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MBC in Press, published online ahead of print March 5, 2004
Mol. Biol. Cell 10.1091/mbc.E03-08-0603

A more recent version of this article appeared on May 1, 2004
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Submitted on August 18, 2003
Revised on January 29, 2004
Accepted on February 13, 2004

Genetic dissection of meiotic cytokinesis in Drosophila males

Maria Grazia Giansanti1, Rebecca M. Farkas2, Silvia Bonaccorsi3, Dan L. Lindsley4, Barbara T. Wakimoto5, Margaret T. Fuller6, and Maurizio Gatti3*

1 Istituto Pasteur Fondazione Cenci Bolognetti and Istituto di Biologia e Patologia Molecolari del CNR, Dipartimento di Genetica e Biologia Molecolare, Universitá "La Sapienza," Rome, Italy; These authors contributed equally to the work
2 Department of Developmental Biology and Department of Genetics, Stanford University School of Medicine, Stanford CA 94305-5329; These authors contributed equally to the work
3 Istituto Pasteur Fondazione Cenci Bolognetti and Istituto di Biologia e Patologia Molecolari del CNR, Dipartimento di Genetica e Biologia Molecolare, Universitá "La Sapienza," Rome, Italy
4 Section of Cell and Developmental Biology, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093-0349
5 Department of Biology and Center for Developmental Biology, University of Washington, Seattle, WA 98195-1800
6 Department of Developmental Biology and Department of Genetics, Stanford University School of Medicine, Stanford CA 94305-5329

* Corresponding author. E-mail address: maurizio.gatti{at}uniroma1.it.

We have used Drosophila male meiosis as a model system for genetic dissection of the cytokinesis mechanism. Drosophila mutants defective in meiotic cytokinesis can be easily identified by their multinucleate spermatids. Moreover, the large size of meiotic spindles allows characterization of mutant phenotypes with exquisite cytological resolution. We have screened a collection of 1955 homozygous mutant male sterile lines for those with multinucleate spermatids, and thereby identified mutations in 19 genes required for cytokinesis. These include 16 novel loci and three genes, diaphanous, four wheel drive and pebble, already known to be involved in Drosophila cytokinesis. To define the primary defects leading to failure of cytokinesis, we analyzed meiotic divisions in males mutant for each of these 19 genes. Examination of preparations stained for tubulin, anillin, KLP3A and F-actin revealed discrete defects in the components of the cytokinetic apparatus, suggesting that these genes act at four major points in a stepwise pathway for cytokinesis. Our results also indicated that the central spindle and the contractile ring are interdependent structures that interact throughout cytokinesis. Moreover, our genetic and cytological analyses provide further evidence for a cell-type specific control of Drosophila cytokinesis, suggesting that several genes required for meiotic cytokinesis in males are not required for mitotic cytokinesis.






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