Encodes a protein truncated at the C-terminal end of the trans-membrane domain.
Carries a splice-donor site mutation that is predicted to generate a Alk protein that is truncated after the transmembrane domain.
An unspecified mutation in the splice donor site. The splice site mutation has been arbitrarily mapped by a FlyBase curator to the first base of the splice donor site.
axon & photoreceptor cell R8 | somatic clone
The central nervous system of Alk8 mutants appears morphologically normal in terms of segmental nerve branching and segmental muscle patterning. Neuropil synaptic differentiation appears normal in these mutants, with comparable labeling intensity, density and distribution of presynaptic and postsynaptic labels.
Alk8 mutant neuromuscular junctions appear correctly and stereotypically formed and elaborated, with no examples of muscle innervation failure or synaptic targeting errors. Mutant presynaptic active zones appear normally formed and with wild-type size.
R8 axons in mosaic adults with Alk8 in the lamina target neurons exhibit thickened terminals and fasciculate with R7/R8 axons in adjacent columns or fail to extend into the medulla neuropil.
Alk8/+ animals have no observable mutant phenotype.
Alk8 is a suppressor of decreased body size | pupal stage phenotype of Nf1E2
Induced on: P{neoFRT}42D chromosome.
Selected as: a mutant that fails to complement the Df(2R)Alk-21 deficiency.