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  • 1
    Publication Date: 2011-07-23
    Description: 5-methylcytosine (5mC) in DNA plays an important role in gene expression, genomic imprinting, and suppression of transposable elements. 5mC can be converted to 5-hydroxymethylcytosine (5hmC) by the Tet (ten eleven translocation) proteins. Here, we show that, in addition to 5hmC, the Tet proteins can generate 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC) from 5mC in an enzymatic activity-dependent manner. Furthermore, we reveal the presence of 5fC and 5caC in genomic DNA of mouse embryonic stem cells and mouse organs. The genomic content of 5hmC, 5fC, and 5caC can be increased or reduced through overexpression or depletion of Tet proteins. Thus, we identify two previously unknown cytosine derivatives in genomic DNA as the products of Tet proteins. Our study raises the possibility that DNA demethylation may occur through Tet-catalyzed oxidation followed by decarboxylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495246/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495246/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Shinsuke -- Shen, Li -- Dai, Qing -- Wu, Susan C -- Collins, Leonard B -- Swenberg, James A -- He, Chuan -- Zhang, Yi -- GM071440/GM/NIGMS NIH HHS/ -- GM68804/GM/NIGMS NIH HHS/ -- P30 ES010126/ES/NIEHS NIH HHS/ -- P30 ES010126-11/ES/NIEHS NIH HHS/ -- P30ES10126/ES/NIEHS NIH HHS/ -- P42 ES005948/ES/NIEHS NIH HHS/ -- P42 ES005948-17/ES/NIEHS NIH HHS/ -- P42ES5948/ES/NIEHS NIH HHS/ -- R01 GM068804/GM/NIGMS NIH HHS/ -- U01 DK089565/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1300-3. doi: 10.1126/science.1210597. Epub 2011 Jul 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21778364" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/*metabolism ; Animals ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; DNA/*metabolism ; DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells/metabolism ; Humans ; Mice ; Oxidation-Reduction ; Proto-Oncogene Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1998-09-04
    Description: The adenomatous polyposis coli gene (APC) is a tumor suppressor gene that is inactivated in most colorectal cancers. Mutations of APC cause aberrant accumulation of beta-catenin, which then binds T cell factor-4 (Tcf-4), causing increased transcriptional activation of unknown genes. Here, the c-MYC oncogene is identified as a target gene in this signaling pathway. Expression of c-MYC was shown to be repressed by wild-type APC and activated by beta-catenin, and these effects were mediated through Tcf-4 binding sites in the c-MYC promoter. These results provide a molecular framework for understanding the previously enigmatic overexpression of c-MYC in colorectal cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, T C -- Sparks, A B -- Rago, C -- Hermeking, H -- Zawel, L -- da Costa, L T -- Morin, P J -- Vogelstein, B -- Kinzler, K W -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1509-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9727977" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Binding Sites ; Cell Line ; Colorectal Neoplasms/*genetics ; Cytoskeletal Proteins/genetics/metabolism ; *Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; *Genes, myc ; HT29 Cells ; Humans ; Mutation ; Promoter Regions, Genetic ; Proto-Oncogene Proteins c-myc/metabolism ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/metabolism ; Transcription, Genetic ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2011-08-06
    Description: The prevalent DNA modification in higher organisms is the methylation of cytosine to 5-methylcytosine (5mC), which is partially converted to 5-hydroxymethylcytosine (5hmC) by the Tet (ten eleven translocation) family of dioxygenases. Despite their importance in epigenetic regulation, it is unclear how these cytosine modifications are reversed. Here, we demonstrate that 5mC and 5hmC in DNA are oxidized to 5-carboxylcytosine (5caC) by Tet dioxygenases in vitro and in cultured cells. 5caC is specifically recognized and excised by thymine-DNA glycosylase (TDG). Depletion of TDG in mouse embyronic stem cells leads to accumulation of 5caC to a readily detectable level. These data suggest that oxidation of 5mC by Tet proteins followed by TDG-mediated base excision of 5caC constitutes a pathway for active DNA demethylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462231/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462231/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yu-Fei -- Li, Bin-Zhong -- Li, Zheng -- Liu, Peng -- Wang, Yang -- Tang, Qingyu -- Ding, Jianping -- Jia, Yingying -- Chen, Zhangcheng -- Li, Lin -- Sun, Yan -- Li, Xiuxue -- Dai, Qing -- Song, Chun-Xiao -- Zhang, Kangling -- He, Chuan -- Xu, Guo-Liang -- 1S10RR027643-01/RR/NCRR NIH HHS/ -- GM071440/GM/NIGMS NIH HHS/ -- R01 GM071440/GM/NIGMS NIH HHS/ -- S10 RR027643/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1303-7. doi: 10.1126/science.1210944. Epub 2011 Aug 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Group of DNA Metabolism, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai 200031, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21817016" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/metabolism ; Animals ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; DNA/*metabolism ; DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells ; HEK293 Cells ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Mice ; Oxidation-Reduction ; Proto-Oncogene Proteins/genetics/*metabolism ; RNA, Small Interfering ; Thymine DNA Glycosylase/genetics/*metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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