P{PZ} insertion 3.2kb downstream of the start of exon 1, within intron 3.
follicle cell & actin filament | somatic clone
In contrast to wild type, single chic05205a γ neurons (generated via MARCM) fail to properly extend their axons in the adult.
Mean filopodium length is reduced compared to wild type in cultured primary neurons derived from chic221/chic05205a and chic05205a/Df(2L)GpdhA embryos.
chic05205a/Df(2L)GpdhA embryos show stalling of motor axons compared to wild type.
Single cell γ neuron mutant clones in the mushroom body show drastic axon growth defects.
In mutant columnar follicle cells, levels of F-actin are markedly decreased at all cortices, although actin filaments are lost preferentially from the basal cortex.
Axon growth from homozygous dissected nerve cords cultured in vitro is reduced compared to wild-type. ISNb axons innervate proximal targets (muscles 6 and 7) and extend to contact muscle 13, but fail to reach the distal target (muscle 12) in hemizygous embryos. chic05205a/chic221 embryos show mild defects in the Fas2-positive longitudinal fascicles of the central nervous system.
chic05205a/chic221 has larval longitudinal connective phenotype, enhanceable by Abl2/Abl[+]
chic05205a/chic221 has larval longitudinal connective phenotype, enhanceable by Abl2/Abl4
chic05205a, ena23/ena[+] has filopodium phenotype
capt10, chic05205a has follicle cell | somatic clone phenotype
Abl2, chic05205a/chic221 has larval longitudinal connective phenotype
Abl4, chic05205a/chic221 has larval longitudinal connective phenotype
Cultured primary neurons derived from chic05205a/+ ena23/+ double heterozygous embryos show a significant reduction in the number of filopodia compared to control neurons.
Ectopic actin filaments do not form in capt10 chic05205a double mutant follicle cell clones, and the level of F-actin in these cells appears to be similar to that in chic05205a single mutant cells. Cells in capt10 chic05205a double mutant follicle cell clones lose their columnar morphology and collapse, forming a thin squamous-like layer of cells. These clones can interfere with the migration of wild-type portions of the follicle cell epithelium. The double mutant clones maintain extensive contacts with adjacent wild-type cells.
The severity of the central nervous system defects of chic05205a/chic221 embryos is enhanced by Abl2/+ and further enhanced by Abl2/Abl4.