Mushroom body defect is required in parallel to Netrin for midline axon guidance in Drosophila

The outgrowth of many neurons within the central nervous system is
initially directed towards or away from the cells lying at the midline.
Recent genetic evidence suggests that a simple model of differential
sensitivity to the conserved Netrin attractants and Slit repellents is
insufficient to explain the guidance of all axons at the midline. In the
Drosophila embryonic ventral nerve cord, many axons still cross the
midline in the absence of the Netrin genes (NetA and NetB) or their
receptor frazzled. Here we show that mutation of mushroom body
defect (mud) dramatically enhances the phenotype of Netrin or
frazzled mutants, resulting in many more axons failing to cross the
midline, although mutations in mud alone have little effect. This
suggests that mud, which encodes a microtubule-binding coiled-coil
protein homologous to NuMA and LIN-5, is an essential component
of a Netrin-independent pathway that acts in parallel to promote
midline crossing. We demonstrate that this novel role of Mud in axon
guidance is independent of its previously described role in neural
precursor development. These studies identify a parallel pathway
controlling midline guidance in Drosophila and highlight a novel role
for Mud potentially acting downstream of Frizzled to aid axon
guidance