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1. Tet2 and Tet3 cooperate with B-lineage transcription factors to regulate DNA modification and chromatin accessibility

Author

Chan-Wang Lio, Jiayuan Zhang, Edahí González-Avalos, Patrick G Hogan, Xing Chang, and Anjana Rao

Subjects
B cell development, DNA methylation, Tet proteins, 5hmC, Medicine, Science, Biology (General), QH301-705.5
Abstract

Ten-eleven translocation (TET) enzymes oxidize 5-methylcytosine, facilitating DNA demethylation and generating new epigenetic marks. Here we show that concomitant loss of Tet2 and Tet3 in mice at early B cell stage blocked the pro- to pre-B cell transition in the bone marrow, decreased Irf4 expression and impaired the germline transcription and rearrangement of the Igκ locus. Tet2/3-deficient pro-B cells showed increased CpG methylation at the Igκ 3’ and distal enhancers that was mimicked by depletion of E2A or PU.1, as well as a global decrease in chromatin accessibility at enhancers. Importantly, re-expression of the Tet2 catalytic domain in Tet2/3-deficient B cells resulted in demethylation of the Igκ enhancers and restored their chromatin accessibility. Our data suggest that TET proteins and lineage-specific transcription factors cooperate to influence chromatin accessibility and Igκ enhancer function by modulating the modification status of DNA.

Published
2016
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2. Tet2 and Tet3 cooperate with B-lineage transcription factors to regulate DNA modification and chromatin accessibility

Author

Anjana Rao, Jiayuan Zhang, Patrick G. Hogan, Edahí González-Avalos, Xing Chang, and Chan-Wang J. Lio

Subjects
0301 basic medicine, Transcription, Genetic, Mouse, QH301-705.5, Cellular differentiation, Science, Immunology, Enhancer RNAs, Biology, General Biochemistry, Genetics and Molecular Biology, Dioxygenases, 03 medical and health sciences, Gene Knockout Techniques, Mice, Proto-Oncogene Proteins, B cell development, Animals, Epigenetics, Biology (General), Enhancer, Transcription factor, B-Lymphocytes, DNA methylation, General Immunology and Microbiology, Tet proteins, General Neuroscience, Cell Differentiation, General Medicine, DNA, Molecular biology, Chromatin, DNA-Binding Proteins, 030104 developmental biology, DNA demethylation, Gene Expression Regulation, Genes and Chromosomes, Interferon Regulatory Factors, 5-Methylcytosine, Medicine, 5hmC, Research Article
Abstract

Ten-eleven translocation (TET) enzymes oxidize 5-methylcytosine, facilitating DNA demethylation and generating new epigenetic marks. Here we show that concomitant loss of Tet2 and Tet3 in mice at early B cell stage blocked the pro- to pre-B cell transition in the bone marrow, decreased Irf4 expression and impaired the germline transcription and rearrangement of the Igκ locus. Tet2/3-deficient pro-B cells showed increased CpG methylation at the Igκ 3’ and distal enhancers that was mimicked by depletion of E2A or PU.1, as well as a global decrease in chromatin accessibility at enhancers. Importantly, re-expression of the Tet2 catalytic domain in Tet2/3-deficient B cells resulted in demethylation of the Igκ enhancers and restored their chromatin accessibility. Our data suggest that TET proteins and lineage-specific transcription factors cooperate to influence chromatin accessibility and Igκ enhancer function by modulating the modification status of DNA. DOI: http://dx.doi.org/10.7554/eLife.18290.001

Published
2016

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