High impact information on SUVH4

• Similarly, the KRYPTONITE histone methyltransferase is required for full DNA methylation in Arabidopsis thaliana [1].
• Loss-of-function kryptonite alleles resemble mutants in the DNA methyltransferase gene CHROMOMETHYLASE3 (CMT3), showing loss of cytosine methylation at sites of CpNpG trinucleotides (where N is A, C, G or T) and reactivation of endogenous retrotransposon sequences [2].
• Control of CpNpG DNA methylation by the KRYPTONITE histone H3 methyltransferase [2].
• The H3K27 methylation present at heterochromatin was not affected by mutations in KYP or in several Arabidopsis PcG related genes including the Enhancer of Zeste homologs, suggesting that a novel pathway controls heterochromatic H3K27 methylation [3].
• Our results suggest a model in which H3K9 methylation by KYP, and H3K27 methylation by an unknown enzyme provide a combinatorial histone code for the recruitment of CMT3 to silent loci [3].

Biological context of SUVH4

• H3 lysine 9 methylation is maintained on a transcribed inverted repeat by combined action of SUVH6 and SUVH4 methyltransferases [4].
• PAI1-PAI4 H3 K9 methylation and DNA methylation are also maintained in an suvh6 mutant, which is defective for a gene closely related to SUVH4 [4].
• CMT3 and KYP targets show similar proximal distributions that correspond to the overall distribution of transposable elements of all types, whereas DRM targets are distributed more distally along the chromosome [5].

Associations of SUVH4 with chemical compounds

• The suvh4 suvh5 suvh6 triple mutant loses both monomethyl and dimethyl H3 K9 at target loci [6].

Other interactions of SUVH4

• Also the SUVH1, SUVH2 and SUVH4 proteins represent heterochromatin-associated proteins and display differential effects on control of heterochromatic histone methylation marks [7].
• Moreover, an unmethylated PAI2 gene could be methylated de novo in the suvh4 mutant background [8].
• This histone methylation is dependent on the KRYPTONITE and DDM1 genes (SU[VAR]3-9 and SWI2/SNF2 homologs, respectively) [9].

Analytical, diagnostic and therapeutic context of SUVH4

• Here we use chromatin immunoprecipitation analysis to show that the transcribed inverted repeat carries H3 K9 methylation, which is maintained even in an suvh4 mutant [4].

References