Mutants do not exhibit a midline crossover phenotype in the pCC/MP2 pathway axons.
The pCC/MP2 pathway forms correctly in homozygous embryos, although the cord may be slightly disorganised.
The longitudinal connectives are slightly disorganised in homozygous embryos, but no axons cross the midline inappropriately.
Homozygous embryos show motor branch truncations, especially the branches of ISNb and ISN. In 76% of hemisegments of the mutant embryos, the ISNb axons fail to extend to muscle 12 and instead stop at earlier choice points beneath muscles 6/7 or 13.
chicsand-1/chic01320 females fail to lay eggs. Lethal in combination with chic221. Embryonic motoneurons extend out into the periphery in chicsand-1/Df(2L)GpdhA embryos, correctly following their initial trajectories, but the growth cones arrest at branching choice points before reaching their final muscle targets. This premature arrest is seen in all motor branches. The stalled growth cones have numerous filopodia and are as large if not larger than their wild-type counterparts. Hemizygous chicsand-1 embryos show a substantial rescue of the "stranded" axonal phenotype if Dp(2;2)C619 (a duplication of the chic locus) is supplied maternally. Axon growth from homozygous dissected nerve cords cultured in vitro is reduced compared to wild-type.
Defective in navigation through a specific choice point during intersegmental nerve and segmental nerve b pathfinding. Intersegmental nerve projections also prematurely terminated. Subtle defects in CNS pathfinding also evident.
chicsand-1 has abnormal neuroanatomy | embryonic stage phenotype, suppressible by Khc::Ggal\MLCKKA.ftz
chicsand-1 is a suppressor of abnormal neuroanatomy | embryonic stage phenotype of Khc::Ggal\MLCKKA.ftz
chicsand-1 has larval intersegmental nerve phenotype, suppressible by Khc::Ggal\MLCKKA.ftz
chicsand-1 is a suppressor of dMP2 neuron phenotype of Rac1V12.UAS, Scer\GAL4ftz.ng
chicsand-1 is a suppressor of pCC neuron phenotype of Rac1V12.UAS, Scer\GAL4ftz.ng
chicsand-1 is a suppressor of vMP2 neuron phenotype of Rac1V12.UAS, Scer\GAL4ftz.ng
chicsand-1 is a suppressor of dMP2 neuron phenotype of Cdc42V12.UAS, Scer\GAL4ftz.ng
chicsand-1 is a suppressor of vMP2 neuron phenotype of Cdc42V12.UAS, Scer\GAL4ftz.ng
chicsand-1 is a suppressor of pCC neuron phenotype of Cdc42V12.UAS, Scer\GAL4ftz.ng
chicsand-1 is a suppressor of pCC neuron phenotype of Khc::Ggal\MLCKKA.ftz
chicsand-1 is a suppressor of vMP2 neuron phenotype of Khc::Ggal\MLCKKA.ftz
chicsand-1 is a non-suppressor of larval intersegmental nerve phenotype of Khc::Ggal\MLCKKA.ftz
The addition of chicsand-1 to any of Rho1N19.Scer\UAS, Rho1V14.Scer\UAS, Rac1N17.Scer\UAS or Cdc42N17.Scer\UAS has no effect on their midline crossover phenotypes in the pCC/MP2 pathway axons. The addition of chicsand-1 to Rac1V12.Scer\UAS suppresses the midline crossover phenotypes in the pCC/MP2 pathway axons. 57.3% of embryos exhibit the phenotype. An average of 1.5 crossovers are seen per embryo. The addition of chicsand-1 to Cdc42V12.Scer\UAS suppresses the midline crossover phenotypes in the pCC/MP2 pathway axons. 45.5% of embryos exhibit the phenotype. An average of 1.9 crossovers are seen per embryo.
The abnormal midline crossing of axons seen in robo1 heterozygotes is suppressed if the embryos are also heterozygous for chicsand-1. However, chicsand-1 robo1 double homozygotes show a severe disruption of the nerve cord. Large numbers of axons cross the midline within segment boundaries and major gaps are seen in the longitudinal connectives.
Pioneer neurons of the pCC/MP2 pathway stall less often and form the pathway with fewer errors in Khc::Ggal\MLCKKA.ftz chicsand-1 double mutant embryos compared to Khc::Ggal\MLCKKA.ftz single mutant embryos; only 15% of hemisegments have gaps in the pCC/MP2 pathway in double homozygous embryos and only 18% of hemisegments have gaps in the pCC/MP2 pathway in Khc::Ggal\MLCKKA.ftz chicsand-1/Khc::Ggal\MLCKKA.ftz + embryos.
Only 16% of double homozygous Khc::Ggal\MLCKKA.ftz chicsand-1 embryos and 18% of Khc::Ggal\MLCKKA.ftz chicsand-1/Khc::Ggal\MLCKKA.ftz + embryos show abnormal midline crossing of axons within the pCC/MP2 pathway (compared to 51% of Khc::Ggal\MLCKKA.ftz single homozygotes).
In Khc::Ggal\MLCKKA.ftz chicsand-1 embryos, all branches of the motor neuron projection are at least partially restored to wild type. Innervation to muscle 12 by the ISNb branch is restored from 24% of hemisegments in chicsand-1 single mutants to 96% of hemisegments in the Khc::Ggal\MLCKKA.ftz chicsand-1 double mutants. Similarly, in 88% of double mutant hemisegments, the ISN branch extends beyond the third branch point to innervate the dorsal-most muscles (1 and 2), compared to only 48% in chicsand-1 single mutants. The subtle overextension phenotype observed at muscle 12 of Khc::Ggal\MLCKKA.ftz single mutants is still seen in the double mutants.