期刊
JOURNAL OF CELL BIOLOGY
卷 155, 期 7, 页码 1185-1197出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200105102
关键词
Abelson kinase; Armadillo; adherens junctions; enabled; Drosophila
类别
资金
- NCI NIH HHS [T32 CA009156, 1T32CA72319, T32 CA072319, 5T3CA09156] Funding Source: Medline
- NIGMS NIH HHS [1F32GM20797, T32 GM007092, R01 GM047857, 5T32GM07092, F32 GM020797, R01 GM47857] Funding Source: Medline
Activation of the nonreceptor tyrosine kinase Abelson (Abl) contributes to the development of leukemia, but the complex roles of AN in normal development are not fully understood. Drosophila Abl links neural axon guidance receptors to the cytoskeleton. Here we report a novel role for Drosophila Abl in epithelial cells, where it is critical for morphogenesis. Embryos completely lacking both maternal and zygotic Abl die with defects in several morphogenetic processes requiring cell shape changes and cell migration. We describe the cellular defects that underlie these problems, focusing on dorsal closure as an example. Further, we show that the Abl target Enabled (Ena), a modulator of actin dynamics, is involved with Abl in morphogenesis. We find that Ena localizes to adherens junctions of most epithelial cells, and that it genetically interacts with the adherens junction protein Armadillo (Arm) during morphogenesis. The defects of abl mutants are strongly enhanced by heterozygosity for shotgun, which encodes DE-cadherin. Finally, loss of Abl reduces Arm and alpha -catenin accumulation in adherens junctions, while having little or no effect on other components of the cytoskeleton or cell polarity machinery. We discuss possible models for Abl function during epithelial morphogenesis in light of these data.
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