|Feature type||allele||Associated gene||Dmel\spg|
|Also Known As||spg242|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: W487@.
|Phenotype Manifest In|
Eggs produced from spg homozygous mothers with a mutant paternal spg allele die early in embryonic development. Homozygous spg or spg/Df(3R)3450 or spg/spg embryos exhibit minor defects in axonal patterns: infrequent breaks in the outer longitudinal tract and occasional thinning of these tracts. Homozygous spg embryos do not exhibit myoblast fusion defects.
|Phenotype Manifest In|
|NOT Enhancer of|
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. In mbc[D11.2]/mbc[D11.2], spg/spg double mutants, myoblasts fail to fuse but still cluster around the founder cells (as in mbc[D11.2]/mbc[D11.2] mutants). There is no significant increase in broken fascicles or the collapse of the outer longitudinal tracts in mbc[D11.2], spg double mutants over mbc[D11.2] mutants alone. However, there is an increase in midline fascicle crossing in the double mutants. Abnormal positioning of the ventral nerve cord is also observed in the double mutants. Df(2L)CadN[Δ14]/+ in a spg homozygous background increases the occurrence of axon outgrowth defects over those seen in spg alone. Df(2L)CadN[Δ14]/Df(2L)CadN[Δ14], spg embryos show more severe defects, with greater than additive increase in ectopic midline crossing.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 2 )|
|Secondary FlyBase IDs|
|References ( 5 )|