Can anyone highlight a study or studies in which PolII occupancy at enhancers or promoters was shown to change independently of, or temporarily preceding, changes in epigenetic chromatin marks (e.g. methylation, acetylation)? Looking for concrete examples rather than speculation on whether this is possible or not. More generally, any good papers out there addressing when changes in chromatin marks may be a lagging rather than leading indicator of gene expression?
http://www.ncbi.nlm.nih.gov/pubmed/22231485
Nat Genet. 2012 Jan 8;44(2):148-56. doi: 10.1038/ng.1064.
Tissue-specific analysis of chromatin state identifies temporal signatures of enhancer activity during embryonic development. Eileen Furlong lab.
http://www.ncbi.nlm.nih.gov/pubmed/22231485
Nat Genet. 2012 Jan 8;44(2):148-56. doi: 10.1038/ng.1064.
Tissue-specific analysis of chromatin state identifies temporal signatures of enhancer activity during embryonic development. Eileen Furlong lab.
Defining the Status of RNA Polymerase at Promoters
Leighton J. Core1, Joshua J. Waterfall1, 4, Daniel A. Gilchrist2, David C. Fargo3, Hojoong Kwak1, Karen Adelman2 and John T. Lis
Cell Rep. 2012 Oct 25;2(4):1025-35. doi: 10.1016/j.celrep.2012.08.034. Epub 2012 Oct 10.
Hi Daniel,
That’s a very good question. I am not sure but I know that the opposite situation does occur. The occupancy of Pol II at some gene promoters doesn't change regardless of their chromatin state. On these gene promoters, Pol II occupancy is independent on their transcriptional status. We have had to treat with one of them (MAT2A). At first glance we thought it was an artifact of the antibody used in the ChIP but it wasn’t. At these genes such as C-FOS, C-MYC, etc…Pol II occupancy is independent of the epigenetic signature of the promoter as it can be associated with Co-repressors and can engage in transcription past the first exon (C-MYC) after which it gets somehow derailed.
Thanks for the excellent references! Many of the observation listed in these references or comments relate to poised enhancers, or PolII pausing at TSSes, which leads to detectable PolII occupancy even in non-permissive chromatin states for gene activation.
Can anyone go one step further to highlight cases where PolII occupancy changes in concert with altered transcription factor or co-factor occupancy (setting aside the known examples of elongation factors), but absent any obvious change in histone marks?
It is hard for me to imagine that kind of scenario. The problem is that most of those co-factors are themselves epigenetic factor acting and counteracting. Yes, if you focus on a specific histone modification.
Concerning pol II occupancy, does anyone know what happens, in S. cerevisiae, in a shift from 30-37 ºC for 30 min, in genes like PMA1, PYK1, etc? (I know Pol II occupancy increases in HSP genes and decreases in RP genes).
Hi Daniel. I think this is an interesting question.
This paper below could ultimately help in leading you down a good path. This is what I got for now. It focuses on Pol III but browse all the way through it because there is some relevant info there, especially in Figure 4, I think.
Nat Struct Mol Biol. 2010 May; 17(5): 620–628.
Published online 2010 April 25. doi: 10.1038/nsmb.1801
PMCID: PMC2945309
Human RNA Polymerase III transcriptomes and relationships to Pol II promoters, enhancer-binding factors and chromatin domains
Andrew J. Oler,Ravi K. Alla, Douglas N. Roberts, Alexander Wong, Peter C. Hollenhorst, Katherine J. Chandler, Patrick A. Cassiday, Cassie A. Nelson, Curt H. Hagedorn, Barbara J. Graves, and Bradley R. Cairns
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