VIM proteins regulate transcription exclusively through the MET1 cytosine methylation pathway

Abstract

In Arabidopsis, variant in methylation (VIM) proteins are required for the maintenance of DNA methylation in the CpG dinucleotide context. VIM1 acts as a cofactor of DNA methyltransferase 1 (MET1), although the mechanism for this co-regulation remains unclear. In this study, we used RNA-seq analysis to profile the transcriptomes of vim1, vim1 vim2 vim3, and met1 null mutants. Consistent with previous studies indicating functional redundancy between these VIM proteins, we found no transcripts that were significantly misregulated in vim1 mutants. However, we identified a large set of VIM protein regulatory targets through analysis of vim1 vim2 vim3 mutants, and we observed that this set is essentially identical to that regulated by MET1. Log2 fold changes in gene expression relative to wild type are strongly correlated between vim1 vim2 vim3 and met1 mutants. While the largest subset of these transcripts is upregulated and enriched with transposable elements, we also found small subsets of downregulated genes in each mutant, which are enriched with protein-coding genes. Together, these results expand on previous studies that profiled cytosine methylation in the vim1 vim2 vim3 mutant, and show that VIM proteins function in transcriptional regulation via their roles in the MET1 DNA methylation pathway.

Azacitidine (5-AzaC)-treatment and mutations in DNA methylase genes affect embryogenic response and expression of the genes that are involved in somatic embryogenesis in Arabidopsis

“…The VIM1 protein contributes to the recruitment of MET1 to a newly replicated DNA strand (Shook and Richards 2014). Consistent with this, we found that the up-regulation of VIM1 was associated with an increased MET1 transcription in SE.…”

“…The impaired embryogenic capacity of the ddm1 and vim1 mutants (present results) suggests that similar to in planta development, the DNA methylation-related proteins VIM1 and DDM1 support the function of MET1 methylases during SE (Zemach et al 2013;Shook and Richards 2014). The VIM1 protein contributes to the recruitment of MET1 to a newly replicated DNA strand (Shook and Richards 2014).…”

“…DNA methylases cooperate with other proteins and the recruitment of MET1 to DNA requires the activity of the variant in methylation (VIM/ORTHRUS) proteins that recognise the hemimethylated CpG sites that are generated during DNA replication (Shook and Richards 2014). The accession of DNA methyltransferases to DNA is supported by DECREASED IN DNA METHYLATION (DDM1), which is a SWI/SNF chromatin-remodeling factor (Jeddeloh et al 1999).…”

EFFECTOR OF TRANSCRIPTION factors are novel plant‐specific regulators associated with genomic DNA methylation in Arabidopsis

“…Regions which reduced CG methylation in et1‐1 et2‐3 (Fig. b) compared to Col‐0 showed the closest similarity to met1 (DNA METHYLTRANSFERASE 1; Kankel et al ., ) and the triple mutant vim1 vim2 vim3 (VARIANT IN METHYLATION; Shook & Richards, ), both defective for CG‐specific maintenance of methylation.…”

“…PCA of hypomethylated hDMRs in et mutants indicated similarities with met1 and vim123 mutants (Kim et al ., ; Shook & Richards, ). This observation indicated the unspecific loss of methylation in genomic regions which are under control of the DNA methylation maintenance pathway.…”