The receptor tyrosine phosphatases DPTP69D and DPTP99A are expressed o
n motor axons in Drosophila embryos. In mutant embryos lacking DPTP69D
protein, motor neuron growth cones stop growing before reaching their
muscle targets, or follow incorrect pathways that bypass these muscle
s. Mutant embryos lacking DPTP99A are indistinguishable from wild type
. Motor axon defects in dptp69D dptp99A double mutant embryos, however
, are much more severe than in embryos lacking only DPTP69D. Our resul
ts demonstrate that DPTP69D and DPTP99A are required for motor axon gu
idance and that they have partially redundant functions during develop
ment of the neuromuscular system.