A number of lines of evidence point to a predominance of cytokinesis d
efects in spermatogenesis in hypomorphic alleles of the Drosophila pol
o gene. In the pre-meiotic mitoses, cytokinesis defects result in cyst
s of primary spermatocytes with reduced numbers of cells that can cont
ain multiple centrosomes. These are connected by a correspondingly red
uced 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 r
ing. In spite of these defects, cyclin B is degraded and the cells exi
t M phase. The resulting spermatids are frequently binuclear or tetran
uclear, in which case they develop either two or four axonemes, respec
tively. A significant proportion of spermatids in which cytokinesis ha
s failed may also show the segregation defects previously ascribed to
polo(1) mutants. We discuss these findings in respect to conserved fun
ctions for the Polo-like kinases in regulating progression through M p
hase, including the earliest events of cytokinesis.