High impact information on MET1

• AGO4 is also found, along with the DNA methyltransferase DRM2, throughout the nucleus at presumed DNA methylation target sites [1].
• Whole-genome tiling-array transcriptional profiling of DNA methyltransferase null mutants identified hundreds of genes and intergenic noncoding RNAs with altered expression levels, many of which may be epigenetically controlled by DNA methylation [2].
• Here we show, however, that depletion of A. thaliana MET1, a homolog of mammalian Dnmt1 (ref. 8), results in immense epigenetic diversification of gametes [3].
• A gene essential for de novo methylation and development in Ascobolus reveals a novel type of eukaryotic DNA methyltransferase structure [4].
• 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 [5].

Biological context of MET1

• The plant genome also has 5-methylcytosine at CpG dinucleotides, which is maintained by METHYLTRANSFERASE1 (MET1), a homolog of Dnmt1 [6].
• Here, we show that Arabidopsis thaliana embryos with loss-of-function mutations in MET1 and CMT3 develop improperly, display altered planes and numbers of cell division, and have reduced viability [6].
• The drm1 drm2 cmt3 triple mutant plants did not affect CpG methylation at any locus tested, suggesting that the primary CpG methylases are encoded by the MET1 class of genes [7].
• In addition, plants have DNA methylation at CpNpG and CpNpN sites, maintained, in part, by the CHROMOMETHYLASE3 (CMT3) DNA methyltransferase [6].
• However, due to the dominant nature of the antisense MET1 transgene, the parent with a hypomethylated genome, its gametophyte, and both the maternal and paternal genomes of the F(1) seed become hypomethylated [8].

Associations of MET1 with chemical compounds

• Genes that specify embryo cell identity are misexpressed, and auxin hormone gradients are not properly formed in abnormal met1 embryos [6].
• DDM1 and MET1 control heterochromatin assembly at chromocenters by their influence on DNA maintenance (CpG) methylation and subsequent methylation of histone H3 lysine 9 [9].
• The female-gametophytic effects on embryo and endosperm development in the Arabidopsis mea, fis, and fie mutants appear to be due to gametic imprinting that can be suppressed by METHYL TRANSFERASE1 antisense (MET1 a/s) transgene expression or by mutation of the DECREASE IN DNA METHYLATION1 (DDM1) gene [10].
• Arabidopsis plants transformed with an antisense construct of an Arabidopsis methyltransferase cDNA (METI) have reduced cytosine methylation in CG dinucleotides [11].
• Treatment with 5-aza-2'-deoxycytidine, an inhibitor of DNA methyltransferase, resulted in the development of altered morphologies in the synthetic allotetraploids, but not in the parents [12].

Regulatory relationships of MET1

• DME activates whereas MET1 suppresses maternal MEA::GFP allele expression in the central cell [13].

Other interactions of MET1

• MET1 is required for DNA methylation of three regions in the MEA promoter in seeds [13].
• Our data suggest that imprinting is controlled in the female gametophyte by antagonism between the two DNA-modifying enzymes, MET1 methyltransferase and DME DNA glycosylase [13].
• Nevertheless, comparison to CMT1 of Cardaminopsis arenosa, an outcrossing relative, indicates conservation for DNA methyltransferase function [14].
• The Arabidopsis DDM1 gene is required for the maintenance of genomic methylation patterns but is a helicase homolog of the SWI2/SNF2 family rather than a DNA methyltransferase [15].
• The FWA imprint depends on the maintenance DNA methyltransferase MET1, as is the case in mammals [16].

References