follicle cell & actin filament | ectopic | somatic clone
follicle cell & actin filament | somatic clone
oocyte & actin filament | ectopic | germ-line clone
Heterozygotes do not show midline crossing errors in the central nervous system.
Mutant follicle cell clones have profound defects in their actin cytoarchitecture; ectopic F-actin accumulates at the apical surface of the cells, close to the germline, while actin filaments at the lateral and basal cortices usually remain unaffected, although F-actin is occasionally lost from the basal surface. In early egg chambers, ectopic actin filaments are first seen accumulating at sites of cell-cell contact.
Ectopic actin filaments first form at the posterior of the oocyte at stage 5-6 in capt10 germ-line clones.
capt10/capt[+] is an enhancer of abnormal neuroanatomy phenotype of sli2
capt10/capt[+] is a non-enhancer of abnormal neuroanatomy | recessive phenotype of robo11, robo3[+]/robo31
Abl2, capt10/capt[+] has abnormal neuroanatomy phenotype
Df(2L)ast2, capt10 has abnormal neuroanatomy phenotype
Abl4, capt10/capt[+] has abnormal neuroanatomy phenotype
Abl2, capt10 has abnormal neuroanatomy phenotype
Abl4, capt10 has abnormal neuroanatomy phenotype
capt10/capt[+] is an enhancer of presumptive embryonic/larval central nervous system phenotype of sli2
capt10/capt[+] is a non-enhancer of presumptive embryonic/larval central nervous system phenotype of robo11, robo3[+]/robo31
Abl2, capt10/capt[+] has presumptive embryonic/larval central nervous system phenotype
Df(2L)ast2, capt10 has presumptive embryonic/larval central nervous system phenotype
Abl4, capt10/capt[+] has presumptive embryonic/larval central nervous system phenotype
capt10, chic05205a has follicle cell | somatic clone phenotype
Central nervous system axons are seen to cross the midline in Abl4 capt10 double heterozygous embryos. Central nervous system axons are seen to cross the midline in Abl2 capt10 double heterozygous embryos. Src64BPI capt10 double heterozygotes do not show significant midline crossing defects in the embryonic central nervous system. The frequency of ectopic crossing of the midline by axons in the central nervous system seen in sli2 heterozygous embryos is increased if they are also heterozygous for capt10. capt10 learobo2-4 double heterozygotes show little if any midline crossing defects in the embryonic central nervous system. capt10 robo31 double heterozygotes show little if any midline crossing defects in the embryonic central nervous system. One copy of capt10 does not enhance the frequency of midline crossing defects seen in robo1 robo31 double mutant heterozygotes. capt10/Df(2L)ast2 embryos show 54% ectopic midline crossing by axons in the central nervous system.
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. F-actin is often seen accumulating at a single, randomly positioned site within the cell in capt10 l(2)gl4 double mutant follicle cell clones. Ectopic actin filaments do not form in enaunspecified capt10 double mutant follicle cell clones and F-actin levels are often decreased. Expression of AblScer\UAS.cFa under the control of Scer\GAL4T155 in capt10 mosaic egg chambers alters both the level and distribution of actin filaments in the capt10 mutant cells. In a few egg chambers, the epithelial morphology is profoundly disrupted.