![]() ![]() ![]() ![]() These data indicate a role of H3K9me3 in restraining genomic distribution and activity of CTCF, with an impact on chromatinīy altering the physical properties of chromatin and providing platforms for the recruitment of effector proteins, histone Increased CTCFīinding to SINE B2 repeats enhanced insulation at hundreds of sites and increased loop formation within topological domainsĬontaining lipopolysaccharide-inducible genes, which correlated with their impaired regulation in response to stimulation. CTCF is an essential regulator of chromatinįolding that restrains DNA looping by cohesin, thus creating boundaries among adjacent topological domains. SINE B2 repeats, a previously unidentified target of SETDB1-mediated repression. In the context of experimentsĪimed at determining the impact of SETDB1 on stimulus-inducible gene expression in macrophages, we found that loss of H3K9me3Ĭaused by SETDB1 depletion was associated with increased recruitment of CTCF to >1600 DNA binding motifs contained within Is recruited to active chromatin domains to silence the expression of endogenous retroviruses. Modification controlling constitutive heterochromatin, gene repression, and silencing of retroelements. Six methyltransferases divide labor in establishing genomic profiles of histone H3 lysine 9 methylation (H3K9me), an epigenomic ![]()
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