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First published online 6 October 2004
doi: 10.1242/dev.01423

Development 131, 5381-5392 (2004)
Published by The Company of Biologists 2004
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FGF and PI3 kinase signaling pathways antagonistically modulate sex muscle differentiation in C. elegans

Isaac E. Sasson and Michael J. Stern*

Yale University School of Medicine, Department of Genetics, I-354 SHM, PO Box 208005, New Haven, CT 06520-8005, USA

* Author for correspondence (e-mail: michael.stern{at}yale.edu)

Accepted 31 August 2004

Myogenesis in vertebrate myocytes is promoted by activation of the phosphatidyl-inositol 3'-kinase (PI3 kinase) pathway and inhibited by fibroblast growth factor (FGF) signaling. We show that hyperactivation of the Caenorhabditis elegans FGF receptor, EGL-15, similarly inhibits the differentiation of the hermaphrodite sex muscles. Activation of the PI3 kinase signaling pathway can partially suppress this differentiation defect, mimicking the antagonistic relationship between these two pathways known to influence vertebrate myogenesis. When ectopically expressed in body wall muscle precursor cells, hyperactivated EGL-15 can also interfere with the proper development of the body wall musculature. Hyperactivation of EGL-15 has also revealed additional effects on a number of fundamental processes within the postembryonic muscle lineage, such as cell division polarity. These studies provide important in vivo insights into the contribution of FGF signaling events to myogenesis.

Key words: FGF receptor, EGL-15, PI3 kinase, Signal transduction, Muscle differentiation, M lineage, Myoblast, SM, Sex muscles


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