Amino acid replacement: ?180term.
C21058738T
Q180term | cpa-PA
?180term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
eye (with cpa43D), with Scer\GAL4αTub84B.PL, cpaUAS.Tag:HA
macrochaeta (with cpa43D), with Scer\GAL4αTub84B.PL, cpaUAS.Tag:HA
wing (with cpa43D), with Scer\GAL4αTub84B.PL, cpaUAS.Tag:HA
Cultured primary neurons derived from mutant embryos show a significant increase in the number of filopodia compared to control neurons.
Early development of egg chambers in females containing homozygous germline clones is relatively normal; mutant germ cells form 16-cell cysts, are encapsulated by follicle cells relatively normally and initially grow in size at a rate relatively similar to wild type. However, as they reach stage 6, mutant egg chambers become morphologically abnormal, taking on a spindle shape. The egg chambers cease increasing in size at this point and ultimately degenerate. Overall actin levels are relatively normal through stage 6/7 in the mutant egg chambers and ring canals appear to form normally.
73% of egg chambers in females containing homozygous germline clones do not contain a properly differentiate oocyte, instead having 16 nuclei that are all larger than that expected for the oocyte (32% of these egg chambers have 16 nuclei equal in size, while 68% have one nucleus that is smaller than the others, but not as small as a normal oocyte nucleus). The oocyte is not precisely positioned at the posterior in 61% of the egg chambers.
Homozygous follicle cell clones accumulate excess actin on their apical and lateral surface in early stage egg chambers. By stages 6-8, some mutant cells begin to lose their monolayer organisation, especially in clones near the posterior end of the egg chamber.
cpa69E mutant cells within wing blade primordium clones accumulate actin filaments around the entire cell cortex. cpa69E clones become extruded from this area of the wing disc. cpa69E cells within notum primordium clones accumulate actin filaments near the apical cell membrane and are not extruded from the disc.
Adults expressing cpaScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4αTub84B.PL in a cpa43D/cpa69E background sometimes show wing, eye or bristle defects.
cpa69E/cpa107E has increased mortality during development phenotype, suppressible by Hsap\CAPZA2K256E.UAS/Scer\GAL4αTub84B.PL
cpa69E/cpa107E has increased mortality during development phenotype, suppressible by Scer\GAL4αTub84B.PL/Hsap\CAPZA2R259L.UAS
cpa69E/cpa107E has increased mortality during development phenotype, suppressible | partially by Hsap\CAPZA2K256E.UAS/Scer\GAL4da.G32
cpa69E/cpa107E has increased mortality during development phenotype, suppressible | partially by Scer\GAL4da.G32/Hsap\CAPZA2R259L.UAS
cpa69E/cpa107E has increased mortality during development phenotype, suppressible by Hsap\CAPZA2UAS.cBa/Scer\GAL4αTub84B.PL
cpa69E/cpa107E has increased mortality during development phenotype, suppressible | partially by Hsap\CAPZA2UAS.cBa/Scer\GAL4da.G32
cpa69E has increased mortality during development phenotype, suppressible by Hsap\CAPZA2UAS.cBa/Scer\GAL4αTub84B.PL
cpa69E/cpa[+] is an enhancer of abnormal cell migration phenotype of CskGD9345, Scer\GAL4ptc-559.1
cpa69E/cpa107E is an enhancer of bristle of mesothoracic tergum phenotype of Hsap\CAPZA2K256E.UAS, Scer\GAL4αTub84B.PL
cpa69E/cpa[+] is an enhancer of bristle of mesothoracic tergum phenotype of Hsap\CAPZA2K256E.UAS, Scer\GAL4αTub84B.PL
cpa69E/cpa[+] is an enhancer of wing disc phenotype of CskGD9345, Scer\GAL4ptc-559.1
Hsap\CAPZA2R259L.UAS, Scer\GAL4αTub84B.PL, cpa69E has bristle of mesothoracic tergum phenotype
Hsap\CAPZA2K256E.UAS, Scer\GAL4αTub84B.PL, cpa69E/cpa107E has filamentous actin | P-stage phenotype
Hsap\CAPZA2R259L.UAS, Scer\GAL4αTub84B.PL, cpa69E/cpa107E has filamentous actin | P-stage phenotype
A cpa69E heterozygous mutant background enhances the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.
Expression of Hsap\CAPZA2UAS.cBa under the control of Scer\GAL4αTub84B.PL in cpa107E/cpa69E background leads to mild defects in notum bristle, such as mild bending or split bristle, when compared to controls.
Expression of Hsap\CAPZA2R259L.UAS under the control of Scer\GAL4αTub84B.PL in cpa107E/cpa69E background leads to severe notum bristle defects (bending, branching, shortening, missing bristles as well as multiple defects of single bristle) in adults and disrupted F-actin organization in notum bristles at pupal stage when compared to controls.
Expression of Hsap\CAPZA2K256E.UAS under the control of Scer\GAL4αTub84B.PL in cpa107E/cpa69E background leads to disrupted F-actin organization in notum bristles at pupal stage when compared to controls.
Expression of Hsap\CAPZA2R259L.UAS under the control of Scer\GAL4αTub84B.PL in cpa69E/+ background leads to defects in notum bristles when compared to controls.
cpa69E/cpa43D is partially rescued by cpaUAS.Tag:HA/Scer\GAL4αTub84B.PL
Ubiquitous expression of cpaScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4αTub84B.PL rescues the lethality of cpa43D/cpa69E mutants, although some of the rescued adults exhibit wing, eye or bristle defects.