Abstract
The presence of H3K27me3 has been demonstrated to correlate with the CpG content. In this work, we tested whether H3K27ac has similar sequence preferences. We performed a translocation of DNA sequences with various properties into a beta-globin locus to control for the local chromatin environment. Our results suggest that in contrast to H3K27me3, H3K27ac gain is unlikely affected by the CpG content of the underlying DNA sequence, while extremely high GC-content might contribute to the gain of the H3K27ac.
Highlights
Modification of histone proteins is a key mechanism of epigenetic regulation
The ligation product was transformed into E. coli Top-10 cells, one of the clones was chosen and the insert was confirmed by Sanger sequencing
None of the GC- and CpG rich promoter regions, that were acetylated in their original genomic loci recovered H3K27ac after relocation to a foreign genomic context in the beta globin locus, suggesting that H3K27ac may not depend directly on such features
Summary
Modification of histone proteins is a key mechanism of epigenetic regulation. Histone modifications vary between cells in some genomic locations but not others. This observation raises the question to what extent histone modifications depend on the underlying nucleotide sequences. It has been reported that the attraction of PRC2 complex and consequent H3K27me[3] is positively correlated with the local density of CpG dinucleotides[1]. More complex sequence patterns, such as transcription factor (TF) binding sites (TFBS), affect the presence of histone modifications. SUZ12, a member of the PRC2 complex, binds DNA in a sequence-specific manner and NRCF and ZBTB33 recruit histone deacetylase. The ENCODE project demonstrated a specific histone modification profile around binding sites of many TFs2
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