Dynein is a minus-end-directed microtubule motor that exists in two forms. Axonemal dynein promotes microtubule sliding for beating of cilia and flagella. Cytoplasmic dynein moves processively along microtubules and, in addition to organelle

INTRODUCTION Dynein is a minus-end-directed microtubule motor that exists in two forms. Axonemal dynein promotes microtubule sliding for beating of cilia and flagella. Cytoplasmic dynein moves processively along microtubules and, in addition to organelle positioning and transport, plays key roles in cell cycle events, including nucleus-centrosome coupling, nuclear envelope breakdown, spindle assembly/positioning and chromosome segregation (Gusnowski and Srayko, 2011; Hebbar et al., 2008; Huang et al., 2011; Salina et al., 2002; Splinter et al., 2010; Stuchell-Brereton et al., 2011; Wainman et al., 2009). Dynein is a large complex composed of four subunit types: heavy (containing motor activity), light, intermediate and light intermediate chains (Höök and Vallee, 2006; Susalka and Pfister, 2000). Dynactin and LIS1 are dynein accessory factors (King and Schroer, 2000; Mesngon et al., 2006). LIS1 directly binds several dynein and dynactin subunits through its C-terminal WD-repeat domain, and LIS1 binding enhances dynein motor activity (Faulkner et al., 2000; Mesngon et al., 2006; Sasaki et al., 2000; Smith et al., 2000; Tai et al., 2002). The importance of LIS1 for dynein function is evidenced by the fact that LIS1 mutants have defects in many dynein-dependent processes (Faulkner et al., 2000; Hebbar et al., 2008; Li et al., 2005; Tai et al., 2002). Loss or mutation of one copy of human LIS1 (PAFAH1B1 – Human Gene Nomenclature Database) causes type I lissencephaly (‘smooth brain’), a brain malformation disorder associated with neuronal migration defects (Gambello et al., 2003; Hirotsune et al., 1998; Vallee and Tsai, 2006; Wynshaw-Boris, 2007). Neuronal migration requires proper migration and positioning of the nucleus (Malone et al., 2003; Tanaka et al., 2004; Tsai and Gleeson, 2005). Dynein plays a major role in regulating these processes by promoting interaction of the nucleus with microtubules and microtubule-organizing centers. The Drosophila homolog of human Lis1 plays key roles during neurogenesis and oogenesis, presumably via its regulation of dynein. Drosophila Lis-1 neuroblasts have defects in centrosome migration, bipolar spindle assembly, centrosomal attachment to spindles and spindle checkpoint function (Siller and Doe, 2008; Siller et al., 2005). In Drosophila oocytes, Lis-1 regulates nuclear migration and positioning (Lei and Warrior, 2000). A detailed characterization of the role of Lis-1 in Drosophila spermatogenesis, however, has not been reported. Drosophila spermatogenesis is an ideal system for studying cell division. Meiotic spindles of spermatocytes are large and, hence, convenient for cytological analysis, relaxed checkpoints facilitate the study of cell cycle mutants and alterations in the highly regular appearance of immature spermatids are diagnostic of meiotic division defects (Cenci et al., 1994; Rebollo and González, 2000). The stages of Drosophila spermatogenesis are well defined (Fuller, 1993). Germline stem cells give rise to spermatogonia, which undergo four synchronous mitotic divisions with incomplete cytokinesis to generate 16-cell cysts of primary spermatocytes. After premeiotic S phase, primary spermatocytes enter G2, a prolonged growth period. Meiosis I yields 32-cell cysts of Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, U-4225 Medical Research Building III, 465 21st Avenue South, Nashville, TN 37232-8240, USA.