Abstract：
:The methylcytosine oxidase TET proteins play important roles in DNA demethylation and development. However, it remains elusive how exactly they target substrates and execute oxidation. Interestingly, we found that, in mice, the full-length TET1 isoform (TET1e) is restricted to early embryos, embryonic stem cells (ESCs), and primordial germ cells (PGCs). By contrast, a short isoform (TET1s) is preferentially expressed in somatic cells, which lacks the N terminus including the CXXC domain, a DNA-binding module that often recognizes CpG islands (CGIs) where TET1 predominantly occupies. Unexpectedly, TET1s can still bind CGIs despite the fact that its global chromatin binding is significantly reduced. Interestingly, global chromatin binding, but not targeted binding at CGIs, is correlated with TET1-mediated demethylation. Finally, mice with exclusive expression of Tet1s failed to erase imprints in PGCs and displayed developmental defects in progeny. These data show that isoform switch of TET1 regulates epigenetic memory erasure and mouse development.
journal_name
Mol Celljournal_title
Molecular cellauthors
Zhang W,Xia W,Wang Q,Towers AJ,Chen J,Gao R,Zhang Y,Yen CA,Lee AY,Li Y,Zhou C,Liu K,Zhang J,Gu TP,Chen X,Chang Z,Leung D,Gao S,Jiang YH,Xie Wdoi
10.1016/j.molcel.2016.10.030subject
Has Abstractpub_date
2016-12-15 00:00:00pages
1062-1073issue
6eissn
1097-2765issn
1097-4164pii
S1097-2765(16)30675-Xjournal_volume
64pub_type
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