Excessive myosin activity in Mbs mutants causes photoreceptor movement out of the Drosophila eye disc epithelium
Excessive myosin activity in Mbs mutants causes photoreceptor movement out of the Drosophila eye disc epithelium
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DOI：
10.1091/mbc.e04-01-0057
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发表时间：
2004-07-01
影响因子：
3.3
通讯作者：
Treisman, JE
中科院分区：
文献类型：
--
作者：
Lee, A;Treisman, JE
神经细胞必须在保持细胞体在其原始位置的同时延伸一个可运动的生长锥。在迁移细胞中，肌凝蛋白收缩提供了将细胞后部拉向前沿的驱动力。我们已经描述了肌球蛋白轻链磷酸酶的功能，它可以下调肌球蛋白活性，在果蝇感光神经元中。编码这种酶的肌球蛋白结合亚基的基因发生突变，导致光感受器从眼盘上皮脱落，并向视柄移动。我们发现这种表型是由于肌凝蛋白调节轻链的过度磷酸化，而不是另一种潜在的底物Moesin，并且它需要非肌肉肌凝蛋白II重链Zipper。肌球蛋白结合亚基突变细胞继续表达顶端上皮标记物，不发生异位顶端收缩。此外，突变细胞留在上皮内，分化出异常的翼毛。我们认为，光感受器神经元中过度的肌球蛋白活性可能会将细胞体拉向生长锥，这一过程类似于正常的细胞迁移。
Neuronal cells must extend a motile growth cone while maintaining the cell body in its original position. In migrating cells, myosin contraction provides the driving force that pulls the rear of the cell toward the leading edge. We have characterized the function of myosin light chain phosphatase, which down-regulates myosin activity, in Drosophila photoreceptor neurons. Mutations in the gene encoding the myosin binding subunit of this enzyme cause photoreceptors to drop out of the eye disc epithelium and move toward and through the optic stalk. We show that this phenotype is due to excessive phosphorylation of the myosin regulatory light chain Spaghetti squash rather than another potential substrate, Moesin, and that it requires the nonmuscle myosin II heavy chain Zipper. Myosin binding subunit mutant cells continue to express apical epithelial markers and do not undergo ectopic apical constriction. In addition, mutant cells in the wing disc remain within the epithelium and differentiate abnormal wing hairs. We suggest that excessive myosin activity in photoreceptor neurons may pull the cell bodies toward the growth cones in a process resembling normal cell migration.