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#H3K9 methylation

2 public questions tagged with this topic.

H3K9 methylation is catalyzed by:

Heterochromatin hallmark histone H3 lysine 9 methylation catalyzed by evolutionary conserved suppressor of variegation 3-9 family enzyme Clr4 in Schizosaccharomyces pombe, mammalian SUV39H1 and SUV39H2 orthologs. Clr4 within CLRC complex comprising Cul4 ubiquitin ligase scaffold, Rik1, Raf1, Raf2, Stc1 adapter transfers methyl group from donor S-adenosylmethionine to H3K9 epsilon amino group producing mono di trimethyl states. H3K9me2 and H3K9me3 recognized by chromodomain proteins Swi6, Chp2, Chp1 aromatic cage mediating chromatin compaction and spreading. Clr4 recruitment requires deacetylated histones and RITS tethering, establishing heterochromatin at centromeres, telomeres, mating type locus crucial for chromosome segregation, sister chromatid cohesion, and genome stability.

Ref: NCBI Bookshelf, Chromatin Modifications: Clr4 – H3K9 Methyltransferase in RNAi Directed Heterochromatin

H3K9 methylation marks:

Histone code marks specific chromatin states. H3 lysine 9 di and trimethylation catalyzed by SUV39H1 and SUV39H2 methyltransferases creates high affinity binding site for heterochromatin protein 1 alpha via its chromodomain, inducing spreading, compaction and transcriptional repression. H3K9 trimethylation enriched at pericentric satellite repeats, subtelomeric repeats and retrotransposons characterizes constitutive heterochromatin, contrasting with H3K4 trimethylation at active promoters. HP1 oligomerization and interaction with DNMTs maintain domain stability. Disruption causes position effect variegation, ectopic transcription and chromosome missegregation defects compromising genome stability severely.

Ref: Bannister et al., Nature 2001; Lodish et al., Molecular Cell Biology, 9th ed., Chapter 8: H3K9 Methylation Heterochromatin Mark