Castor Gene Involvement in the Cardiogenesis of Drosophilia Melanogaster
Mutations in the human zinc-finger transcription factor-encoding gene CASZI are associated with cardiac abnormalities or defects such as dilated cardiomyopathy, ventricular septal defect, and left ventricular noncompaction cardiomyopathy. Disruption of the orthologs of CASZlin Xenopus and mice also lead to aberrant heart development, indicating its conserved role in cardiogenesis. Phenotypic analysis of a null mutation of castor (cas), the Drosophila ortholog of CASZI shows that cos has two potential roles in cardiogenesis. First, COS is required for mediating all three categories of cardiac progenitor cell division: asymmetric, symmetric, and cell division at an earlier stage. Second, cas prevents subsets of cells in the most anterior region of the heart, the anterior aorta, from becoming specified as seven up- expressing cardial cells (Svp-CCs). Svp-CCs are present in the posterior aorta and the even more posterior heart proper, sections of the heart determined by the expression of the Hox genes Ultmbithorax (Ubx) and abdominal A (abd-A). Intriguingly, both Ubx and abd-A repress cas, and ectopic expression of either of these two Hox genes in the anterior aorta leads to the ectopic specification of Svp-CCs there. Collectively, these data raise the possibility that Ubx and abd-A specify Svp-CCs in the posterior aorta and the heart proper by repressing cos in those regions, a hypothesis that is being tested currently.