|Feature type||allele||Associated gene||Dmel\Cam|
|Map ( GBrowse )|
|Allele class||hypomorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: E31K.
Amino acid replacement: E31K. FlyBase curator comment: The Figure shows lesion as an E to K change. The Figure Legend incorrectly reports a Q to K change.
|Phenotype Manifest In|
bouton & abdominal 2 ventral longitudinal muscle 2
bouton & abdominal 3 ventral longitudinal muscle 2
bouton & abdominal 4 ventral longitudinal muscle 2
bouton & abdominal 5 ventral longitudinal muscle 2
bouton & abdominal 6 ventral longitudinal muscle 2
bouton & abdominal 7 ventral longitudinal muscle 2
Cam3c1 heterozygotes exhibit little effect on the average period of free-running.
Cam3c1/Camn339 flies exhibit reduced locomotion, coordination and flight ability. A slight dominant effect can be detected for both Cam3c1 and Camn339. The recessive mutant effects are more substantial. In the larval neuromuscular junction voltage clamp preparation, working on muscle 6, ejc amplitude for Cam3c1/Camn339 is normal. Ejc amplitude is increased approximately three fold by quinidine at low external calcium concentrations (at 0.4mM external calcium quinidine has no effect. The mejc amplitude and frequency is unchanged, suggesting the increase in ejc reflects increased neurotransmitter release. Cam3c1/Camn339 larvae show structural synaptic abnormalities: the terminal arbor forms a thickened, or large, misshapen structure with few distinct boutons. This results in a reduced number of boutons and a nearly complete lack of terminal branching in pleural external longitudinal muscle 13. Muscle 13 shows the same ejc phenotype as ventral internal longitudinal muscle 6. No abnormalities in nerve terminals on muscles ventral internal longitudinal muscle 6, 7 or pleural external longitudinal muscle 12 have been observed. Cam3c1/Cam3c1 homozygous larvae show normal synaptic transmission, even in the presence of quinidine, and normal structure of synaptic boutons.
Electrophysiological and physiological defects. Mutation has a detectable maternal effect on egg hatch rate. Mutation may also interfere with male mating behaviour. Transheterozygous combinations with other Cam mutations produces an incompletely penetrant ectopic wing vein phenotype and either lateral or bilateral cuticular 'scabs' on the notum.
|Phenotype Manifest In|
|Complementation & Rescue Data|
|Stocks ( 1 )|
|Notes on Origin|
The Cam3c1 mutation might effect Ca2+ buffering or interfere with the activation or inhibition of a calmodulin target distinct from that encoded by CaMKII or calmodulin activated adenylyl cyclase, rut.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 1 )|
|Secondary FlyBase IDs|
|References ( 3 )|