|Gunsalus, K. C., Bonaccorsi,
S., Williams, E., Verni, F., Gatti, M. & Goldberg, M. L. (1995)
Mutations in twinstar, a Drosophila gene encoding a
cofilin/ADF homologue, result in defects in centrosome migration and
cytokinesis. J. Cell Biol. 131, 1243-1259.
describe the phenotypic and molecular characterization of twinstar (tsr),
an essential gene in Drosophila melanogaster. Two P-element induced
alleles of tsr (tsr1 and tsr2) result in late larval or pupal lethality.
Cytological examination of actively dividing tissues in these mutants
reveals defects in cytokinesis in both mitotic (larval neuroblast) and
meiotic (larval testis) cells. In addition, mutant spermatocytes show
defects in aster migration and separation during prophase/prometaphase
of both meiotic divisions. We have cloned the gene affected by these
mutations and shown that it codes for a 17-kD protein in the cofilin/ADF
family of small actin severing proteins. A cDNA for this gene has
previously been described by Edwards et al. (1994). Northern analysis
shows that the tsr gene is expressed throughout development, and that
the tsr1 and tsr2 alleles are hypomorphs that accumulate decreased
levels of tsr mRNA. These findings prompted us to examine actin behavior
during male meiosis to visualize the effects of decreased twinstar
protein activity on actin dynamics in vivo. Strikingly, both mutants
exhibit abnormal accumulations of F-actin. Large actin aggregates are
seen in association with centrosomes in mature primary spermatocytes.
Later, during ana/telophase of both meiotic divisions, aberrantly large
and misshaped structures appear at the site of contractile ring
formation and fail to disassemble at the end of telophase, in contrast
with wild-type. We discuss these results in terms of possible roles of
the actin-based cytoskeleton in centrosome movement and in cytokinesis.