Search results
Results from the WOW.Com Content Network
Trithorax-group (trxG) proteins maintain the active state of gene expression while the Polycomb-group (PcG) proteins counteract this activation with a repressive function that is stable over many cell generations and can only be overcome by germline differentiation processes.
Methylation of lysines H3K4 and H3K36 is correlated with transcriptional activation while demethylation of H3K4 is correlated with silencing of the genomic region. Methylation of lysines H3K9 and H3K27 is correlated with transcriptional repression. [5] Particularly, H3K9me3 is highly correlated with constitutive heterochromatin. [6]
Histone methylation can be associated with either transcriptional repression or activation. For example, trimethylation of histone H3 at lysine 4 ( H3K4me3 ) is an active mark for transcription and is upregulated in hippocampus one hour after contextual fear conditioning in rats.
In genetics and cell biology, repression is a mechanism often used to decrease or inhibit the expression of a gene. Removal of repression is called derepression.This mechanism may occur at different stages in the expression of a gene, all resulting with increasing the overall RNA or protein products.
EZH2, as a part of PRC2, catalyzes trimethylation of H3K27 (), which is a histone modification that has been characterized as part of the histone code.[16] [20] [21] [22] The histone code is the theory that chemical modifications, such as methylation, acetylation, and ubiquitination, of histone proteins play distinctive roles in epigenetic regulation of gene transcription.
Methylation of lysines H3K4 and H3K36 is correlated with transcriptional activation while demethylation of H3K4 is correlated with silencing of the genomic region. Methylation of lysines H3K9 and H3K27 is correlated with transcriptional repression. [4] Particularly, H3K9me3 is highly correlated with constitutive heterochromatin. [5]
In activators, E2F binding with pRB has been shown to mask the transactivation domain responsible for transcription activation. [5] In repressors E2F4 and E2F5, pocket protein binding (more often p107 and p130 than pRB) mediates recruitment of repression complexes to silence target genes. [6]
Once the pool of LexA decreases, repression of the SOS genes goes down according to the level of LexA affinity for the SOS boxes. [7] Operators that bind LexA weakly are the first to be fully expressed. In this way LexA can sequentially activate different mechanisms of repair.