Cardiac-specific developmental and epigenetic functions of Jarid2 during embryonic development.

ABSTRACT: Epigenetic regulation is critical in normal cardiac development. We have demonstrated that the deletion of Jarid2 (Jumonji (Jmj) A/T-rich interaction domain 2) in mice results in cardiac malformations recapitulating human congenital cardiac disease and dysregulation of gene expression. However, the precise developmental and epigenetic functions of Jarid2 within the developing heart remain to be elucidated. Here, we determined the cardiac-specific functions of Jarid2 and the genetic networks regulated by Jarid2. Jarid2 was deleted using different cardiac-specific Cre mice. The deletion of Jarid2 by Nkx2.5-Cre mice (Jarid2^Nkx) caused cardiac malformations including ventricular septal defects, thin myocardium, hypertrabeculation, and neonatal leth

SUBMITTER: Cho E 

PROVIDER: S-EPMC6066322 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature