RT Journal Article
SR Electronic
T1 A new coactivator complex required for retinoic acid-dependent regulation of embryonic symmetry
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 089201
DO 10.1101/089201
A1 Goncalo C. Vilhais-Neto
A1 Marjorie Fournier
A1 Jean-Luc Plassat
A1 Mihaela E. Sardiu
A1 Anita Saraf
A1 Jean-Marie Garnier
A1 Mitsuji Maruhashi
A1 Laurence Florens
A1 Michael P. Washburn
A1 Olivier Pourquié
YR 2016
UL http://biorxiv.org/content/early/2016/11/22/089201.abstract
AB Bilateral symmetry is a striking feature of the vertebrate body plan organization. Vertebral precursors, called somites, provide one of the best illustrations of embryonic symmetry. Maintenance of somitogenesis symmetry requires Retinoic acid (RA) and its coactivator Rere/Atrophin2. Here, using a proteomic approach we identify a protein complex, containing Wdr5, Hdac1, Hdac2 and Rere (named WHHERE), which regulates RA signalling and controls embryonic symmetry. We demonstrate that Wdr5, Hdac1 and Hdac2 are required for RA signalling in vitro and in vivo. Mouse mutants for Wdr5 and Hdac1 exhibit asymmetrical somite formation characteristic of RA-deficiency. We also identify the Rere-binding histone methyltransferase Ehmt2/G9a, as a RA coactivator controlling somite symmetry. Upon RA treatment, WHHERE and Ehmt2 become enriched at RA target genes to promote RNA Polymerase II recruitment. Our work identifies a novel protein complex linking key epigenetic regulators acting in the molecular control of embryonic bilateral symmetry.