期刊
JOURNAL OF CELL BIOLOGY
卷 198, 期 1, 页码 57-67出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201112114
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资金
- Canadian Institute for Health Research [MOP 114899, MOP 106548, MOP 115171]
- National Sciences and Engineering Research Council [355641]
- Canadian Cancer Society Research Institute [700824]
Membrane trafficking has well-defined roles during cell migration. However, its regulation is poorly characterized. In this paper, we describe the first screen for putative Rab-GTPase-activating proteins (GAPs) during collective cell migration of Drosophila melanogaster border cells (BCs), identify the uncharacterized Drosophila protein Evi5 as an essential membrane trafficking regulator, and describe the molecular mechanism by which Evi5 regulates BC migration. Evi5 requires its Rab-GAP activity to fulfill its functions during migration and acts as a GAP protein for Rab11. Both loss and gain of Evi5 function blocked BC migration by disrupting the Rab11-dependent polarization of active guidance receptors. Altogether, our findings deepen our understanding of the molecular machinery regulating endocytosis and subsequently cell signaling during migration.
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