Abstract
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.
