Novel Cell Lines Isolated From Mouse Embryonic Stem Cells Exhibiting De Novo Methylation of the E-Cadherin Promoter

Stem Cells ◽  
2014 ◽  
Vol 32 (11) ◽  
pp. 2869-2879 ◽  
Author(s):  
Kate Hawkins ◽  
Maria Keramari ◽  
Francesca Soncin ◽  
Joe M. Segal ◽  
Lisa Mohamet ◽  
...  
2017 ◽  
Vol 50 (1) ◽  
pp. 83-95 ◽  
Author(s):  
Nipun Verma ◽  
Heng Pan ◽  
Louis C. Doré ◽  
Abhijit Shukla ◽  
Qing V. Li ◽  
...  

PLoS ONE ◽  
2011 ◽  
Vol 6 (7) ◽  
pp. e21463 ◽  
Author(s):  
Francesca Soncin ◽  
Lisa Mohamet ◽  
Sarah Ritson ◽  
Kate Hawkins ◽  
Nicoletta Bobola ◽  
...  

Stem Cells ◽  
2009 ◽  
Vol 27 (9) ◽  
pp. 2069-2080 ◽  
Author(s):  
Francesca Soncin ◽  
Lisa Mohamet ◽  
Dominik Eckardt ◽  
Sarah Ritson ◽  
Angela M. Eastham ◽  
...  

Gene ◽  
2002 ◽  
Vol 289 (1-2) ◽  
pp. 41-48 ◽  
Author(s):  
Jonathan E. Dodge ◽  
Bernard H. Ramsahoye ◽  
Z.Galen Wo ◽  
Masaki Okano ◽  
En Li

2019 ◽  
Author(s):  
Botao Zhao ◽  
Chunsun Fan

AbstractMicroRNAs (miRNAs) are a class of non-coding small RNAs that function in almost every known cellular activity. MiRNAs play an important role in gene regulation that controls embryonic stem cell (ESC) pluripotency and differentiation, as well as induced pluripotent stem cell (iPSC) reprogramming. In this study, we identified nine novel miRNAs by mining the deep sequencing dataset from mouse embryonic stem cells, mouse embryonic fibroblasts (MEF) and three kinds of reprogrammed pluripotent cells. Most of them are non-conserved but species-specific and cell-specific miRNAs. Eight miRNAs are derived from gene introns, including a “mirtron” miRNA, miR-novel-41. We also showed that miR-novel-27 is a mouse-specific miRNA and the 5′ arm of its precursor hairpin, embedding the mature miR-novel-27, uniquely exists in mouse species but not in any other Placentalia animals. Notably, the 5′ arm of the pre-miR-novel-27 hairpin shows nearly perfect palindrome to the 3′ arm suggesting that it was generated by inverted duplication of the 3′ arm. By this mechanism, the pre-miR-novel-27 hairpin was de novo gained in the mouse genome. This is a new type of de novo miRNA emergence mechanism in animals, which we called “inverted local half hairpin duplication” here. In addition, very limited nucleotide mutants accumulated on the newly emerged 5′ arm since its birth suggesting an especially young evolutionary history of the miR-novel-27 gene.


Development ◽  
1996 ◽  
Vol 122 (10) ◽  
pp. 3195-3205 ◽  
Author(s):  
H. Lei ◽  
S.P. Oh ◽  
M. Okano ◽  
R. Juttermann ◽  
K.A. Goss ◽  
...  

It has been a controversial issue as to how many DNA cytosine methyltransferase mammalian cells have and whether de novo methylation and maintenance methylation activities are encoded by a single gene or two different genes. To address these questions, we have generated a null mutation of the only known mammalian DNA methyltransferase gene through homologous recombination in mouse embryonic stem cells and found that the development of the homozygous embryos is arrested prior to the 8-somite stage. Surprisingly, the null mutant embryonic stem cells are viable and contain low but stable levels of methyl cytosine and methyltransferase activity, suggesting the existence of a second DNA methyltransferase in mammalian cells. Further studies indicate that de novo methylation activity is not impaired by the mutation as integrated provirus DNA in MoMuLV-infected homozygous embryonic stem cells become methylated at a similar rate as in wild-type cells. Differentiation of mutant cells results in further reduction of methyl cytosine levels, consistent with the de novo methylation activity being down regulated in differentiated cells. These results provide the first evidence that an independently encoded DNA methyltransferase is present in mammalian cells which is capable of de novo methylating cellular and viral DNA in vivo.


2008 ◽  
Vol 15 (3) ◽  
pp. 259-267 ◽  
Author(s):  
Lasse Sinkkonen ◽  
Tabea Hugenschmidt ◽  
Philipp Berninger ◽  
Dimos Gaidatzis ◽  
Fabio Mohn ◽  
...  

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Marie MacLennan ◽  
Marta García-Cañadas ◽  
Judith Reichmann ◽  
Elena Khazina ◽  
Gabriele Wagner ◽  
...  

Mobilization of retrotransposons to new genomic locations is a significant driver of mammalian genome evolution, but these mutagenic events can also cause genetic disorders. In humans, retrotransposon mobilization is mediated primarily by proteins encoded by LINE-1 (L1) retrotransposons, which mobilize in pluripotent cells early in development. Here we show that TEX19.1, which is induced by developmentally programmed DNA hypomethylation, can directly interact with the L1-encoded protein L1-ORF1p, stimulate its polyubiquitylation and degradation, and restrict L1 mobilization. We also show that TEX19.1 likely acts, at least in part, through promoting the activity of the E3 ubiquitin ligase UBR2 towards L1-ORF1p. Moreover, loss of Tex19.1 increases L1-ORF1p levels and L1 mobilization in pluripotent mouse embryonic stem cells, implying that Tex19.1 prevents de novo retrotransposition in the pluripotent phase of the germline cycle. These data show that post-translational regulation of L1 retrotransposons plays a key role in maintaining trans-generational genome stability in mammals.


1990 ◽  
Vol 10 (8) ◽  
pp. 4396-4400 ◽  
Author(s):  
M Szyf ◽  
G Tanigawa ◽  
P L McCarthy

Although DNA can be extensively methylated de novo when introduced into pluripotent cells, the CpG island in the Thy-1 gene does not become methylated either in the mouse embryo or in embryonic stem cells. A 214-base-pair region near the promoter of the Thy-1 gene protects itself as well as heterologous DNA sequences from de novo methylation. We propose that this nucleotide sequence is representative of a class of important signals that limits de novo methylation in the embryo and establishes the pattern of hypomethylated CpG dinucleotides found in somatic tissues.


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