Practice question

DNA methylation at 5-methylcytosine within CpG context catalyzed by DNMT1 maintenance during replication and DNMT3A/3B de novo enzymes generally correlates with stable gene silencing. Methyl-CpG recruits methyl-binding domain proteins MeCP2, MBD1, MBD2 which recruit histone deacetylase complexes and H3K9 methyltransferases, generating compact repressive chromatin impeding transcription factor access. Promoter methylation blocks initiation and maintains X inactivation and genomic imprinting. Removal via TET-mediated hydroxymethylation restores activity, confirming methylation predominantly represses transcription rather than activating replication or recombination alone in differentiated tissues.