A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\Cam3c1

General Information
SymbolDmel\Cam3c1SpeciesD. melanogaster
NameFlyBase IDFBal0083600
Feature typealleleAssociated geneDmel\Cam
Map ( GBrowse ) GBrowse View Helpdetailed view FBal0083599 FBal0083600 FBal0083598 FBal0083596 FBal0083597
Allele classhypomorphic allele - genetic evidence
Mutagenethyl methanesulfonate
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
point mutation
comment=Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
evidence=experimental
pr_change=E32K|Cam-PB,E32K|Cam-PA
reported_pr_change=E31K
na_change=G8152338A
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
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.
Cytology
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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
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Statement
Reference
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.
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Statement
Reference
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Statement
Reference
In combination with l(2)C43C43 mutants exhibit markedly reduced viability.
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Statement
Reference
A heterozygous Cam3c1 background in flies expressing Mmmm\PVScer\UAS.T:Hsap\MYC under the control of Scer\GAL4P2.4.Pdf has no effect on the length of the free-running period, compared to controls, after 1-5 weeks in constant darkness.
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Partially complements
Rescued by
Comments
Defects can be completely rescued by expression of Camhs.PN.
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Bloomington
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Discoverer
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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.
Allelic series of the relative strength of the lethal mutations: Cam8t > Cam7 > Cam6c4 > Cam5 > Cam4c1 > Cam3c1.
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Reported As
Symbol Synonym
Name Synonym
Secondary FlyBase IDs
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Research paper
Harrisingh et al., 2007, J. Neurosci. 27(46): 12489--12499
Intracellular Ca[2+] Regulates Free-Running Circadian Clock Oscillation In Vivo. [FBrf0204998]
Arredondo et al., 1998, Genetics 150(1): 265--274
Increased transmitter release and aberrant synapse morphology in a Drosophila calmodulin mutant. [FBrf0104398]
Nelson et al., 1997, Genetics 147(4): 1783--1798
Calmodulin point mutations affect Drosophila development and behavior. [FBrf0099767]