Df(3L)banΔ1 mutant clones in the larval brain exhibit a reduction in type I and type II neuroblast size, a decrease in the number and size of secondary neuroblasts, and decreases in the nucleolar sizes of neuroblasts and secondary neuroblasts, as compared to control clones.
Df(3L)banΔ1/+ mutants display severe germline stem cell loss following irradiation.
Homozygotes show 100% lethality when reared with their heterozygous siblings. Some lethality is seen during the larval stage and some during the pupal stage. Survival is improved if mutant larvae are raised isolated from their heterozygous siblings.
Intestinal stem cell differentiation is unaffected in Df(3L)banΔ1 mutant clones, but the clones contain fewer cells than controls.
There is no obvious improvement in axon regeneration of class IV da neurons in the ventral nerve cord (after axon severing at the commissure junction at 48 hours after egg laying) in mutant larvae compared to wild type controls.
The dendrites of ddaC neurons of mutant larvae show enhanced regeneration (after dendrite severing at 48 hours after egg laying) compared to wild-type controls. 81.2% of dendrites show regeneration in the mutant larvae (compared to 49.4% in controls). No substantial dendrite regeneration is seen after dendrite severing at 72 hours after egg laying.
Df(3L)banΔ1 mutant larvae show a decrease in the number of glial cells in the eye disc and brain.
Df(3L)banΔ1 mutants display a dendrite overgrowth phenotype with the first sign of larval growth defects at 72 hours after egg laying. Dendrites of individual class IV neurons occupy a larger proportion of the body wall in Df(3L)banΔ1 mutant third instar larvae. Dendrites in Df(3L)banΔ1 mutants promiscuously cross boundaries that are observed by dendrites of wild-type neurons. The exuberant growth of dendrites in Df(3L)banΔ1 mutants is manifested throughout the arbor, not just at the boundaries. In addition to these defects in dendrite coverage, class IV neurons in Df(3L)banΔ1 mutants show significant increase in the number of dendrites, the density of dendrites, and overall dendrite length. Class III dendrites are defective in scaling of dendrite growth to hemisegment size in Df(3L)banΔ1 mutants. In contrast, larval class I dendrites show no obvious defects in dendrite coverage in Df(3L)banΔ1 mutants.
Unlike wild-type controls, following ablation at 48 hours after egg laying, dendrites in Df(3L)banΔ1 mutants extensively fill unoccupied space.
Df(3L)banΔ1 heterozygotes show significantly reduced eclosion after irradiation with 0-8000 R of X-rays.
Df(3L)banΔ1 mutant germline stem cells (GSCs) generated during the adult stages show maintenance and cell division defects, with loss of approximately 14% of Df(3L)banΔ1 mutant GSCs per day. When Df(3L)banΔ1 clones are generated during the larval and pupal stages GSC loss is less severe, with loss of only around 6% of GSCs per day.
Df(3L)banΔ1 mutant clones are very small compared to their sister twinspots when induced at 60 hours of development and examined in the late third instar. Df(3L)banΔ1 clones remain relatively small even when given a growth advantage using the Minute technique. These clones do not induce a rough eye phenotype and show no evidence of increased apoptosis when induced in the wing.
When Df(3L)banΔ1 somatic clones are made in the wing disc, they are on average 1/3 of the size of wild-type twins. No obvious increase in apoptosis is seen in these clones.
The body mass of heterozygotes is 89% that of control flies. The wing blade surface area is 94.9% that of controls. Cell size in the wing blade is 100.5% of controls and cell number in the wing blade is 94.4% that of controls.
Homozygotes die at early pupal stages. Homozygous larvae lack detectable imaginal discs.