|Also Known As||banΔ1, bantamΔ1|
|Computed Breakpoints include|
|Member of large scale dataset(s)|
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|Nature of the Aberration|
|Class of aberration (relative to progenitor)|
|Formalized genetic data|
|Genetic mapping information|
|Comments on Cytology|
|Gene Deletion & Duplication Data|
|Genes Deleted / Disrupted|
|Completely deleted / disrupted|
|Genes NOT Deleted / Disrupted|
|Genes NOT Duplicated|
|In combination with other aberrations|
|NOT in combination with other aberrations|
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)ban[Δ1] mutant larvae show a decrease in the number of glial cells in the eye disc and brain.
Df(3L)ban[Δ1] 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)ban[Δ1] mutant third instar larvae. Dendrites in Df(3L)ban[Δ1] mutants promiscuously cross boundaries that are observed by dendrites of wild-type neurons. The exuberant growth of dendrites in Df(3L)ban[Δ1] 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)ban[Δ1] 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)ban[Δ1] mutants. In contrast, larval class I dendrites show no obvious defects in dendrite coverage in Df(3L)ban[Δ1] mutants. Unlike wild-type controls, following ablation at 48 hours after egg laying, dendrites in Df(3L)ban[Δ1] mutants extensively fill unoccupied space. Loss of ban function in homozygous Df(3L)ban[Δ1] mutant sensory neuron clones has no significant effect on dendrite coverage of class IV neurons.
Df(3L)ban[Δ1] heterozygotes show significantly reduced eclosion after irradiation with 0-8000 R of X-rays. A W heterozygous background suppresses lethality found in Df(3L)ban[Δ1] mutants to generate wild-type levels of survival when larvae are irradiated with 0-8000 R of X-rays.
Df(3L)ban[Δ1] mutant germline stem cells (GSCs) generated during the adult stages show maintenance and cell division defects, with loss of approximately 14% of Df(3L)ban[Δ1] mutant GSCs per day. When Df(3L)ban[Δ1] 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.
|Stocks ( 0 )|
|Notes on Origin|
|Balancer / Genotype Variants of the Aberration|
|Synonyms & Secondary IDs ( 7 )|
|Secondary FlyBase IDs|
|References ( 15 )|