Genome-wide hydroxymethylcytosine pattern changes in response to oxidative stress

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作者
Benjamin Delatte
Jana Jeschke
Matthieu Defrance
Martin Bachman
Catherine Creppe
Emilie Calonne
Martin Bizet
Rachel Deplus
Laura Marroquí
Myriam Libin
Mirunalini Ravichandran
Françoise Mascart
Decio L. Eizirik
Adele Murrell
Tomasz P. Jurkowski
François Fuks
机构
[1] Laboratory of Cancer Epigenetics,
[2] Faculty of Medicine,undefined
[3] ULB,undefined
[4] CRUK Cambridge Institute,undefined
[5] University of Cambridge,undefined
[6] ULB,undefined
[7] Center for Diabetes Research,undefined
[8] Faculty of Medicine,undefined
[9] ULB,undefined
[10] Laboratory of Vaccinology and Mucosal Immunity,undefined
[11] Faculty of Medicine,undefined
[12] ULB,undefined
[13] Institute of Biochemistry,undefined
[14] Stuttgart University,undefined
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摘要
The TET enzymes convert methylcytosine to the newly discovered base hydroxymethylcytosine. While recent reports suggest that TETs may play a role in response to oxidative stress, this role remains uncertain and results lackin vivomodels. Here we show a global decrease of hydroxymethylcytosine in cells treated with buthionine sulfoximine and in mice depleted for the major antioxidant enzymesGPx1 and 2. Furthermore, genome-wide profiling revealed differentially hydroxymethylated regions in coding genes and intriguingly in microRNA genes, both involved in response to oxidative stress. These results thus suggest a profound effect ofin vivooxidative stress on the global hydroxymethylome.
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