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Development 129, 1283-1294 (2002)
© 2002 The Company of Biologists Limited

DEVELOPMENT AND DISEASE

The Kallmann syndrome gene homolog in C. elegans is involved in epidermal morphogenesis and neurite branching

Elena I. Rugarli1,*,{dagger}, Elia Di Schiavi2,*, Massimo A. Hilliard2, Salvatore Arbucci2, Cristina Ghezzi1, Anna Facciolli2, Giuseppe Coppola2, Andrea Ballabio1,3 and Paolo Bazzicalupo2,{dagger}

1 Telethon Institute of Genetics and Medicine (TIGEM), via P. Castellino III, 80131 Naples, ltaly
2 International Institute of Genetics and Biophysics (IIGB), via P. Castellino III, 80131 Naples, ltaly
3 Faculty of Medicine, II University of Naples, Naples, ltaly
* These two authors contributed equally to this work

{dagger}Authors for correspondence (e-mail: rugarli{at}tigem.it and bazzical{at}iigb.na.cnr.it)

Accepted 11 December 2001

Kallmann syndrome is an inherited disorder defined by the association of anosmia and hypogonadism, owing to impaired targeting and migration of olfactory axons and gonadotropin-releasing hormone secreting neurons. The gene responsible for the X-linked form of Kallmann syndrome, KAL-1, encodes a secreted protein of still elusive function. It has been proposed that KAL-1 might be involved in some aspects of olfactory axon guidance. However, the unavailability of a mouse model, and the difficulties in studying cellular and axonal migration in vertebrates have hampered an understanding of its function. We have identified the C. elegans homolog, kal-1, and document its function in vivo. We show that kal-1 is part of a mechanism by which neurons influence migration and adhesion of epidermal cells undergoing morphogenesis during ventral enclosure and male tail formation. We also show that kal-1 affects neurite outgrowth in vivo by modulating branching. Finally, we find that human KAL-1 cDNA can compensate for the loss of worm kal-1 and that overexpression of worm or human KAL-1 cDNAs in the nematode results in the same phenotypes. These data indicate functional conservation between the human and nematode proteins and establish C. elegans as a powerful animal in which to investigate KAL function in vivo. Our findings add a new player to the set of molecules, which appear to underlie both morphogenesis and axonal/neuronal navigation in vertebrates and invertebrates.

Key words: Kallmann syndrome, C. elegans, Morphogenesis, Neurite branching


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