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First published online 2 December 2004
doi: 10.1242/dev.01568
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1 Molecular Biology, Cell Biology, and Biochemistry Department, Brown
University, Providence, RI 02912, USA
2 Molecular Biology and Virology Laboratory, The Salk Institute for Biological
Studies, La Jolla, CA 92037, USA
3 Department of Biology, University of California, San Diego, La Jolla, CA
92093, USA
4 Department of Zoology, Oregon State University, Corvallis, OR 97331, USA
Author for correspondence (e-mail:
michael_mckeown{at}brown.edu)
Accepted 4 November 2004
Mutations in the Drosophila retained/dead ringer (retn) gene lead to female behavioral defects and alter a limited set of neurons in the CNS. retn is implicated as a major repressor of male courtship behavior in the absence of the fruitless (fru) male protein. retn females show fru-independent male-like courtship of males and females, and are highly resistant to courtship by males. Males mutant for retn court with normal parameters, although feminization of retn cells in males induces bisexuality. Alternatively spliced RNAs appear in the larval and pupal CNS, but none shows sex specificity. Post-embryonically, retn RNAs are expressed in a limited set of neurons in the CNS and eyes. Neural defects of retn mutant cells include mushroom body ß-lobe fusion and pathfinding errors by photoreceptor and subesophageal neurons. We posit that some of these retn-expressing cells function to repress a male behavioral pathway activated by fruM.
Key words: Courtship, Behavior, retained, fruitless, Neuronal pathfinding, Drosophila
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