Mutated residue Gly249 is a conserved residue in car homologues of different species.
Amino acid replacement: L26V.
Amino acid replacement: G249V.
C19566417G
L26V | car-PA; L26V | car-PB; L26V | car-PC
L26V
One of two amino acid substitutions observed in car1 mutant. Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
G19567087T
G249V | car-PA; G249V | car-PB; G249V | car-PC
G249V
One of two amino acid substitutions observed in car1 mutant. Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
car1 homozygotes or heterozygotes do not exhibit a significant increase in the proportion of hyperplastic testes, as compared to controls.
car1 mutant males exhibit ~40% less spermatogonial cyst death compared to controls.
car1 mutants exhibit an endosome clustering phenotype.
car1 mutants exhibit retinal degeneration after 9-days of constant light.
Both number and morphology of LysoTracker-positive puncta and lipid droplets during ecdysone-induced autophagy in car1 male wandering third instar larvae is comparable to wild-type.
Mutant flies show some decrease in ommochrome pigment levels and a significant reduction in drosopterin pigment levels compared to wild type.
Mutant males have a shortened adult life span compared to controls, with a mean life span of 17.42 days at 25o.
Hemocyte endosomal degradation is significantly reduced in car1 mutants compared to wild-type cells. This reduction also correlates with an increased severity of eye-colour defect. car1 mutants show a small but significant impairment in endosomal degradation. There is no difference between in the morphology and formation of the multi-vesicular body and the small dense organelle between car1 and wild-type cells. Cells from car1 animals exhibit a block in transition of small dense vesicles to tubular-vesicular compartments. Endosomes in car1 mutant cells exhibit wild-type fusion characteristics and mature into fusion-inaccessible small dense structures.
Brain histology abnormal.
Malpighian tubule colour: pale yellow; hard to distinguish from wild type before third instar.
Eye color autonomous in transplant into wild-type host.
Eye colour: dark ruby. Body shape and proportions seem rounded.
Scer\GAL4arm.PS, car1, rushUAS.GFP has partially lethal - majority live phenotype, suppressible by sta+t4.4/Df(1)rush4
car[+]/car1 is an enhancer of visible phenotype of Scer\GAL4GMR.PF, bchsEP2299
car1 is a suppressor of decreased body size | pupal stage phenotype of Nf1E2
Scer\GAL4arm.PS, car1, rushUAS.GFP has partially lethal - majority live phenotype
car1, dor1 has lethal | prepupal stage phenotype
car1, ltunspecified has lethal phenotype
car1, dor1 has lethal | pupal stage phenotype
car1 has ommatidium phenotype, suppressible by CysGMR.PK
car1 has rhabdomere phenotype, suppressible by CysGMR.PK
car[+]/car1 is an enhancer of eye phenotype of Scer\GAL4GMR.PF, bchsEP2299
car1 is a suppressor of eye phenotype of Scer\GAL4GMR.PF, Sk2UAS.cYa
car1 is a suppressor of photoreceptor neuron phenotype of Scer\GAL4GMR.PF, Sk2UAS.cYa
car1 is a suppressor of ommatidium phenotype of Scer\GAL4GMR.PF, Sk2UAS.cYa
car1 is a suppressor of rhabdomere phenotype of Scer\GAL4GMR.PF, Sk2UAS.cYa
Dp(1;Y)1E, car1 has late endosome phenotype
car1, lt1 has larval brain phenotype
car1, lt1 has ventral nerve cord phenotype
Expression of rushScer\UAS.T:Avic\GFP under the control of Scer\GAL4arm.PS decreases the fraction of car1 flies eclosing. This effect is rescued by Df(1)rush4, sta+t4.4.
The reduction in drosopterin pigment levels that is seen in car1 flies is not affected by HPS4W515X.
The reduction in drosopterin pigment levels seen in flies carrying wdsRNA.GMR is not enhanced by car1.
A car1 mutant background suppresses the retinal degeneration seen upon expression of Sk2Scer\UAS.cYa under the control of Scer\GAL4GMR.PF in the developing eye through enhanced lysosomal degradation.
The double mutant, car1 dor1 does not survive beyond the prepupal stage. In cell culture, car1 dor1 cells exhibit the most severe defect in endosomal degradation, compared to either single mutant. There is a small but significant difference between the degradation defect in dor1 car1 and dor1, consistent with a role for both car and dor in endosomal degradation. Endosomes in cells from car1 dor1 mutants, although incapable of a morphological transition to small dense vesicles, are capable of fusion at early times and normal maturation. The presence of Dp(1;Y)1E in car1 mutants blocks the transition from large to small endosomes during maturation.
Dies as larva when mother car1; ltunspecified/+ or car1/+; ltunspecified and as pupa when mother car1/+; ltunspecified/+.
Reduced recovery in gynandromorphs with male parts car dor.
Lethal focus domineering; fate maps to ventral nervous system.