article is published as Zhang, Weiguo, Huai Deng, Xiaomin Bao, Stephanie Lerach, Jack Girton, Jørgen Johansen, and Kristen M. Johansen. "The JIL-1 histone H3S10 kinase regulates dimethyl H3K9 modifications and heterochromatic spreading in Drosophila." Development 133, no. 2 (2006): 229-235. doi: 10.1242/dev.02199. Posted with permission.

Copyright Owner

The Authors

Language

en

File Format

application/pdf

Share

COinS