TET enzymes, DNA demethylation and pluripotency.
cell differentiation
epigenetics
epigenomics
methylation
model organisms
pluripotency
Journal
Biochemical Society transactions
ISSN: 1470-8752
Titre abrégé: Biochem Soc Trans
Pays: England
ID NLM: 7506897
Informations de publication
Date de publication:
28 06 2019
28 06 2019
Historique:
received:
02
04
2019
revised:
19
05
2019
accepted:
20
05
2019
pubmed:
19
6
2019
medline:
18
12
2019
entrez:
19
6
2019
Statut:
ppublish
Résumé
Ten-eleven translocation (TET) methylcytosine dioxygenases (TET1, TET2, TET3) actively cause demethylation of 5-methylcytosine (5mC) and produce and safeguard hypomethylation at key regulatory regions across the genome. This 5mC erasure is particularly important in pluripotent embryonic stem cells (ESCs) as they need to maintain self-renewal capabilities while retaining the potential to generate different cell types with diverse 5mC patterns. In this review, we discuss the multiple roles of TET proteins in mouse ESCs, and other vertebrate model systems, with a particular focus on TET functions in pluripotency, differentiation, and developmental DNA methylome reprogramming. Furthermore, we elaborate on the recently described non-catalytic roles of TET proteins in diverse biological contexts. Overall, TET proteins are multifunctional regulators that through both their catalytic and non-catalytic roles carry out myriad functions linked to early developmental processes.
Identifiants
pubmed: 31209155
pii: BST20180606
doi: 10.1042/BST20180606
doi:
Substances chimiques
Dioxygenases
EC 1.13.11.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
875-885Informations de copyright
© 2019 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.