期刊
SCIENCE
卷 343, 期 6171, 页码 649-652出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1243126
关键词
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资金
- NIH/National Institute of General Medical Sciences
- March of Dimes
- Burroughs Wellcome Fund
- Uehara Memorial Foundation
- Kanae Foundation for the Promotion of Medical Science
Despite our understanding of actomyosin function in individual migrating cells, we know little about the mechanisms by which actomyosin drives collective cell movement in vertebrate embryos. The collective movements of convergent extension drive both global reorganization of the early embryo and local remodeling during organogenesis. We report here that planar cell polarity (PCP) proteins control convergent extension by exploiting an evolutionarily ancient function of the septin cytoskeleton. By directing septin-mediated compartmentalization of cortical actomyosin, PCP proteins coordinate the specific shortening of mesenchymal cell-cell contacts, which in turn powers cell interdigitation. These data illuminate the interface between developmental signaling systems and the fundamental machinery of cell behavior and should provide insights into the etiology of human birth defects, such as spina bifida and congenital kidney cysts.
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