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doi: 10.1242/10.1242/dev.00148

1 Centre de Génétique Moléculaire et Cellulaire, CNRS
UMR-5534, Université Claude Bernard Lyon-1, 69622 Villeurbanne,
France
2 Department of Neurobiology and Behavior, The State University of New York at
Stony Brook, Stony Brook, New York 11794, USA
3 Karolinska Institute, Department of Biosciences, Södertörn
University College, Section of Natural Sciences, S-14189 Huddinge,
Sweden
Author for correspondence (e-mail:
durand-b{at}univ-lyon1.fr)
Accepted 3 September 2002
Ciliated neurons play an important role in sensory perception in many animals. Modified cilia at dendrite endings serve as sites of sensory signal capture and transduction. We describe Drosophila mutations that affect the transcription factor RFX and genetic rescue experiments that demonstrate its central role in sensory cilium differentiation. Rfx mutant flies show defects in chemosensory and mechanosensory behaviors but have normal phototaxis, consistent with Rfx expression in ciliated sensory neurons and neuronal precursors but not in photoreceptors. The mutant behavioral phenotypes are correlated with abnormal function and structure of neuronal cilia, as shown by the loss of sensory transduction and by defects in ciliary morphology and ultrastructure. These results identify Rfx as an essential regulator of ciliated sensory neuron differentiation in Drosophila.
Key words: Ciliated sensory neuron, RFX, Drosophila
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