TY - JOUR
T1 - A role for Drosophila IAP1-mediated caspase inhibition in Rac-dependent cell migration
AU - Geisbrecht, Erika R.
AU - Montell, Denise J.
N1 - Funding Information:
Thanks to researchers who contributed reagents and/or flies. This work was supported by a grant from the NIH (GM46425) to D.J.M.
PY - 2004/7/9
Y1 - 2004/7/9
N2 - Border cell migration in the Drosophila ovary is a relatively simple and genetically tractable model for studying the conversion of epithelial cells to migratory cells. Like many cell migrations, border cell migration is inhibited by a dominant-negative form of the GTPase Rac. To identify new genes that function in Rac-dependent cell motility, we screened for genes that when overexpressed suppressed the migration defect caused by dominant-negative Rac. Overexpression of the Drosophila inhibitor of apoptosis 1 (DIAP1), which is encoded by the thread (th) gene, suppressed the migration defect. Moreover, loss-of-function mutations in th caused migration defects but, surprisingly, did not cause apoptosis. Mutations affecting the Dark protein, an activator of the upstream caspase Dronc, also rescued RacN17 migration defects. These results indicate an apoptosis-independent role for DIAP1-mediated Dronc inhibition in Rac-mediated cell motility.
AB - Border cell migration in the Drosophila ovary is a relatively simple and genetically tractable model for studying the conversion of epithelial cells to migratory cells. Like many cell migrations, border cell migration is inhibited by a dominant-negative form of the GTPase Rac. To identify new genes that function in Rac-dependent cell motility, we screened for genes that when overexpressed suppressed the migration defect caused by dominant-negative Rac. Overexpression of the Drosophila inhibitor of apoptosis 1 (DIAP1), which is encoded by the thread (th) gene, suppressed the migration defect. Moreover, loss-of-function mutations in th caused migration defects but, surprisingly, did not cause apoptosis. Mutations affecting the Dark protein, an activator of the upstream caspase Dronc, also rescued RacN17 migration defects. These results indicate an apoptosis-independent role for DIAP1-mediated Dronc inhibition in Rac-mediated cell motility.
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U2 - 10.1016/j.cell.2004.06.020
DO - 10.1016/j.cell.2004.06.020
M3 - Article
C2 - 15242648
AN - SCOPUS:3142598843
SN - 0092-8674
VL - 118
SP - 111
EP - 125
JO - Cell
JF - Cell
IS - 1
ER -