Faculty Opinions recommendation of De novo DNA methylation activity of methyltransferase 1 (MET1) partially restores body methylation in Arabidopsis thaliana.

Author(s):  
Elizabeth Dennis
PLoS Genetics ◽  
2010 ◽  
Vol 6 (10) ◽  
pp. e1001182 ◽  
Author(s):  
Ian R. Henderson ◽  
Angelique Deleris ◽  
William Wong ◽  
Xuehua Zhong ◽  
Hang Gyeong Chin ◽  
...  

2009 ◽  
Vol 16 (12) ◽  
pp. 1325-1327 ◽  
Author(s):  
Israel Ausin ◽  
Todd C Mockler ◽  
Joanne Chory ◽  
Steven E Jacobsen

2016 ◽  
Vol 113 (14) ◽  
pp. E2083-E2092 ◽  
Author(s):  
Mélanie Rigal ◽  
Claude Becker ◽  
Thierry Pélissier ◽  
Romain Pogorelcnik ◽  
Jane Devos ◽  
...  

Genes and transposons can exist in variable DNA methylation states, with potentially differential transcription. How these epialleles emerge is poorly understood. Here, we show that crossing an Arabidopsis thaliana plant with a hypomethylated genome and a normally methylated WT individual results, already in the F1 generation, in widespread changes in DNA methylation and transcription patterns. Novel nonparental and heritable epialleles arise at many genic loci, including a locus that itself controls DNA methylation patterns, but with most of the changes affecting pericentromeric transposons. Although a subset of transposons show immediate resilencing, a large number display decreased DNA methylation, which is associated with de novo or enhanced transcriptional activation and can translate into transposon mobilization in the progeny. Our findings reveal that the combination of distinct epigenomes can be viewed as an epigenomic shock, which is characterized by a round of epigenetic variation creating novel patterns of gene and TE regulation.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Roza H. Ali Masalmeh ◽  
Francesca Taglini ◽  
Cristina Rubio-Ramon ◽  
Kamila I. Musialik ◽  
Jonathan Higham ◽  
...  

AbstractThe aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.


2017 ◽  
Author(s):  
James Walker ◽  
Hongbo Gao ◽  
Jingyi Zhang ◽  
Billy Aldridge ◽  
Martin Vickers ◽  
...  

SUMMARYDNA methylation controls eukaryotic gene expression and is extensively reprogrammed to regulate animal development. However, whether developmental methylation reprogramming during the sporophytic life cycle of flowering plants regulates genes is presently unknown. Here we report a distinctive, gene-targeted RNA-directed DNA methylation (RdDM) activity in the Arabidopsis thaliana male sexual lineage that regulates gene expression in meiocytes. Loss of sexual lineage-specific RdDM causes mis-splicing of the MPS1/PRD2 gene, thereby disrupting meiosis. Our results establish a regulatory paradigm in which de novo methylation creates a cell-lineage-specific epigenetic signature that controls gene expression and contributes to cellular function in flowering plants.


Author(s):  
Chuck Haggerty ◽  
Helene Kretzmer ◽  
Christina Riemenschneider ◽  
Abhishek Sampath Kumar ◽  
Alexandra L. Mattei ◽  
...  

AbstractDNA methylation plays a critical role during development, particularly in repressing retrotransposons. The mammalian methylation landscape is dependent on the combined activities of the canonical maintenance enzyme Dnmt1 and the de novo Dnmts, 3a and 3b. Here, we demonstrate that Dnmt1 displays de novo methylation activity in vitro and in vivo with specific retrotransposon targeting. We used whole-genome bisulfite and long-read Nanopore sequencing in genetically engineered methylation-depleted mouse embryonic stem cells to provide an in-depth assessment and quantification of this activity. Utilizing additional knockout lines and molecular characterization, we show that the de novo methylation activity of Dnmt1 depends on Uhrf1, and its genomic recruitment overlaps with regions that enrich for Uhrf1, Trim28 and H3K9 trimethylation. Our data demonstrate that Dnmt1 can catalyze DNA methylation in both a de novo and maintenance context, especially at retrotransposons, where this mechanism may provide additional stability for long-term repression and epigenetic propagation throughout development.


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