|Feature type||allele||Associated gene||Dmel\Ced-12|
|Also Known As||elmo19F3|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: Y393@.
|Phenotype Manifest In|
Embryos homozygous for Ced-12[19F3] 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-12[19F3] 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-12[19F3] embryos have a large number of unfused myoblasts as well as missing muscles. Germline clone embryos mutant for Ced-12[19F3] die prior to myogenesis.
|Phenotype Manifest In|
Compared to Ced-12[19F3]/Ced-12[19F3] or spg/spg 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-12[19F3]/Ced-12[19F3], spg/spg double mutant embryos appears wild type. Ced-12[19F3], Df(2L)CadN[Δ14] 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.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 2 )|
|Secondary FlyBase IDs|
|References ( 2 )|