Nucleotide substitution: C?T.
Amino acid replacement: Q489term.
C19160840T
C?T
Q489term | ena-PA; Q638term | ena-PB; Q489term | ena-PC; Q492term | ena-PD; Q489term | ena-PE; Q785term | ena-PF; Q469term | ena-PG
Q489term
actin filament & egg chamber | germ-line clone
22% of eggs derived from females carrying homozygous germline clones show a "dumpless" phenotype.
Egg chambers in females with homozygous germline clones have defects in the cytoplasmic filaments (the bundled cytoplasmic actin filaments extending from the cortex to nuclei). No defects in ring canal formation or growth are seen in mutant egg chambers.
Dorsal cluster dendritic arborisation neurons show dendritic defects in mutant embryos. At 16 hours after egg laying (AEL), extension of the dorsal dendrites toward the dorsal midline appears more or less normal, but there are significantly fewer dynamic transient lateral fine branches compared to controls (suggesting a defect in the initiation of new branches). At 18-20 hours AEL, the number of lateral dendrites that extend toward or reach the adjacent segment boundaries is reduced compared to wild type.
Third larval instar single cell homozygous ddaB, ddaC, ddaE and ddaF neuron clones show a significant decrease in the number of dendritic ends compared to control clones.
Third larval instar ddaE neurons show a significant decrease in the amount of quarternary, tertiary and secondary dendritic branching compared to controls, while primary branching is not significantly affected.
Heterozygous third instar larvae show a slight decrease in the number of dendritic ends extending from the main dorsal dendrites of the vpda neurons compared to wild type.
Exhibits misrouting in the dorsal cluster of embryonic dendrites. The early budding and extension of lateral branches appear normal; however at a late stage, some lateral branches turn dorsally instead of extending toward segment boundaries, resulting in an apparent reduction of the number of lateral branches. About 60% of embryos exhibit this phenotype. Mutants show no gross defects in anterior-posterior or dorsal-ventral patterning. The development of epidermis and muscle patterning also appears to be normal.
ena46 has abnormal neuroanatomy | third instar larval stage phenotype, enhanceable by p120ctn308
ena[+]/ena46 is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4A9, ShrmA.UAS
ena[+]/ena46 is a suppressor | partially of decreased size | adult stage phenotype of Scer\GAL4A9, ShrmA.UAS
ena[+]/ena46 is a suppressor | partially of decreased size | adult stage phenotype of Scer\GAL4lz-gal4, ShrmA.UAS
ena[+]/ena46 is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4lz-gal4, ShrmA.UAS
ena46 has abdominal posterior ventral multidendritic neuron vdap phenotype, enhanceable by p120ctn308
ena[+]/ena46 is a suppressor | partially of wing phenotype of Scer\GAL4A9, ShrmA.UAS
ena[+]/ena46 is a suppressor | partially of wing disc ventral compartment phenotype of Scer\GAL4A9, ShrmA.UAS
ena[+]/ena46 is a suppressor | partially of eye phenotype of Scer\GAL4lz-gal4, ShrmA.UAS
p120ctn308 enhances the decrease in the number of dendritic ends extending from the main dorsal dendrites of the vpda neurons which is seen in ena46/+ third instar larvae.
Induced on: a chromosome containing Avic\GFPS65T.Scer\UAS driven by Scer\GAL4109(2)80.