Isolation and initial characterization of the mouse &lt;i&gt;Dnmt3l&lt;/i&gt; gene

Aapola, Ulla; Lyle, Robert; Krohn, Kai; Antonarakis, Stylianos E.; Peterson, Pärt

doi:10.1159/000056881

Cited by 67 publications

(42 citation statements)

References 13 publications

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“…The identification of the murine DNMT3L gene (Aapola et al, 2001), which is 61% identical to its human counterpart, soon followed. Similarity between DNMT3L and DNMT3a and DNMT3b is restricted mainly to the cysteine-rich region encompassing the PHD/ATRX-like region in the amino terminus of DNMT3L.…”

Section: Dnmt3lmentioning

confidence: 99%

DNA methylation and chromatin – unraveling the tangled web

2002

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Methylation of cytosines within the CpG dinucleotide by DNA methyltransferases is involved in regulating transcription and chromatin structure, controlling the spread of parasitic elements, maintaining genome stability in the face of vast amounts of repetitive DNA, and X chromosome inactivation. Cellular DNA methylation is highly compartmentalized over the mammalian genome and this compartmentalization is essential for embryonic development. When the complicated mechanisms that control which DNA sequences become methylated go awry, a number of inherited genetic diseases and cancer may result. Much new information has recently come to light regarding how cellular DNA methylation patterns may be established during development and maintained in somatic cells. Emerging evidence indicates that various chromatin states such as histone modifications (acetylation and methylation) and nucleosome positioning (modulated by ATP-dependent chromatin remodeling machines) determine DNA methylation patterning. Additionally, various regulatory factors interacting with the DNA methyltransferases may direct them to specific DNA sequences, regulate their enzymatic activity, and allow their use as transcriptional repressors. Continued studies of the connections between DNA methylation and chromatin structure and the DNA methyltransferaseassociated proteins, will likely reveal that many, if not all, epigenetic modifications of the genome are directly connected. Such studies should also yield new insights into treating diseases involving aberrant DNA methylation.

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Section: Dnmt3lmentioning

confidence: 99%

DNA methylation and chromatin – unraveling the tangled web

2002

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“…DNA cytosine-5-methyltrasferase3 Like (DNMT3L) was originally identified by database analysis of the human genome sequences and subsequently a mouse homolog was characterized [26][27][28]. This enzyme lacks amino acids essential for the catalytic activity of methyltransferase.…”

Section: Dna Cytosine-5-methyltrasferase3 Likementioning

confidence: 99%

Dynamic and reversibility of heterochromatic gene silencing in human disease

et al. 2005

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In eukaryotic organisms cellular fate and tissue specific gene expression are regulated by the activity of proteins known as transcription factors that by interacting with specific DNA sequences direct the activation or repression of target genes. The post genomic era has shown that transcription factors are not the unique key regulators of gene expression. Epigenetic mechanisms such as DNA methylation, post-translational modifications of histone proteins, remodeling of nucleosomes and expression of small regulatory RNAs also contribute to regulation of gene expression, determination of cell and tissue specificity and assurance of inheritance of gene expression levels. The relevant contribution of epigenetic mechanisms to a proper cellular function is highlighted by the effects of their deregulation that cooperate with genetic alterations to the development of various diseases and to the establishment and progression of tumors.

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“…The first DNMT to be identified was DNMT1 and it is likely the most important for the maintenance of DNA methylation patterns in the mammalian genome (Bestor et al 1988). More recently four related enzymes, namely DNMT2 , DNMT3a, DNMT3b (Okano et al 1998) and DNMT3L (Aapola et al 2001;Bourc'his et al 2001), have been characterised. Of the DNMTs, only DNMT1, DNMT3a and DNMT3b are thought to methylate DNA in vivo; DNMT3L works in concert with the two other DNMT3 enzymes (Chedin et al 2002;Hata et al 2002;Goll and Bestor 2005).…”

Section: Introductionmentioning

confidence: 99%

Gamete imprinting: setting epigenetic patterns for the next generation

Trasler¹

2006

Reprod. Fertil. Dev.

120

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Abstract. The acquisition of genomic DNA methylation patterns, including those important for development, begins in the germ line. In particular, imprinted genes are differentially marked in the developing male and female germ cells to ensure parent-of-origin-specific expression in the offspring. Abnormalities in imprints are associated with perturbations in growth, placental function, neurobehavioural processes and carcinogenesis. Based, for the most part, on data from the well-characterised mouse model, the present review will describe recent studies on the timing and mechanisms underlying the acquisition and maintenance of DNA methylation patterns in gametes and early embryos, as well as the consequences of altering these patterns.

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Isolation and initial characterization of the mouse <i>Dnmt3l</i> gene

Cited by 67 publications

References 13 publications

DNA methylation and chromatin – unraveling the tangled web

DNA methylation and chromatin – unraveling the tangled web

Dynamic and reversibility of heterochromatic gene silencing in human disease

Gamete imprinting: setting epigenetic patterns for the next generation

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