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

Author:

Bergeret Evelyne1,Pignot-Paintrand Isabelle2,Guichard Annabel3,Raymond Karine1,Fauvarque Marie-Odile1,Cazemajor Michel4,Griffin-Shea Ruth1

Affiliation:

1. DBMS-CNRS UMR 5092 1 and

2. DBMS-IFR 27 INSERM, 2 CEA-Grenoble, Grenoble, and

3. Biology Department, University of California at San Diego, San Diego, California3

4. CNRS UMR 7592, University of Paris VII, Jussieu, Paris, 4 France, and

Abstract

ABSTRACT 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.

Publisher

American Society for Microbiology

Subject

Cell Biology,Molecular Biology

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