The Plexin PLX-2 and the Ephrin EFN-4 Have Distinct Roles in MAB-20/Semaphorin 2A Signaling in Caenorhabditis elegans Morphogenesis

Author:

Nakao Fumi1,Hudson Martin L2,Suzuki Motoshi1,Peckler Zachary2,Kurokawa Rie1,Liu Zhicen1,Gengyo-Ando Keiko3,Nukazuka Akira1,Fujii Takashi1,Suto Fumikazu1,Shibata Yukimasa1,Shioi Go1,Fujisawa Hajime1,Mitani Shohei3,Chisholm Andrew D2,Takagi Shin1

Affiliation:

1. Division of Biological Science, Nagoya University Graduate School of Science, Chikusa-ku, Nagoya 464-8602, Japan

2. Department of Molecular, Cell and Developmental Biology, Sinsheimer Laboratories, University of California, Santa Cruz, California 95064 and

3. Department of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo 162-8666, Japan

Abstract

Abstract Semaphorins are extracellular proteins that regulate axon guidance and morphogenesis by interacting with a variety of cell surface receptors. Most semaphorins interact with plexin-containing receptor complexes, although some interact with non-plexin receptors. Class 2 semaphorins are secreted molecules that control axon guidance and epidermal morphogenesis in Drosophila and Caenorhabditis elegans. We show that the C. elegans class 2 semaphorin MAB-20 binds the plexin PLX-2. plx-2 mutations enhance the phenotypes of hypomorphic mab-20 alleles but not those of mab-20 null alleles, indicating that plx-2 and mab-20 act in a common pathway. Both mab-20 and plx-2 mutations affect epidermal morphogenesis during embryonic and in postembryonic development. In both contexts, plx-2 null mutant phenotypes are much less severe than mab-20 null phenotypes, indicating that PLX-2 is not essential for MAB-20 signaling. Mutations in the ephrin efn-4 do not synergize with mab-20, indicating that EFN-4 may act in MAB-20 signaling. EFN-4 and PLX-2 are coexpressed in the late embryonic epidermis where they play redundant roles in MAB-20-dependent cell sorting.

Publisher

Oxford University Press (OUP)

Subject

Genetics

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