A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\cknK.Δ324-331

General Information
SymbolDmel\cknK.Δ324-331SpeciesD. melanogaster
NameFlyBase IDFBal0265796
Feature typealleleAssociated geneDmel\ckn
Allele classamorphic allele - genetic evidence
Mutagenethyl methanesulfonate
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Description
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FB2013_03
FB2013_02
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Treatment with 22mM ethyl methanesulfonate generates a deletion removing residues 324-331, but does not result in a frameshift.
Cytology
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Statement
Reference
ckn[K.Δ324-331] homozygous or ckn[K.Δ324-331]/Df(2R)BSC330 mutant embryos display consistent motor axon projection defects, exhibiting classic ISNb 'bypass' phenotypes, where ISNb axons fail to innervate the ventrolateral muscle field. These axons appear to defasciculate normally from the primary ISN branch at the exit junction, but fail to enter the ventral muscle field, instead bypassing their targets as they extend parallel to the primary ISN fascicle. Frequently, mis-targeted ISNb axons reach back from the dorsal edge of muscle 12 to innervate the ventrolateral muscle field. In the majority of affected nerves, ISNb axons are visible as a distinct fascicle next to the ISN. ckn[K.Δ324-331] heterozygous embryos do not exhibit ISNb guidance defects.
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Reference
cknK.Δ324-331 has neuroanatomy defective | embryonic stage phenotype, non-enhanceable by Ptp69D[+]/Ptp69D7
cknK.Δ324-331 has neuroanatomy defective | embryonic stage phenotype, non-enhanceable by Ptp69D1/Ptp69D[+]
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cknK.Δ324-331 has neuroanatomy defective | embryonic stage phenotype, non-suppressible by Ptp69D[+]/Ptp69D7
cknK.Δ324-331 has neuroanatomy defective | embryonic stage phenotype, non-suppressible by Ptp69D1/Ptp69D[+]
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cknK.Δ324-331 has intersegmental nerve | embryonic stage phenotype, non-enhanceable by Ptp69D[+]/Ptp69D7
cknK.Δ324-331 has intersegmental nerve | embryonic stage phenotype, non-enhanceable by Ptp69D1/Ptp69D[+]
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Reference
cknK.Δ324-331 has intersegmental nerve | embryonic stage phenotype, non-suppressible by Ptp69D[+]/Ptp69D7
cknK.Δ324-331 has intersegmental nerve | embryonic stage phenotype, non-suppressible by Ptp69D1/Ptp69D[+]
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Statement
Reference
Lar[5.5] ckn[K.Δ324-331] double heterozygous embryos display bypass phenotypes with 39% penetrance. A heterozygous or homozygous Ptp69D[1] background fails to affect the penetrance of the ISNb bypass phenotype found in ckn[K.Δ324-331] heterozygotes or homozygotes. A heterozygous or homozygous Ptp69D[7] background fails to affect the penetrance of the ISNb bypass phenotype found in ckn[K.Δ324-331] heterozygotes or homozygotes. ISNb pathfinding is delayed in approximately 23% of dock[3] ckn[K.Δ324-331] double heterozygotes. A heterozygous ckn[K.Δ324-331] background enhances ISNb pathfinding defects in dock[3] homozygotes, from 6% to 43% of hemisegments. dock[3] ckn[K.Δ324-331] double homozygotes exhibit delayed 'immature' ISNb axons in 65% of hemisegments. Motor axons in the affected nerves are loosely organised with multiple projections and resemble wild-type axons at earlier stages. Furthermore, the ISNd branch is frequently absent or reduced in size. Examination of the ISNb/d choice point reveals defects in ISNb/d branch segregation. The lateral two longitudinal Fas2-positive fascicles are poorly fasciculated and discontinuous in these double mutants.
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Reported As
Symbol Synonym
cknK.Δ324-331
 
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Research paper
Weng et al., 2011, J. Neurosci. 31(12): 4421--4433
The Cytoplasmic Adaptor Protein Caskin Mediates Lar Signal Transduction during Drosophila Motor Axon Guidance. [FBrf0213321]