Deletion which removes ckn residues 324-331, but does not result in a frameshift.
cknK.Δ324-331 homozygous or cknK.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.
cknK.Δ324-331 heterozygous embryos do not exhibit ISNb guidance defects.
cknK.Δ324-331 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by Ptp69D1/Ptp69D[+]
cknK.Δ324-331 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by Ptp69D[+]/Ptp69D7
cknK.Δ324-331 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Ptp69D1/Ptp69D[+]
cknK.Δ324-331 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Ptp69D[+]/Ptp69D7
cknK.Δ324-331 is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of Lar5.5
cknK.Δ324-331, dock3 has abnormal neuroanatomy | embryonic stage phenotype
cknK.Δ324-331 has larval intersegmental nerve | embryonic stage phenotype, non-enhanceable by Ptp69D1/Ptp69D[+]
cknK.Δ324-331 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-enhanceable by Ptp69D1/Ptp69D[+]
cknK.Δ324-331 has larval intersegmental nerve | embryonic stage phenotype, non-enhanceable by Ptp69D[+]/Ptp69D7
cknK.Δ324-331 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-enhanceable by Ptp69D[+]/Ptp69D7
cknK.Δ324-331 has larval intersegmental nerve | embryonic stage phenotype, non-suppressible by Ptp69D1/Ptp69D[+]
cknK.Δ324-331 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-suppressible by Ptp69D1/Ptp69D[+]
cknK.Δ324-331 has larval intersegmental nerve | embryonic stage phenotype, non-suppressible by Ptp69D[+]/Ptp69D7
cknK.Δ324-331 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-suppressible by Ptp69D[+]/Ptp69D7
cknK.Δ324-331 is an enhancer of larval intersegmental nerve branch ISNb of A1-7 phenotype of dock3
cknK.Δ324-331 is an enhancer of larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype of Lar5.5
cknK.Δ324-331/ckn[+] is an enhancer of larval intersegmental nerve branch ISNb of A1-7 phenotype of dock3
cknK.Δ324-331, dock3 has larval intersegmental nerve branch ISNd of A1-7 phenotype
cknK.Δ324-331, dock3 has lateral longitudinal fascicle | embryonic stage phenotype
cknK.Δ324-331, dock3 has intermediate longitudinal fascicle | embryonic stage phenotype
Lar5.5 cknK.Δ324-331 double heterozygous embryos display bypass phenotypes with 39% penetrance.
A heterozygous or homozygous Ptp69D1 background fails to affect the penetrance of the ISNb bypass phenotype found in cknK.Δ324-331 heterozygotes or homozygotes.
A heterozygous or homozygous Ptp69D7 background fails to affect the penetrance of the ISNb bypass phenotype found in cknK.Δ324-331 heterozygotes or homozygotes.
ISNb pathfinding is delayed in approximately 23% of dock3 cknK.Δ324-331 double heterozygotes.
A heterozygous cknK.Δ324-331 background enhances ISNb pathfinding defects in dock3 homozygotes, from 6% to 43% of hemisegments.
dock3 cknK.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.