Abstract
The early morphogenetic mechanisms involved in heart formation are evolutionarily conserved. A screen for genes that control Drosophila heart development revealed a cardiac defect in which pericardial and cardial cells dissociate, which causes loss of cardiac function and embryonic lethality. This phenotype resulted from mutations in the genes encoding HMG-CoA reductase, downstream enzymes in the mevalonate pathway, and G protein Gγ1, which is geranylgeranylated, thus representing an end point of isoprenoid biosynthesis. Our findings reveal a cardial cell-autonomous requirement of Gγ1 geranylgeranylation for heart formation and suggest the involvement of the mevalonate pathway in congenital heart disease.
Original language | English (US) |
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Pages (from-to) | 1301-1303 |
Number of pages | 3 |
Journal | Science |
Volume | 313 |
Issue number | 5791 |
DOIs | |
State | Published - Sep 1 2006 |
ASJC Scopus subject areas
- General