The GEX-2 and GEX-3 proteins are required for tissue morphogenesis and cell migrations in C. elegans (original) (raw)
- Martha C. Soto1,2,5,
- Hiroshi Qadota3,5,
- Katsuhisa Kasuya3,
- Makiko Inoue3,
- Daisuke Tsuboi3,4,
- Craig C. Mello1,2,6, and
- Kozo Kaibuchi3,4
- 1Program in Molecular Medicine and Cell Biology,2Howard Hughes Medical Institute, University of Massachusetts Cancer Center, Worcester, Massachusetts 01605, USA; 3Division of Signal Transduction, Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara 630-0101, Japan;4Department of Cell Pharmacology, Nagoya University, Graduate School of Medicine, Showa, Nagoya, Aichi 466-8550, Japan
Abstract
During body morphogenesis precisely coordinated cell movements and cell shape changes organize the newly differentiated cells of an embryo into functional tissues. Here we describe two genes, gex-2 and_gex-3_, whose activities are necessary for initial steps of body morphogenesis in Caenorhabditis elegans. In the absence of_gex-2_ and gex-3 activities, cells differentiate properly but fail to become organized. The external hypodermal cells fail to spread over and enclose the embryo and instead cluster on the dorsal side. Postembryonically gex-3 activity is required for egg laying and for proper morphogenesis of the gonad. GEX-2 and GEX-3 proteins colocalize to cell boundaries and appear to directly interact. GEX-2 and GEX-3 are highly conserved, with vertebrate homologs implicated in binding the small GTPase Rac and a GEX-3_Drosophila_ homolog, HEM2/NAP1/KETTE, that interacts genetically with Rac pathway mutants. Our findings suggest that GEX-2 and GEX-3 may function at cell boundaries to regulate cell migrations and cell shape changes required for proper morphogenesis and development.
Footnotes
↵5 These authors contributed equally to this work.
↵6 Corresponding author.
E-MAIL craig.mello{at}umassmed.edu; FAX (508) 856-4289.
Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.955702.
- Received October 22, 2001.
- Accepted January 10, 2002.
Cold Spring Harbor Laboratory Press