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

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 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 and 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.

Rebelled epigenome: histone H3S10 phosphorylation and H3S10 kinases in cancer biology and therapy

“…Of note, even though H3S10ph facilitates transcription, it is not a prerequisite for the transcription to occur. In stress-induced system in Drosophila melanogaster, H3S10ph was not upregulated in the genes activated in response to the heat shock, nor was it needed for the transcription of those genes in H3S10 kinase mutant [77,78]. These findings indicate that H3S10ph affects chromatin structure/function both directly and indirectly, by modifying the composition of chromatin binding protein platforms.…”