BIOL 483 Lecture Notes - Lecture 50: X-Inactivation, Heterochromatin, Dna Replication
Document Summary
In eukaryotes ename happens at cpg ( c followed by g) or chg or chh in specialised cell types (neurons) Typically dname is a repressive mark -> prevent dna binding proteins and enhance methyl binding proteins that lead to repression. Important for imprinting, x inactivation, genome stability, dysregulated in aging, cancer. Most methyl binding proteins have other repressive chromatin modifiers (hdac, hmt, Important because once c gets methylated, they can be deaminated -> t over time. But cgis (normal expected cpg levels) are unmethylated, differentially methylated - important for tf binding, can be actively demethylated or inaccessible to dnmt. Exist at: promoters -> repressive, unmethylated cgis silenced by polycomb, intragenic -> prevent cryptic transcription, activating, enhancers -> variable methylation states recruit different factors to modulate gene expression. Active: dnmt and tet = active demethylation enzymes, oxidase that convert c -> mc. Passive: methylation not maintained after replication, diluted over time. Overall functional role of modifications are not well understood.
