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Published online September 29, 2008
doi:10.1083/jcb.200807049
The Journal of Cell Biology, Vol. 183, No. 1, 157-168
The Rockefeller University Press, 0021-9525 $30.00
© 2008 Kunwar et al.
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Article

 Tre1 GPCR initiates germ cell transepithelial migration by regulating Drosophila melanogaster E-cadherin

Prabhat S. Kunwar1,2, Hiroko Sano1,2, Andrew D. Renault1,2, Vitor Barbosa1,2, Naoyuki Fuse3, and Ruth Lehmann1,2

1 Howard Hughes Medical Institute and 2 Kimmel Center for Biology and Medicine at the Skirball Institute for Biomolecular Medicine, Department of Cell Biology, New York University School of Medicine, New York, NY 10016
3 Global Center of Excellence Program, Division of Biological Science, Kyoto University, Kyoto 606-8502, Japan

Correspondence to Ruth Lehmann: lehmann{at}saturn.med.nyu.edu

Despite significant progress in identifying the guidance pathways that control cell migration, how a cell starts to move within an intact organism, acquires motility, and loses contact with its neighbors is poorly understood. We show that activation of the G protein–coupled receptor (GPCR) trapped in endoderm 1 (Tre1) directs the redistribution of the G protein Gβ as well as adherens junction proteins and Rho guanosine triphosphatase from the cell periphery to the lagging tail of germ cells at the onset of Drosophila melanogaster germ cell migration. Subsequently, Tre1 activity triggers germ cell dispersal and orients them toward the midgut for directed transepithelial migration. A transition toward invasive migration is also a prerequisite for metastasis formation, which often correlates with down-regulation of adhesion proteins. We show that uniform down-regulation of E-cadherin causes germ cell dispersal but is not sufficient for transepithelial migration in the absence of Tre1. Our findings therefore suggest a new mechanism for GPCR function that links cell polarity, modulation of cell adhesion, and invasion.

P.S. Kunwar and H. Sano contributed equally to this paper.

P.S. Kunwar's present address is Anderson Laboratory, Division of Biology, California Institute of Technology, Pasadena, CA 91125.

H. Sano's present address is Ochadai Academic Production, Division of Advanced Sciences, Ochanomizu University, Bunkyo-ku, Tokyo 112-8610, Japan.

A.D. Renault's present address is Max Planck Institute for Developmental Biology, Tübingen, D-72076 Germany.

Abbreviations used in this paper: AEL, after egg laying; DE-cadherin, Drosophila melanogaster E-cadherin; EMT, epithelial–mesenchymal transition; GPCR, G protein–coupled receptor; shg, shotgun; tre1, trapped in endoderm 1; tud, tudor; UAS, upstream activation sequence.

© 2008 Kunwar et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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Tre1 says when, and where, to go
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