RhoL controls invasion and Rap1 localization during immune cell transmigration in Drosophila.

ABSTRACT: Human immune cells have to penetrate an endothelial barrier during their beneficial pursuit of infection and their destructive infiltration of tissues in autoimmune diseases. This transmigration requires Rap1 GTPase to activate integrin affinity. We define a new model system for this process by demonstrating, with live imaging and genetics, that during embryonic development Drosophila melanogaster immune cells penetrate an epithelial, Drosophila E-cadherin (DE-cadherin)-based tissue barrier. A mutant in RhoL, a GTPase homologue that is specifically expressed in haemocytes, blocks this invasive step but not other aspects of guided migration. RhoL mediates integrin adhesion caused by Drosophila Rap1 overexpression and moves Rap1 away from a concentration in the cytoplasm to the leading edge

SUBMITTER: Siekhaus D 

PROVIDER: S-EPMC3006444 | biostudies-literature | 2010 Jun

REPOSITORIES: biostudies-literature