The GEX-2 and GEX-3 proteins are required for tissue morphogenesis and cell migrations in C. elegans
- 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 andgex-3, whose activities are necessary for initial steps of body morphogenesis in Caenorhabditis elegans. In the absence ofgex-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-3Drosophila 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.
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Footnotes
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↵5 These authors contributed equally to this work.
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↵6 Corresponding author.
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E-MAIL craig.mello{at}umassmed.edu; FAX (508) 856-4289.
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Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.955702.
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- Received October 22, 2001.
- Accepted January 10, 2002.
- Cold Spring Harbor Laboratory Press
