作者: Jocelyn A. McDonald , Anna Khodyakova , George Aranjuez , Colleen Dudley , Denise J. Montell
DOI: 10.1016/J.CUB.2008.09.041
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摘要: Summary Background Many cells that migrate during normal embryonic development or in metastatic cancer first detach from an epithelium. However, this step is often difficult to observe directly in vivo, and the mechanisms controlling ability of cells leave epithelium are poorly understood. In addition, once detach, they must assume a migratory phenotype, involving changes cytoskeletal signaling dynamics. Drosophila border provide model system in which combination of forward genetics live-cell imaging can allow researchers investigate cellular and molecular epithelial cell detachment migration in vivo. Results We identified homolog serine/threonine kinase PAR-1 (MARK/Kin1) screen for mutations that disrupt migration. Previous studies two proteins, Apontic Notch, indirectly affect by regulating transcription downstream targets. contrast, modulates apical-basal polarity between cells to promote detachment. Furthermore, PAR-1, but not apical complex protein PAR-3, promotes directionality transient protrusions, which cells require sensing chemoattractant gradient. Conclusions conclude PAR-1-dependent required proper neighboring cells. Moreover, controlled influences migratory cells sense direction, critical feature Thus, work reveals new insights into distinct, essential, steps