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J. Cell Biol.,
Volume 143, Number 3, November 2, 1998 659-671
* CRC Cell Cycle Group, Cancer Research Campaign Laboratories, Department of Anatomy and Physiology, Medical Sciences
Institute, University of Dundee, Dundee DD1 4HN, Scotland; and A number of lines of evidence point to a predominance of cytokinesis defects in spermatogenesis in
hypomorphic alleles of the Drosophila polo gene. In
the pre-meiotic mitoses, cytokinesis defects result in
cysts of primary spermatocytes with reduced numbers
of cells that can contain multiple centrosomes. These are connected by a correspondingly reduced number of
ring canals, structures formed by the stabilization of the
cleavage furrow. The earliest defects during the meiotic
divisions are a failure to form the correct mid-zone and
mid-body structures at telophase. This is accompanied
by a failure to correctly localize the Pavarotti kinesin-
like protein that functions in cytokinesis, and of the septin Peanut and of actin to be incorporated into a
contractile ring. In spite of these defects, cyclin B is degraded and the cells exit M phase. The resulting spermatids are frequently binuclear or tetranuclear, in
which case they develop either two or four axonemes,
respectively. A significant proportion of spermatids in
which cytokinesis has failed may also show the segregation defects previously ascribed to polo1 mutants. We
discuss these findings in respect to conserved functions for the Polo-like kinases in regulating progression
through M phase, including the earliest events of cytokinesis.
Dipartimento di Biologia Evolutiva, Università di Siena, Via
Mattioli 4, 53100 Siena, Italy
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