dunkKG09309/dunkKG09309 mutant embryos show defects in myosin organization at the invagination front shortly after the onset of cellularization and throughout the flow phase (but not the recruitment phase), with myosin preferentially accumulating at the vertices and being depleted from the edges, and is not due to loss or redistribution of F-actin, although at later stages, F-actin distribution becomes abnormal likely due to the defective morphology of the invagination front. The rate of myosin turnover at the cortex does not appear to be affected. The hexagonal symmetry of the ingressing furrows is disrupted in these mutants, subsequently leading to irregularly shaped actomyosin rings, but basal closure still occurs, there are no obvious defects in the rate of furrow ingression, and subsequent development is normal.
dunkKG09309 has embryo | blastoderm stage phenotype, enhanceable by Df(2L)Exel6016/Df(2L)Exel6016
dunkKG09309/dunkKG09309, Df(2L)Exel6016/Df(2L)Exel6016 double mutant embryos exhibit more severe defects in myosin organization during cellularization as compared to single mutants. These embryos display loss of myosin recruitment to the invagination front during the recruitment phase of cellularization. Myosin never forms an interconnected network, the subsequent organization into individual contractile rings completely fails, and the actomyosin network completely breaks down into discrete foci.
