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Molecular and Cellular Biology, September 2001, p. 6280-6291, Vol. 21, No. 18
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.18.6280-6291.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

RotundRacGAP Functions with Ras during Spermatogenesis and Retinal Differentiation in Drosophila melanogaster

Evelyne Bergeret,¹ Isabelle Pignot-Paintrand,^2, Annabel Guichard,³ Karine Raymond,¹ Marie-Odile Fauvarque,¹ Michel Cazemajor,^4, and Ruth Griffin-Shea^1,*

DBMS-CNRS UMR 5092¹ and DBMS-IFR 27 INSERM,² CEA-Grenoble, Grenoble, and CNRS UMR 7592, University of Paris VII, Jussieu, Paris,⁴ France, and Biology Department, University of California at San Diego, San Diego, California³

Received 12 January 2001/Returned for modification 27 February 2001/Accepted 21 June 2001

Our analysis of rotund (rn) null mutations in Drosophila melanogaster revealed that deletion of the rn locus affects both spermatid and retinal differentiation. In the male reproductive system, the absence of RnRacGAP induced small testes, empty seminal vesicles, short testicular cysts, reduced amounts of interspermatid membrane, the absence of individualization complexes, and incomplete mitochondrial condensation. Flagellar growth continued within the short rn null cysts to produce large bulbous terminations of intertwined mature flagella. Organization of the retina was also severely perturbed as evidenced by grossly misshapen ommatidia containing reduced numbers of photoreceptor and pigment cells. These morphological phenotypes were rescued by genomic rnRacGAP transgenes, demonstrating that RnRacGAP function is critical to spermatid and retinal differentiation. The testicular phenotypes were suppressed by heterozygous hypomorphic mutations in the Dras1 and drk genes, indicating cross talk between RacGAP-regulated signaling and that of the Ras pathway. The observed genetic interactions are consistent with a model in which Rac signaling is activated by Ras and negatively regulated by RnRacGAP during spermatid differentiation. RnRacGAP and Ras cross talk also operated during retinal differentiation; however, while the heterozygous hypomorphic drk mutation continued to act as a suppressor of the rn null mutation, the heterozygous hypomorphic Dras1 mutation induced novel retinal phenotypes.

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^* Corresponding author. Mailing address: DBMS-CNRS UMR 5092, CEA-Grenoble, 17 Rue des Martyrs, F-38054 Grenoble Cedex 9, France. Phone: 33-4-38-78-30-90. Fax: 33-4-38-78-51-85. E-mail: ruth.griffin-shea{at}cea.fr.

Present address: CNRS-CERMAV, 38041 Grenoble Cedex 9, France.

Present address: ENSAR-INRA, Laboratoire Ecologie et Sciences Phytosanitaires, CS 84215, F-35042 Rennes Cedex, France.

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Molecular and Cellular Biology, September 2001, p. 6280-6291, Vol. 21, No. 18
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.18.6280-6291.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

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