TET1 is a DNA-binding protein that modulates DNA methylation and gene transcription via hydroxylation of 5-methylcytosine

Zhang, Haikuo; Zhang, Xin; Clark, Erin; Mulcahey, Michelle A.; Huang, Stephen; Shi, Yujiang Geno

doi:10.1038/cr.2010.156

Cited by 171 publications

(134 citation statements)

References 10 publications

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“…This is possibly due to the presence of a CpG-binding CXXC zinc finger domain in Tet1 ( Fig. 1; Iyer et al 2009;Zhang et al 2010). Interestingly, the CXXC domain has also been found in other epigenetic regulators such as Cfp1 (CXXC finger protein 1) and the H3K36me2 (dimethylated H3K36) histone demethylase Kdm2a that are enriched at unmethylated CGIs (Blackledge et al 2010;Thomson et al 2010), raising the possibility that these CXXC domain-containing proteins may cooperate in contributing to the establishment of a transcriptionally permissive chromatin state at CGIs (Deaton and Bird 2011).…”

Section: Genomic Distribution Of Tet1 and 5hmc And Their Role In Tramentioning

confidence: 99%

Mechanisms and functions of Tet protein-mediated 5-methylcytosine oxidation

Wu¹,

Zhang²

2011

Genes Dev.

581

497

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Ten-eleven translocation 1-3 (Tet1-3) proteins have recently been discovered in mammalian cells to be members of a family of DNA hydroxylases that possess enzymatic activity toward the methyl mark on the 5-position of cytosine (5-methylcytosine [5mC]), a well-characterized epigenetic modification that has essential roles in regulating gene expression and maintaining cellular identity. Tet proteins can convert 5mC into 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC) through three consecutive oxidation reactions. These modified bases may represent new epigenetic states in genomic DNA or intermediates in the process of DNA demethylation. Emerging biochemical, genetic, and functional evidence suggests that Tet proteins are crucial for diverse biological processes, including zygotic epigenetic reprogramming, pluripotent stem cell differentiation, hematopoiesis, and development of leukemia. Insights into how Tet proteins contribute to dynamic changes in DNA methylation and gene expression will greatly enhance our understanding of epigenetic regulation of normal development and human diseases.

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Section: Genomic Distribution Of Tet1 and 5hmc And Their Role In Tramentioning

confidence: 99%

Mechanisms and functions of Tet protein-mediated 5-methylcytosine oxidation

Wu¹,

Zhang²

2011

Genes Dev.

581

497

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“…11 However, we note that this conclusion is in direct contrast with a previous study demonstrating a role of Tet1 enzymatic activity in transcriptional regulation. 16 Further studies are needed to determine whether the capacity of Tet1 in regulating gene expression requires its enzymatic activity.…”

Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tmentioning

confidence: 99%

“…preference of Tet1 for CGI-containing gene promoters, probably due to the fact that Tet1 possesses a CXXC zinc-finger domain, which has a high affinity for nonmethylated CpG sequences. 16 The convergence of multiple CXXC domain containing epigenetic regulators such as Cfp1, 17 Kdm2a, 18 and Tet1 at CpG-rich sequences indicates that they may synergistically contribute to the establishment of a distinct chromatin environment at CGIs. In this scenario, Cfp1 confers trimethylation of lysine 4 on histone 3 (H3K4me3) by recruiting the H3K4me3 methyltransferase Setd1; Kdm2a binding results in the depletion of H3K36me2; Tet1 maintains a DNA hypomethylated state at CGIs.…”

Section: Introductionmentioning

confidence: 99%

Tet1 and 5-hydroxymethylation

Zhang

2011

Cell Cycle

115

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“…Following these two studies, many other laboratories have confirmed and extended these results using various methods. [24][25][26][27]30,31 5hmC as an Intermediate of Active DNA Demethylation: Indirect Evidence…”

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confidence: 99%

“…35 Shi and colleagues reported that TET1 overexpression led to active demethylation of artificially methylated plasmid DNA. 31 The TET1 gene was originally identified through its translocation in acute myeloid leukemia (AML). 36,37 Later, TET2 was also found to be frequently mutated in various forms of myeloid malignancies.…”

mentioning

confidence: 99%