102D6;102F

102D2;4Rt;[102D2-102D2];[4Rt-4Rt];

Df(4)C3/+ embryos exhibit an increase in embryonic ISNb motor axon defects as compared to controls (both controls and Df(4)C3/+ flies contain Sema1a^UAS.cYa without a GAL4 driver).

Homozygous embryos show ISNb motor axon guidance defects (70.8% of hemisegments) and SNa motor axon guidance defects (74.2% of hemisegments).

The lateral Fas2-positive tract of the central nervous system is often thin and discontinuous in mutant embryos, but the intermediate Fas2-positive tract appears normal. Chordotonal organ axons show normal terminal bifurcations along the intermediate Fas2-positive tract.

Most homozygous Df(4)C3 mutants die at late embryonic stage, although some mutants reach the third-instar larval stage.

R1-R6 growth cones scatter around the lamina termination region in Df(4)C3 homozygous third instar larvae, leading to the appearance of a discontinuous termination layer in the lamina.

Df(4)C3 mutant embryos exhibit a v'ch1 sensory neuron mis-projection phenotype. The sensory neuron mis-projects anteriorly to the ISN, and one or more axons of the 1ch5 sensory neurons misproject to the SN. Df(4)C3 mutant embryos exhibit normal projection of the ISN and SN axons in all hemisegments in which v'ch1 and dorsal sensory axon defects occur.

Df(4)C3 homozygous embryos exhibit defects in the innervation of the ventral muscles in most of the segments examined.

The most distal SNa axon is often unable to separate from the dorsal SNa bundle in Df(4)C3 homozygous embryos and so fails to innervate muscle 24, resulting in a 'stall' phenotype.

In Df(4)C3 mutants, the outermost fascicle visible with Fas2 is reduced in thickness and is discontinuous along its entire length.

60.8% of homozygous hemisegments show defects in muscle 6/7 innervation and 47.3% show defects in muscle 12/13 innervation (these defects in ISNb axons include axons stalling, bypassing targets and absent or decreased muscle innervation). 74.3% of homozygous hemisegments show SNa pathway defects, failing to make the two characteristic turns between muscles 22 and 23 and muscles 23 and 24.

Mutants exhibit an axon guidance phenotype. The SNa often branches abnormally, and the ISNb nerve also sometimes branches abnormally.

Homozygous embryos show axon guidance defects both in the central nervous system and in the projections of motor nerves to their muscle targets in the periphery. ISNb growth cones often fail to defasciculate from one another at any or all three of the ISNb choice points. Occasionally they fail to exit the intersegmental nerve (ISN) and therefore bypass the ventral muscles, in some cases they innervate their ventral muscle targets via small projections made directly from the main branch of the ISN. More often, they exit the ISN but fail to defasciculate at choice points 2 and/or 3, leading to a thickened, stalled nerve branch and failure to innervate muscles 6 and 7 and/or 12. The segmental nerve is also often abnormal; SNa axons fail to defasciculate from one another at the second choice point in approximately 70% of segments and instead extend dorsally as a single branch. The outermost Fas2-positive longitudinal connective is often disrupted and is sometimes fused with the middle Fas2-positive longitudinal connective. Growth cones from the transverse nerve extend ectopic projections onto ventral muscles in 36.5% of segments.