VIM proteins regulate transcription exclusively through the MET1 cytosine methylation pathway.
VIM proteins regulate transcription exclusively through the MET1 cytosine methylation pathway.
复制标题
VIM蛋白专门通过MET1胞嘧啶甲基化途径调节转录。
DOI：
10.4161/epi.28906
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发表时间：
2014-07
期刊：
影响因子：
3.7
通讯作者：
Richards EJ
中科院分区：
文献类型：
--
作者：
Shook MS;Richards EJ
在拟南芥中，甲基化变体（Vim）蛋白是维持CpG二核苷酸背景下的DNA甲基化所必需的。VIM 1作为DNA甲基转移酶1（MET 1）的辅因子，尽管这种共调节的机制仍不清楚。在这项研究中，我们使用RNA-seq分析来分析vim 1，vim 1 vim 2 vim 3和met 1无效突变体的转录组。与以前的研究表明，这些Vim蛋白之间的功能冗余一致，我们没有发现明显失调的VIM 1突变体的转录本。然而，我们通过分析vim 1 vim 2 vim 3突变体确定了大量的Vim蛋白调控靶点，我们观察到这一组与MET 1调控的靶点基本相同。相对于野生型，基因表达的对数2倍变化在vim 1、vim 2、vim 3和met 1突变体之间强烈相关。虽然这些转录本的最大子集是上调和丰富的转座因子，我们也发现在每个突变体，这是丰富的蛋白质编码基因的下调基因的小子集。总之，这些结果扩展了以前的研究，在vim 1 vim 2 vim 3突变体中的胞嘧啶甲基化，并表明Vim蛋白通过其在MET 1 DNA甲基化途径中的作用在转录调控中发挥作用。
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.