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TET1-mediated hydroxymethylation facilitates hypoxic gene induction in neuroblastoma.

Abstract：

:The ten-eleven-translocation 5-methylcytosine dioxygenase (TET) family of enzymes catalyzes the conversion of 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC), a modified cytosine base that facilitates gene expression. Cells respond to hypoxia by inducing a transcriptional program regulated in part by oxygen-dependent dioxygenases that require Fe(II) and α-ketoglutarate. Given that the TET enzymes also require these cofactors, we hypothesized that the TETs regulate the hypoxia-induced transcriptional program. Here, we demonstrate that hypoxia increases global 5-hmC levels, with accumulation of 5-hmC density at canonical hypoxia response genes. A subset of 5-hmC gains colocalize with hypoxia response elements facilitating DNA demethylation and HIF binding. Hypoxia results in transcriptional activation of TET1, and full induction of hypoxia-responsive genes and global 5-hmC increases require TET1. Finally, we show that 5-hmC increases and TET1 upregulation in hypoxia are HIF-1 dependent. These findings establish TET1-mediated 5-hmC changes as an important epigenetic component of the hypoxic response.

journal_name

Cell Rep

journal_title

Cell reports

authors

Mariani CJ,Vasanthakumar A,Madzo J,Yesilkanal A,Bhagat T,Yu Y,Bhattacharyya S,Wenger RH,Cohn SL,Nanduri J,Verma A,Prabhakar NR,Godley LA

doi

10.1016/j.celrep.2014.04.040

subject

Has Abstract

pub_date

2014-06-12 00:00:00

pages

1343-1352

issue

5

issn

2211-1247

pii

S2211-1247(14)00342-8

journal_volume

7

pub_type

杂志文章

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