Allele Dmel\cknK.Δ324-331
| General Information | |||
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| Symbol | Dmel\cknK.Δ324-331 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0265796 | |
| Feature type | allele | Associated gene | Dmel\ckn |
| Allele class | amorphic allele - genetic evidence | ||
| Mutagen | ethyl methanesulfonate | ||
Recent Updates
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| Description |
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| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mutations Mapped to the Genome | |||
Type Location Additional Notes References | |||
| Associated Sequence Data | |||
| DDBJ
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
| UniProtKB/Swiss-Prot | |||
| UniProtKB/TrEMBL | |||
| Progenitor genotype | |||
| Nature of the lesion | Statement Reference Treatment with 22mM ethyl methanesulfonate generates a deletion removing residues 324-331, but does not result in a frameshift. | ||
| Cytology | |||
Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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Detailed Description
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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. | |||
External Data
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| Linkouts | |||
Interactions
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Phenotypic Class
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NOT Enhanced by | |||
Statement 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[+] | |||
NOT suppressed by | |||
Statement Reference 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[+] | |||
Enhancer of | |||
Statement Reference | |||
Other | |||
Statement Reference | |||
Phenotype Manifest In
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NOT Enhanced by | |||
Statement Reference 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[+] cknK.Δ324-331 has intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-enhanceable by Ptp69D[+]/Ptp69D7 cknK.Δ324-331 has intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-enhanceable by Ptp69D1/Ptp69D[+] | |||
NOT suppressed by | |||
Statement 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[+] cknK.Δ324-331 has intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-suppressible by Ptp69D[+]/Ptp69D7 cknK.Δ324-331 has intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-suppressible by Ptp69D1/Ptp69D[+] | |||
Enhancer of | |||
Statement Reference cknK.Δ324-331 is an enhancer of intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype of Lar5.5 | |||
Other | |||
Statement Reference | |||
Additional Comments
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Genetic Interactions
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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. | |||
Xenogenetic Interactions
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Statement Reference | |||
Complementation & Rescue Data
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| Rescues | |||
| Comments | |||
Stocks
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Notes on Origin
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| Discoverer | |||
External Crossreferences & Linkouts
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| Other Crossreferences | |||
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Synonyms & Secondary IDs
( 2 ) | |||
| Reported As | |||
| Symbol Synonym | cknK.Δ324-331 cknK | ||
| Name Synonym | |||
| Secondary FlyBase IDs | |||
References
( 1 ) | |||
| Research paper |
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Recent Updates
External Crossreferences & Linkouts