In sliunspecified mutant embryos, all axons collapse on the midline.
The longitudinal tracts are collapsed at the midline in mutant embryos.
The fascicles of the longitudinal connectives are fused at the midline in mutant embryos. Nearly all ganglionic branches are misrouted and branches do not migrate in the same dorsoventral plane. 17% of ganglionic branches stall outside or inside the central nervous system and 37% cross the midline. The migration of dorsal tracheal branches towards the heart is disrupted in stage 16 mutant embryos. 20% of the branches are either completely missing or stalled at various lengths. 28% of the fusion events that normally interconnect the tracheal network over the dorsal midline are disrupted. All primary visceral branches grow towards the gut in mutant embryos, but the migration of the secondary branches appears irregular in some embryos, with some projections extending more dorsally or ventrally along the midgut than normal.
The heterozygote Df(1)NP5 phenotype is not enhanced in embryos also heterozygous for sliunspecified. In contrast, the frequency of midline guidance errors is increased in sliunspecified/+ embryos also heterozygous for Df(1)NP5. sliunspecified, in trans to a deficiency uncovering sli, such as Df(2R)Jp4 or Df(2R)Jp1 has complete midline fusion of all axon tracts. The semidominant interaction of sliunspecified and scbunspecified is also observed in sliunspecified/Df(2R)XTE-18 embryos.
In contrast to wild-type, the nuclear division and cytokinesis of GMC-1 in sli mutant embryos is symmetric producing two nuclei of equal sizes.
Embryos show collapse of axon fascicles at the central nervous system midline.
sli null mutants show a characteristic collapse of all axons onto the central nervous system midline.
No gross dentritic defects are seen in mutant embryos.
Collapsed CNS axon phenotype with frequent breaks in the longitudinal connectives. Midline glial cells become displaced ventrally during stage 12 onward.
sliunspecified mutant embryos show abnormal head involution. Abdominal transformations occur in combination with Pc like mutants.
sliunspecified has abnormal neuroanatomy phenotype, enhanceable by mewM6
sliunspecified has abnormal neuroanatomy phenotype, enhanceable by LanA9-32/scbunspecified
sliunspecified has abnormal neuroanatomy phenotype, enhanceable by LanA9-32
sliunspecified has abnormal neuroanatomy phenotype, enhanceable by ifk27e
sliunspecified has abnormal neuroanatomy phenotype, enhanceable by scbunspecified
sliunspecified/robo1unspecified is an enhancer of abnormal neuroanatomy | embryonic stage 16 phenotype of kuzunspecified
sliunspecified is an enhancer of abnormal neuroanatomy phenotype of LanA9-32
Tigx, sliunspecified has abnormal neuroanatomy phenotype
sliunspecified has fascicle phenotype, enhanceable by scbunspecified
sliunspecified has fascicle phenotype, enhanceable by mewM6
sliunspecified has fascicle phenotype, enhanceable by LanA9-32/scbunspecified
sliunspecified has fascicle phenotype, enhanceable by ifk27e
sliunspecified has phenotype, non-enhanceable by kuz[+]/kuzunspecified
sliunspecified has larval ventral nerve cord phenotype, non-suppressible by communspecified
sliunspecified/robo1unspecified is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of kuzunspecified
sliunspecified/robo1unspecified is an enhancer of commissure | embryonic stage 16 phenotype of kuzunspecified
sliunspecified/scbunspecified is an enhancer of fascicle phenotype of LanA9-32
sliunspecified is an enhancer of fascicle phenotype of LanA9-32
robo1unspecified, sliunspecified has larval longitudinal connective phenotype
LanA9-32, scbunspecified, sliunspecified has central nervous system phenotype
Tigx, sliunspecified has fascicle phenotype
kuzunspecified, sliunspecified/sli[+] has presumptive embryonic/larval central nervous system phenotype
The positioning of the longitudinal tracts in sliunspecified ; NetAunspecified NetBunspecified double mutant embryos is as seen in NetAunspecified NetBunspecified mutant embryos.
Longitudinal tracts collapse at the midline in sliunspecified robounspecified double mutant embryos.
The frequency of midline crossing is much higher in mewM6/Y;sliunspecified/+ and ifk27e/Y;sliunspecified mutants and also involves more lateral tracts. The semidominant interaction of sliunspecified and scbunspecified is also observed in sliunspecified/Df(2R)XTE-18 embryos. Tigx has a semidominant interaction with sliunspecified, Fas2 labelling of fascicles between segments is reduced and midline guidance defects are observed in one in three segments. LanA9-32 mutants, when double heterozygous with sliunspecified, exhibit midline crossover of Fas2-labelled axons in over 30% of segments. The degree of defasciculation and midline guidance errors in all axon tracts of the triple heterozygote of scbunspecified/sliunspecified;LanA9-32/+, appears to be additive of the individual phenotypes. In addition, a narrowing of the central nervous system and the medial displacement of all axon tracts is also seen in this mutant combination.
Fas2-positive axons cross the central nervous system midline in about 12% of sliunspecified kuzunspecified double heterozygotes, in contrast to either single heterozygote. kuzunspecified homozygotes that are also heterozygous for sliunspecified have a central nervous system (CNS) phenotype similar to kuzunspecified single mutants, but the position of the longitudinal connectives is shifted towards the CNS midline. Removal of one copy of kuz+ in a sliunspecified homozygous background does not enhance the sli mutant phenotype.
The addition of communspecified to sliunspecified mutants has no effect on the sliunspecified phenotype.
Commissures are formed in communspecified sliunspecified double mutant embryos but in an irregular pattern.
sliunspecified is partially rescued by Scer\GAL4sli.PS/sliUncleave.UAS
sliunspecified is partially rescued by sliUAS.cUa/Scer\GAL4sli.PS
Expression of sliScer\UAS.cUa under the control of Scer\GAL4sli.PS rescues the midline crossing phenotype seen in sliunspecified, but does not restore proper lateral position of the FasII-positive fascicles.
Expression of sliUncleave.Scer\UAS under the control of Scer\GAL4sli.PS rescues the midline crossing phenotype seen in sliunspecified, but does not restore proper lateral position of the FasII-positive fascicles.
