Medial longitudinal tracts often cross the midline in mutant embryos (one or two segments in 9% of embryos).
No axons cross the midline in mutant embryos and as a result no commissures are formed. 97% of ganglionic branches stall or turn to migrate dorsally and posteriorly prematurely, before reaching the midline.
No commissures are seen in homozygous embryos.
Almost no axons cross the midline in communspecified mutant embryos.
communspecified has abnormal neuroanatomy phenotype, enhanceable by sli2/sli[+]
communspecified is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA
communspecified has larval longitudinal connective phenotype, enhanceable by sli2/sli[+]
communspecified is a non-enhancer of larval ventral nerve cord commissure phenotype of robo1unspecified
communspecified is a non-suppressor of larval ventral nerve cord phenotype of sliunspecified
The midline crossing defects of axons seen in Scer\GAL4eg-Mz360-driven fraΔC.Scer\UAS.T:Ivir\HA-expressing embryos are enhanced in a heterozygous communspecified/+ genetic background.
The longitudinal tract midline crossing phenotype seen in communspecified mutants is significantly enhanced by sli2/+, both in terms of the numbers of segments and the number of embryos affected.
The addition of communspecified to robounspecified embryos does not affect the number of commissure crossing the midline. The addition of communspecified to sliunspecified mutants has no effect on the sliunspecified phenotype.
Some axons can cross the midline in communspecified kusunspecified double mutant embryos, but in most neuromeres the comm mutant phenotype is epistatic to the kus mutant phenotype. However, if commissural axons have crossed the midline, then this neuromere shows a kus mutant phenotype. Commissures are formed in communspecified sliunspecified double mutant embryos but in an irregular pattern.
