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First published online 17 March 2004
doi: 10.1242/dev.01069

Development 131, 1777-1786 (2004)
Published by The Company of Biologists 2004
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Intercellular signaling of reproductive development by the C. elegans DAF-9 cytochrome P450

Ho Yi Mak and Gary Ruvkun*

Department of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, Boston, MA 02114, USA

* Author for correspondence (e-mail: ruvkun{at}molbio.mgh.harvard.edu)

Accepted 12 January 2004

Parallel pathways control C. elegans reproductive development in response to environmental cues. Attenuation of daf-2 insulin-like or daf-7 TGFß-like signaling pathways cause developmental arrest at the stress resistant and long-lived dauer stage. Loss-of-function mutations in the cytochrome P450 gene daf-9 also cause dauer arrest and defects in cell migration. A rescuing daf-9::GFP fusion gene driven by the daf-9 promoter is expressed in two head cells at all stages, in the hypodermis from mid-second larval stage (L2) to the fourth larval stage (L4), and in the spermatheca of the adult hermaphrodite. Although the level of daf-9::GFP expression in the head cells and spermatheca is constant, hypodermal daf-9::GFP expression is modulated by multiple inputs. In particular, daf-9::GFP expression in the hypodermis is absolutely dependent on daf-12, the nuclear receptor that is negatively regulated by daf-9 gene activity, suggesting feedback control between daf-9 and daf-12 in this tissue. daf-9 expression exclusively in the hypodermis is sufficient to restore reproductive development in daf-9 mutant animals, suggesting that daf-9 functions in a cell nonautonomous manner. Furthermore, constitutive expression of daf-9 in the hypodermis suppresses dauer arrest of daf-7 mutant animals and inhibits dauer remodelling of some tissues in daf-2 mutant animals. Thus, daf-9 may integrate outputs from daf-2 and daf-7 signaling pathways to relay neuroendocrine signals through synthesis of a lipophilic hormone.

Key words: daf-9, daf-12, Dauer, Gonadal migration, Cytochrome P450, Insulin, C. elegans, TGFß


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