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Vol. 15, Issue 5, 2509-2522, May 2004
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* Istituto Pasteur Fondazione Cenci Bolognetti and Istituto di Biologia e Patologia Molecolari del CNR, Dipartimento di Genetica e Biologia Molecolare, Universitá "La Sapienza," Rome, 00185 Italy;
Department of Developmental Biology and Department of Genetics, Stanford University School of Medicine, Stanford, California 94305-5329;
Section of Cell and Developmental Biology, Division of Biological Sciences, University of California, San Diego, La Jolla, California 92093-0349; and
|| Department of Biology and Center for Developmental Biology, University of Washington, Seattle, Washington 98195-1800
Submitted August 18, 2003;
Revised January 29, 2004;
Accepted February 13, 2004
Monitoring Editor: Ted Salmon
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 male mutants 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.
Online version of this article contains supporting material. Online version is available at www.molbiolcell.org.
These authors contributed equally to this work.
¶ Corresponding author. E-mail address: maurizio.gatti{at}uniroma1.it.
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