Df(1)jub^II maternal-zygotic mutants are pupal lethal, and some die as embryos and larvae; maternal-only mutants survive to adulthood.

Both Df(1)jub^II maternal-zygotic and maternal-only mutant embryos show an increased number of shrinking edges that join rosette structures during axis elongation, leading to a higher Rosette:T1 structure ratio than controls (~ 1:1 ratio, instead of the expected ~ 1:2 ratio).

Both maternal-zygotic and maternal-only mutant embryos also show a significant increase in the proportion of shrinking edges forming rosettes through sequential contraction, but not in through simultaneous contraction, as compared to controls. Often there are aberrant gaps between cells, which are most pronounced in rosettes, and there is a delay in the resolution of high-order vertices both in T1 structures and rosettes, leading to some unresolved shrinking edges and defective rosettes. Maternal-only mutant embryos exhibit a similar number of overall shrinking edges, as compared to controls.

Zygotic-only Df(1)jub^II mutant embryos exhibit a similar peak retraction velocity of laser-ablated vertical and horizontal cell interfaces, as compared to controls.

Maternal-zygotic Df(1)jub^II mutant embryos show mild-to-moderate dorsal closure defects, with small gaps between the lateral epithelium and the amnioserosa during its final zippering phase.

The higher Rosette:T1 structure ratio observed in maternal-only Df(1)jub^II mutants is fully rescued by the Scer\GAL4^{VP16.mat.αTub67C}-driven expression of either jub^{UASp.FL.msVenus} or jub^{preLIM+12.UASp.msVenus}, and only partially rescued by the Scer\GAL4^{VP16.mat.αTub67C}-driven expression of jub^{preLIM+3.UASp.msVenus}.

The dorsal closure defects observed in Df(1)jub^II maternal-zygotic mutant embryos are enhanced by shg² heterozygosity.