Campus Units

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

Document Type

Article

Publication Version

Published Version

Publication Date

2017

Journal or Book Title

Development

Volume

144

Issue

18

First Page

3232

Last Page

3240

DOI

10.1242/dev.151134

Abstract

A model has been proposed in which JIL-1 kinase-mediated H3S10 and H2Av phosphorylation is required for transcriptional elongation and heat shock-induced chromatin decondensation. However, here we show that although H3S10 phosphorylation is indeed compromised in the H2Av null mutant, chromatin decondensation at heat shock loci is unaffected in the absence of JIL-1 as well as of H2Av and that there is no discernable decrease in the elongating form of RNA polymerase II in either mutant. Furthermore, mRNA for the major heat shock protein Hsp70 is transcribed at robust levels in both H2Avand JIL-1 null mutants. Using a different chromatin remodeling paradigm that is JIL-1 dependent, we provide evidence that ectopic tethering of JIL-1 and subsequent H3S10 phosphorylation recruits PARP-1 to the remodeling site independently of H2Av phosphorylation. These data strongly suggest that H2Av or H3S10 phosphorylation by JIL-1 is not required for chromatin decondensation or transcriptional elongation in Drosophila.

Comments

This article is published as Li, Yeran, Chao Wang, Weili Cai, Saheli Sengupta, Michael Zavortink, Huai Deng, Jack Girton, Jørgen Johansen, and Kristen M. Johansen. "H2Av facilitates H3S10 phosphorylation but is not required for heat shock-induced chromatin decondensation or transcriptional elongation." Development 144, no. 18 (2017): 3232-3240. doi: 10.1242/dev.151134. Posted with permission.

Copyright Owner

The Authors

Language

en

File Format

application/pdf

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