Fig. 6.

Cardiac progenitor cell division defects associated with Myb loss of function. (A) A heart from a wild-type embryo bearing the svp-lacZ enhancer trap showing hemisegments consisting of four Tin-CCs (green), two Svp-CCs (yellow) and two Svp-PCs (red). (B-D) Hearts from embryos that are hemizygous for the Myb^MH30 null mutation demonstrating mutant hemisegments with either excess or too few CCs (dashed ovals) and illustrating the two distinct types of progenitor cell division defects that underlie these cardiac phenotypes. (E) Schematic showing cell lineage relationships in a wild-type heart, and the three previously characterized cardiac progenitor cell divisions defects known to be responsible for localized changes in heart cell number (Ahmad et al., 2012). Note that only two types of developmental errors, those involved in symmetric cell divisions and those involved in an earlier step to determine the number of Svp progenitors, are primarily responsible for the Myb cardiac phenotypes. (F) Fraction of hemisegments exhibiting each type of cardiac progenitor cell division defect in embryos that are wild type or hemizygous for the Myb^MH30 mutation. The significance of each type of cell division defect in the Myb mutants compared with wild-type embryos is shown.