Unknown

Dataset Information

0

Hopx and Hdac2 interact to modulate Gata4 acetylation and embryonic cardiac myocyte proliferation.


ABSTRACT: Regulation of chromatin structure via histone modification has recently received intense attention. Here, we demonstrate that the chromatin-modifying enzyme histone deacetylase 2 (Hdac2) functions with a small homeodomain factor, Hopx, to mediate deacetylation of Gata4, which is expressed by cardiac progenitor cells and plays critical roles in the regulation of cardiogenesis. In the absence of Hopx and Hdac2 in mouse embryos, Gata4 hyperacetylation is associated with a marked increase in cardiac myocyte proliferation, upregulation of Gata4 target genes, and perinatal lethality. Hdac2 physically interacts with Gata4, and this interaction is stabilized by Hopx. The ability of Gata4 to transactivate cell cycle genes is impaired by Hopx/Hdac2-mediated deacetylation, and this effect is abrogated by loss of Hdac2-Gata4 interaction. These results suggest that Gata4 is a nonhistone target of Hdac2-mediated deacetylation and that Hdac2, Hopx, and Gata4 coordinately regulate cardiac myocyte proliferation during embryonic development.

SUBMITTER: Trivedi CM 

PROVIDER: S-EPMC2947937 | BioStudies | 2010-01-01

REPOSITORIES: biostudies

Similar Datasets

2010-08-19 | E-GEOD-23700 | ArrayExpress
2010-08-19 | GSE23700 | GEO
2017-01-01 | S-EPMC5296651 | BioStudies
2013-01-01 | S-EPMC3597510 | BioStudies
2020-01-01 | S-EPMC6954403 | BioStudies
1000-01-01 | S-EPMC5576510 | BioStudies
2015-06-01 | GSE67253 | GEO
2015-06-01 | GSE67252 | GEO
1000-01-01 | S-EPMC4612678 | BioStudies
2014-01-01 | S-EPMC4015328 | BioStudies