|Feature type||allele||Associated gene||Dmel\Alk|
|Map ( GBrowse )|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Encodes a protein truncated in the first 'MAM' domain.
The stop mutation causes truncation of the Alk protein at the beginning of the first 'MAM' domain
Amino acid replacement: Q306@.
|Phenotype Manifest In|
axon & photoreceptor cell R8 | somatic clone
Homozygous Alk mutant longitudinal visceral muscle (LVM) founder cells in stage 12 embryos migrate normally towards the trunk visceral mesoderm (TVM) and very few dying cells are seen. At stage 13 the front migrating cells reach the anterior end of the trunk visceral mesoderm as in wild type. However during late stage 13 the migration becomes disordered and progressive founder cell death is seen.
The central nervous system of Alk 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. Alk 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. Homozygous Alk mutants exhibit reduced hatching and mutant larval movement is typically sluggish and highly limited. Locomotory movement in Alk mutants is decreased to 35% of the control level, characterised by slower contractions and extended pauses. Severely impaired and motionless larvae remain capable of briefly resuming movement when stimulated, suggesting a defect in the central circuit output driving locomotion. Alk mutant neuromuscular junctions exhibit visible glutamate-driven muscle contractions, and consistently large and robust postsynaptic current amplitudes compared to controls. In Alk mutant neuromuscular junctions, no large or patterned EJCs are recorded (maximum amplitude 429nA), and overall EJC frequency is below 1Hz in 80% of active cells.
Third instar larvae that have Alk function removed in the lamina target neurons, by the presence of Alk1 clones, show normal R cell guidance. Additionally, adults with eyes made mutant for Alk1 by the presence of clones show no R cell guidance defects. Adult mosaic Alk1 animals, in which lamina target neurons are mutant for Alk1, show R8 axon guidance defects. R8 cells exhibit thickened terminals and frequently fail to terminate in their appropriate layer. These axons either project into the R7 layer (7%), stop at the distal border of the medulla neuropil (12%), or project to neighbouring columns (9%). The vast majority of R7 terminals target normally but a small proportion extend into an adjacent medulla column. At the pupal stage, animals with lamina target neuron Alk1 clones exhibit normal R cell projections up to 40 hours after puparium formation. At around 55 hours, R cell projection defects become apparent. These include thickened terminals, fasciculation with neighbouring columns and stalling of the axons at the distal medulla neuropil border ot projection into an adjacent column. In adults carrying Alk1 clones in the lamina target neurons, the array of cartridges consisting of R1-R6 terminals in the lamina is disrupted and the size and shape of lamina cartridges is variable. Cartridges containing homozygous mutant target lamina are likely to be distributed randomly throughout the lamina. The visceral mesoderm is disrupted in stage 14 Alk1 embryos.
Alk1 homozygous larvae do not ingest food, and lack discernible intestinal structures. In stage 13 Alk1 homozygous embryos, the visceral mesoderm is disorganized. At stage 11, the earliest stage at which a mutant phenotype in the visceral mesoderm can clearly be observed, these embryos lack muscle founder cells. However, myoblasts do form in the visceral mesoderm, and go on to contribute to somatic muscle (i.e.- they are fusion competent.)
|Phenotype Manifest In|
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 2 )|
|Secondary FlyBase IDs|
|References ( 9 )|