Thank you very much! It becomes clearer. So, is it true that the data from the Chip-seq experiment correspond to the active state? Or is it an inactive state, but with histone marks that are there all the time?
Hello!
I'm trying to deal with histone mark and their localization on the genome. I read that marks H3K4me3 are localized in the promoter regions. But I know that promoters are free of nucleosomes. How is this possible? Do I understand correctly that the presence of histone marks from an experiment Chip-seq means the presence of a nucleosome in this region? I read several articles, but did not find the answer.
I will be glad to any answer, especially useful articles on this topic.
1 answer
Promoters are not free of nucleosomes but there is a nucleosome-free stretch of DNA at which the DNA-binding machinery assembles. This is flanked by histones that undergo modifications at, e.g. their lysin tails (K4).

From what I understand H3K4me3 is often referred to as a "promoter mark", even though it boils down to an indication for active transcription.
There is some research that has found H3K4me3 is generally found in all high CpG promoters (the majority in human) regardless of transcriptional activity, but are only present at low CpG promoters when the gene is actively transcribed (https://www.nature.com/articles/nature06008 ). H3K27ac may be more predictive of active transcription at promoters/TSS than H3K4me3 (see https://www.pnas.org/content/107/7/2926 ).
Thank you for these articles! Exactly what is needed!
While interesting literature, be aware that many of these "old" papers are based on a selection of regions using ChIP-Chip experiments instead of ChIP-seq. It therefore might well be that the results, while accurate for the regions the authors investigated, might not be as representative for the entire genome and all classes of regulatory elements and genes as one might imagine. If you scan the literature that follows up on this, H3K27ac seems to be more associated to distal regulatory elements while H3K4me3 kind of got a reputation to be a promoter/TSS mark that is (if memory serves) associated with (among others) paused polymerase processes etc.
Both papers I linked used ChIP-seq data, not ChIP-Chip. The Nature paper is, I believe, the paper that introduced ChIP-seq.
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