期刊
JOURNAL OF CELL BIOLOGY
卷 167, 期 6, 页码 1019-1024出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200408090
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资金
- NCI NIH HHS [P30 CA042014, P30CA42014, P30 CA042014-16] Funding Source: Medline
- NCRR NIH HHS [P41 RR011823, RR11823-08] Funding Source: Medline
- NIGMS NIH HHS [R01 GM050877-10, T32 GM007464, R01 GM056498, R01 GM50877, R01 GM050877, T32 GM07464-27] Funding Source: Medline
Cell adhesion and migration are dynamic processes requiring the coordinated action of multiple signaling pathways, but the mechanisms underlying signal integration have remained elusive. Drosophila embryonic dorsal closure (DC) requires both integrin function and c-Jun amino-terminal kinase (JNK) signaling for opposed epithelial sheets to migrate, meet, and suture. Here, we show that PINCH, a protein required for integrin-dependent cell adhesion and actin-membrane anchorage, is present at the leading edge of these migrating epithelia and is required for DC. By analysis of native protein complexes, we identify RSU-1, a regulator of Ras signaling in mammalian cells, as a novel PINCH binding partner that contributes to PINCH stability. Mutation of the gene encoding RSU-1 results in wing blistering in Drosophila, demonstrating its role in integrin-dependent cell adhesion. Genetic interaction analyses reveal that both PINCH and RSU-1 antagonize JNK signaling during DC. Our results suggest that PINCH and RSU-1 contribute to the integration of JNK and integrin functions during Drosophila development.
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