The histone code hypothesis represents a useful paradigm for understanding how histone marks deposited by writer proteins (for example, HMTs) recruit mark readers to gene promoters, which triggers the transition between permissive and non-permissive chromatin that ultimately regulates gene transcription.
Less is known about the role of these factors in recruiting negative marks of transcription to their target genes when the cells exit the cell cycle and reach a postmitotic status.
Apparently, a move towards online marking left the OCR without half the markers it previously had recruited to mark the Classical Civilisation exam papers.
The 19S regulatory complex recruits substrates marked for degradation and prepares them for translocation into the 20S core complex.
In good agreement with our data, it has been reported that several vertebrate transcription factors involved in the cell cycle progression recruit active marks of transcription.
In this context, EZH2-containing repressive complexes are further recruited, fully "marking" the histones via H3K27 methylation to establish a stable PPARG silencing by blocking transcription elongation (Figure 6).
More complex scenarios are of course possible such as phosphorylated H3T45 acting as binding platform for recruiting a histone mark reader which then coordinates H3K56 acetylation.
This histone mark recruits the BMI1-containing PRC1 that silences the genes marked by PRC2.
PRC2 and its constituent enzyme EZH2 stimulate H3K27 trimethylation 7; this epigenetic mark recruits PRC1, a stimulator of chromatin compaction.
Although trimethylation in the H3 K9 mark recruits HP1 and contributes for condensed heterochromatin, the mono- and di-methylations of the same have been associated with regulatory repressive function in euchromatic regions.
