H2Av facilitates H3S10 phosphorylation but is not required for heat shock-induced chromatin decondensation or transcriptional elongation

被引:2
作者
Li, Yeran [1 ]
Wang, Chao [1 ]
Cai, Weili [1 ]
Sengupta, Saheli [1 ]
Zavortink, Michael [1 ]
Deng, Huai [1 ]
Girton, Jack [1 ]
Johansen, Jorgen [1 ]
Johansen, Kristen M. [1 ]
机构
[1] Iowa State Univ, Roy J Carver Dept Biochem Biophys & Mol Biol, Ames, IA 50011 USA
来源
DEVELOPMENT | 2017年 / 144卷 / 18期
基金
美国国家卫生研究院;
关键词
JIL-1; kinase; Chromatin structure; Histone H3S10 phosphorylation; Drosophila; H2Av; His2Av; POSITION-EFFECT VARIEGATION; HISTONE H3 PHOSPHORYLATION; JIL-1 TANDEM KINASE; DOSAGE COMPENSATION; IN-VIVO; PROTEIN; VARIANT; HETEROCHROMATIN; SU(VAR)3-9; DOMAIN;
D O I
10.1242/dev.151134
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 H2Av and 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.
引用
收藏
页码:3232 / 3240
页数:9
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