JIL-1 and Transcriptionn Figure 8. Correlations of H3K36me3, H4K16ac, and JIL-1 binding. Pair-wise correlations of JIL-1 versus ePol, H3K36me3, H4K16ac and the sum of H3K36me3 and H4K16ac signals in unified 200 bp sampling windows. (A) Results for the X chromosome (B) for autosomes (C) and for the entire genome. Pearson correlation coefficients are provided for each panel. doi:10.1371/journal.pgen.1001327.g008 chromosome except for JIL-1 and the JIL-1-dependent phospho- acetyl mark. An appealing model for JIL-1 targeting is that its general recruitment mode (correlating with H3K36me3) would be the same on all chromosomes. The additional presence of H4K16ac might enhance the access of JIL-1 to the first targeting principle, since it has been shown that H4K16ac prevents the folding of the nucleosomal fibre into more compact structures [27]. Effects of H3S10 phosphorylation by JIL-1 It has been observed that histone H3S10ph can enhance acetylation of histone H3K14 [50,51] and inhibit methylation of histone H3K9 [52]. The biochemical analysis of JIL-1 kinase showed that a number of other modifications of the H3 N- terminus are compatible with the phosphorylation by JIL-1. Therefore, JIL-1 phosphorylation is compatible with the prior existence of other modifications, consistent with a downstream function of JIL-1. Our data suggest that in Drosophila the function of H3S10ph may at least in part differ from that in other organisms, where it is implicated in the fast and transient induction of promoters in response to various inducers [13,16,53,54]. In Drosophila, JIL-1 is not particularly enriched at promoters, but associates with genes along their entire length. This distribution is more compatible with a role in fine-tuning transcriptional elongation. The effects of JIL-1 may – at least in part – be mediated by 14-3-3 proteins, which are able to recognize the interphase H3S10ph mark [17,54]. The depletion of JIL-1 has a clear but small effect on overall transcription. The fact that JIL-1 binds gene bodies rather that promoters and the the binding is independent of actual transcription rates leads us to speculate that the kinase may influence transcription efficiency only very indirectly by reinforc- ing the active chromatin state – once established by co-activators – by protecting it from neighbouring repressive chromatin. This could become important when moderately active genes are not PLoS Genetics | www.plosgenetics.org 12 March 2011 | Volume 7 | Issue 3 | e1001327