Amino acid replacement: Y393term.
T12099482A
Y393term | Ced-12-PA
Y393term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change. Could alternatively be a T to G nucleotide change; unspecified.
Detached muscle fibres are present in Ced-1219F3/Ced-12KO zygotic mutant stage 16-17 embryos.
Stage 16-17 Ced-1219F3/Ced-12KO zygotic mutant embryos exhibit muscle attachment sites that are reduced in size and a decreased number of mature tendon cells.
Embryos homozygous for Ced-1219F3 exhibit minor defects in axonal patterning. Longitudinal fascicles show a nearly wild type pattern, while occasional thinning of these tracks and increased length of adjacent segments is observed.
Ced-1219F3 border cell clones display sever migration defects, with 35% showing no migration and the remaining 65% arresting their journey when only 25% complete.
Df(2L)HO55/Ced-1219F3 embryos have a large number of unfused myoblasts as well as missing muscles.
Germline clone embryos mutant for Ced-1219F3 die prior to myogenesis.
Ced-1219F3 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by spg2
Ced-1219F3 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by Df(2L)CadNΔ14
Ced-1219F3 is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of spg2
Ced-12KO/Ced-1219F3 has visceral muscle fiber | embryonic stage phenotype, enhanceable by msk4/msk[+]
Ced-1219F3 is an enhancer of lateral longitudinal fascicle phenotype of spg2
Ced-12[+]/Ced-1219F3 is a suppressor of eye phenotype of Ced-12UAS.cGa, Scer\GAL4Mef2.PR, mbcUAS.cBa
Ced-1219F3, Df(2L)CadNΔ14 has lateral longitudinal fascicle phenotype
The presence of msk4/+ increases the severity of muscle attachment defects in Ced-1219F3/Ced-12KO embryos.
Compared to Ced-1219F3/Ced-1219F3 or spg2/spg2 single mutants, a consistent increase in longitudinal axon defects is observed in the double homozygous mutants. There is also an increase in axons that inappropriately cross the midline, and abnormalities in the spacing between adjacent segments is enhanced.
The final muscle pattern in Ced-1219F3/Ced-1219F3, spg2/spg2 double mutant embryos appears wild type.
Ced-1219F3, Df(2L)CadNΔ14 double mutant exhibit a consistent enhancement of axonal breaks, although no increase in midline guidance errors. These embryos also show collapsed outer longitudinal axon tracts onto the MP1 fascicle, a phenotype that is not observed in either single mutant.
The rough eye phenotype resulting from Scer\GAL4GMR.PU-mediated expression of Ced-12Scer\UAS.cGa and mbcScer\UAS.cBa is suppressed by heterozygosity for Ced-1219F3.
Ced-12KO/Ced-1219F3 is partially rescued by Scer\GAL4Mef2.PR/Ced-12UAS.cGa
Ced-12KO/Ced-1219F3 is partially rescued by Scer\GAL4how-24B/Ced-12UAS.cGa
Ced-12KO/Ced-1219F3 is partially rescued by Scer\GAL4Mef2.PR/Ced-12ΔN.UAS
Ced-12KO/Ced-1219F3 is partially rescued by Scer\GAL4how-24B/Ced-12ΔN.UAS
Ced-12KO/Ced-1219F3 is not rescued by Scer\GAL4sr-md710/Ced-12UAS.cGa
Ced-12KO/Ced-1219F3 is not rescued by Ced-12ΔC.UAS/Scer\GAL4Mef2.PR
Ced-12KO/Ced-1219F3 is not rescued by Scer\GAL4how-24B/Ced-12ΔC.UAS
Scer\GAL4sr-md710-mediated expression of Ced-12Scer\UAS.cGa in tendon cells does not improve the muscle detachment phenotype of Ced-1219F3/Ced-12KO embryos.
Scer\GAL4Mef2.PR- or Scer\GAL4how-24B-mediated expression of Ced-12Scer\UAS.cGa in muscles or mesoderm, respectively, efficiently but not completely rescues the muscle detachment phenotype of Ced-1219F3/Ced-12KO embryos.
Scer\GAL4Mef2.PR- or Scer\GAL4how-24B-mediated expression of Ced-12ΔC.Scer\UAS in muscles or mesoderm, respectively, does not improve the muscle detachment phenotype of Ced-1219F3/Ced-12KO embryos.