zip2/zipIIX62 embryos show a dorsal closure phenotype with a low penetrance. Time-lapse imaging shows that in affected embryos there is a decrease in the rate of closure at end stages and the distribution of F-actin in leading-edge cells is disorganized as closure progresses. Additionally, there is a failure in the structural integrity of the amnioserosa, leading-edge cells, and the junction between them.
zip1/zipIIX62 embryos exhibit dramatic defects in head involution. 58% of zip1/zipIIX62 embryos have a clear dorsal hole (i.e.- dorsal closure is incomplete). The remaining embryos complete dorsal closure, although they frequently show puckering or segment misalignments along the closed midline seam. During dorsal closure the leading edge in zip1/zipIIX62 embryos is very disporganized and extends a broader extent of lamellipodial and filopodial protrusions per unit length of leading edge than wild-type.
Embryos fail to complete dorsal closure as the mutant myosin fails to contribute sufficient myosin to drive dorsal closure to completion.