Homozygous embryos show complete muscle detachment (quantified as greater than 40% shortening of the dorsal muscles). 38% of homozygotes fail to undergo germband retraction.
Homozygous clones in the wing result in wing blisters in more than 95% of wings.
Adult Df(3L)79a homozygous mutant intestinal stem cell clones have reduced maintenance 7 days and 14 days after clone induction compared to control clones; remaining clones contain fewer cells by day 14.
Df(3L)79a mutant embryos display major architectural defects in muscle attachment. The overall area of the muscle attachment is reduced by 84%, and the length of muscle attachment is reduced by 68% compared to wild-type embryos. Embryos display a "tail-up" appearance, with defects in germ band retraction.
Df(3L)79a dorsal branch terminal cell clones in third instar larvae show more than 25 lumen, while wild-type clones show a single lumen.
Df(3L)79a mutant terminal clones derived in Df(3L)79a/+ larvae from Df(3L)79a germline clones and wild-type fathers show a phenotype indistinguishable from that of Df(3L)79a clones in larvae from 2 wild-type parents.
Homozygous female germline clones do not show any abnormal phenotypes and complete oogenesis normally. Homozygous follicle cell clones that are not situated at the posterior of the egg chamber cause mislocalisation of the oocyte in 75% of egg chambers, while homozygous follicle cell clones at the posterior of the egg chamber do not cause oocyte mispositioning. In egg chambers where there is mislocalisation of the oocyte, the oocyte is in contact with the mutant follicle cell clone in 96% of cases.
Embryos maternally and zygotically homozygous for Df(3L)79a exhibit a failure of germ-band retraction and a more severe muscle detachment phenotype than embryos that are only zygotically mutant.
