comm⁵ mutant embryos exhibit a commissureless phenotype.

Mitotically recombined neuronal clones homozygous for comm⁵ cross the ventral midline in 58% of cases, compared to 85% of wild-type instances.

When single comm⁺ neurectoderm cells are transplanted into dorsocentral positions within the thoracic or abdominal neurectoderm of a comm⁵ host, 40% of these clones include neurons with contralateral projections, which contrasts with comm⁵ embryos in which only all such neurons project ipsilaterally. However when comm⁺ cells are transplanted into comm⁺ embryos 83% of these neurons project contralaterally. When single comm⁵ neurectoderm cells are transplanted into dorsocentral positions within the thoracic or abdominal neurectoderm of a comm⁺ host, contralateral projections are lacking in 69% of clones, compared to just 17% in controls. When the NB3-1 and NB5-6 are examined specifically, only ipsilateral projections ae seen, which contrasts with wild-type where contralateral projections are generated.

Homozygous embryos lack commissural axons.

comm⁵ embryos (in which the neuromuscular synaptogenesis defects have been specifically rescued, independent of the CNS midline defects, by expression of comm^Scer\UAS.cWa under the control of Scer\GAL4⁰⁰⁵) do not have commissural tracts. However, several axons can cross the midline. Cells near the midline are laterally dislocated. Cell bodies of the RP3, RP2 and aCC neurons are present in all half-segments examined and are laterally displaced. Axon terminals are present on muscles 6 and 7 in 90% of half-segments, on muscle 12 in 89% of half-segments, muscle 2 in 100% of half-segments and muscle 1 in 95% of half-segments. In 75% of cases in comm⁵ embryos (in which the neuromuscular synaptogenesis defects have been specifically rescued, independent of the CNS midline defects, by expression of comm^Scer\UAS.cWa under the control of Scer\GAL4⁰⁰⁵) the RP3 axon innervating muscles 6 and 7 is ipsilateral (has not crossed the midline), in contrast to wild type where the RP3 axon innervating muscles 6 and 7 has always crossed the midline. In the remaining 25% of cases, the RP3 axon innervating muscles 6 and 7 is contralateral (has crossed the midline). Regardless of its midline decision, in all cases the subsequent axon pathways of the RP3 neuron remain the same as in wild-type embryos. 47% of V motorneurons cross the midline in comm⁵ embryos (in which the neuromuscular synaptogenesis defects have been specifically rescued, independent of the CNS midline defects, by expression of comm^Scer\UAS.cWa under the control of Scer\GAL4⁰⁰⁵), in contrast to wild-type embryos where they always cross the midline. In all cases, subsequent growth cone guidance accuracy of the V motorneuron is normal. The axon pathway of the aCC neurons is normal in comm⁵ embryos (in which the neuromuscular synaptogenesis defects have been specifically rescued, independent of the CNS midline defects, by expression of comm^Scer\UAS.cWa under the control of Scer\GAL4⁰⁰⁵), and no aCC neurons cross the midline, as in wild type.

Muscles appear morphologically normal in homozygous embryos. The axon pathways of the aCC and RP2 motoneurons remain normal both within the central nervous system and periphery until the axons reach near the normal target muscles. The RP3 and RP5 motoneuron axon pathways extend ipsilaterally instead of crossing the midline as in wild-type embryos, however their subsequent pathways both in the central nervous system and periphery are normal until the axons reach near the normal target muscles. The motoneuron growth cones fail to initiate synaptogenesis on contacting their target muscles in homozygous or comm¹/comm⁵ embryos. The axons either stall just short of synaptic targets or they extend beyond the normal stopping points without apparently settling on alternative targets. These phenotypes are seen in the five motoneuron nerve groups (the ISN, SNa, SNb, SNc and SNd).

Both pairs of commissures are missing in all thoracic and abdominal segments. Many commissural growth cones initially extend toward the midline; however they soon retract and join longitudinal pathways without crossing the midline.

comm⁵/comm[+] is an enhancer of symmetrical commissure phenotype of elav⁵

comm⁵/comm[+] is an enhancer of connective phenotype of elav⁵