scbunspecified mutants exhibit midline fusions as well as transient merging of lateral fascicles. scbunspecified, in trans to a deficiency uncovering only scb, such as Df(2R)XTE-18, has an integrin-like mutant phenotype. The heterozygote Df(1)NP5 phenotype is not enhanced in embryos also heterozygous for scbunspecified. The medial Fas2-labelled fascicles, in scbunspecified/Df(2R)Jp1 embryos, which lack all scb function and are heterozygous for sli, make midline guidance errors in all segments. Fusion is also observed of the two most medial but not the most lateral axon fascicles. The semidominant interaction of sliunspecified and scbunspecified is also observed in scbunspecified/Df(2R)Jp4 embryos.
Embryos have a small mid-dorsal hole, which has a necrotic rim.
scbunspecified has abnormal neuroanatomy phenotype, enhanceable by sli2
scbunspecified has abnormal neuroanatomy phenotype, suppressible by LanA9-32
LanA9-32/scbunspecified is an enhancer of abnormal neuroanatomy phenotype of sliunspecified
scbunspecified is an enhancer of abnormal neuroanatomy phenotype of sliunspecified
scbunspecified is a suppressor of abnormal neuroanatomy phenotype of LanA9-32
LanA9-32, scbunspecified, sli2 has abnormal neuroanatomy phenotype
scbunspecified has fascicle phenotype, enhanceable by sli2/LanA9-32
scbunspecified has fascicle phenotype, enhanceable by sli2
scbunspecified has central nervous system phenotype, suppressible by LanA9-32
sliunspecified/scbunspecified is an enhancer of fascicle phenotype of LanA9-32
LanA9-32/scbunspecified is an enhancer of fascicle phenotype of sliunspecified
scbunspecified is an enhancer of fascicle phenotype of sliunspecified
LanA9-32, scbunspecified has fascicle phenotype
LanA9-32, scbunspecified, sliunspecified has central nervous system phenotype
In scbunspecified/+ sli2/+ double heterozygous mutants the frequency of midline guidance errors is increased over the level observed in scbunspecified homozygous mutants. 58% of segments had midline guidance defects (as assayed by Fas2). scbunspecified/+ sli2/+ double heterozygotes exhibit defects in the middle and most lateral axon tracts. The semidominant interaction of sliunspecified and scbunspecified is also observed in scbunspecified/Df(2R)Jp4 embryos. Midline guidance errors are not visible in LanA9-32/+; scbunspecified/+ double mutants, in contrast to single mutant heterozygotes. However, defasciculation and interruptions to the Fas2-labelling of the most lateral fascicle are observed. 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.
