No detectable P element.
Grossly abnormal CNS and sensory nervous system. Outgrowth of motor axons from the CNS is greatly delayed. Larval muscle formation and maintenance are not affected, though there is a higher frequency of mild muscle pattern aberrations than in wild type, primarily in abdominal segments 4 and 5. The adult muscle prepattern, revealed by persistent twi-expressing cells, is unaffected. Myotube uncoupling is unaffected. The maturation and maintenance of the contractile and electrical properties of the muscle are unaffected.
Innervation of muscles during embryogenesis fails or is delayed.
Severe CNS defects. The aCC and pCC neurons have abnormal axon morphology. Cells involved in the circumferential or mediolateral condensation of the CNS may be defective: nerve cord condensation along the mediolateral axis is retarded and there are often gaps along the midline.
C. Doe.
In pros mutants, where innervation of muscles fails, connectin and Fas3 are expressed on muscle surface beginning in same developmental pattern as in wild type. However Fas3 expression declines towards the end of embryogenesis, whereas it persists in wild type. In pros mutants functional glutamate receptors are expressed at normal time and distribution over the muscle surface but subsequently fail to cluster to the neuromuscular junction as they would in wild type, and second phase of glutamate receptor synthesis characteristic of wild type fails to occur. The few pros mutants where innervation occurs but is delayed show late clustering and late second phase synthesis of glutamate receptors, indicating that these events are innervation-dependent.