Desai C J, Gindhart J G, Goldstein L S, Zinn K
Division of Biology, California Institute of Technology, Pasadena, 91125, USA.
Cell. 1996 Feb 23;84(4):599-609. doi: 10.1016/s0092-8674(00)81035-1.
The receptor tyrosine phosphatases DPTP69D and DPTP99A are expressed on 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 muscles. 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 results demonstrate that DPTP69D and DPTP99A are required for motor axon guidance and that they have partially redundant functions during development of the neuro-muscular system.
受体酪氨酸磷酸酶DPTP69D和DPTP99A在果蝇胚胎的运动轴突上表达。在缺乏DPTP69D蛋白的突变胚胎中，运动神经元生长锥在到达其肌肉靶点之前停止生长，或者沿着绕过这些肌肉的错误路径延伸。缺乏DPTP99A的突变胚胎与野生型没有区别。然而，dptp69D dptp99A双突变胚胎中的运动轴突缺陷比仅缺乏DPTP69D的胚胎严重得多。我们的结果表明，DPTP69D和DPTP99A是运动轴突导向所必需的，并且它们在神经肌肉系统发育过程中具有部分冗余功能。
