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Research Article |
1 Gene Discovery Research Center, National Institute of Advanced Industrial
Science and Technology (AIST), Tsukuba, Ibaraki 305-8562, Japan
2 Department of Cell Genetics, Exelixis Inc., South San Francisco, CA
94083-0511, USA
* Author for correspondence (e-mail: t-uyeda{at}aist.go.jp )
Accepted 21 February 2002
Myosin-II-null cells of Dictyostelium discoideum cannot divide in suspension, consistent with the dogma that myosin II drives constriction of the cleavage furrow and, consequently, cytokinesis (cytokinesis A). Nonetheless, when grown on substrates, these cells exhibit efficient, cell-cycle-coupled division, suggesting that they possess a novel, myosin-II-independent, adhesion-dependent method of cytokinesis (cytokinesis B). Here we show that double mutants lacking myosin II and either AmiA or coronin, both of which are implicated in cytokinesis B, are incapable of cell-cycle-coupled cytokinesis. These double mutants multiplied mainly by cytokinesis C, a third, inefficient, method of cell division, which requires substrate adhesion and is independent of cell cycle progression. In contrast, double mutants lacking AmiA and coronin were no sicker than each of the single mutants, indicating that the severe defects of myosin II-/AmiA- or myosin II-/coronin- mutants are not simple additive effects of two mutations. We take this as genetic evidence for two parallel pathways both of which lead to cell-cycle-coupled cytokinesis. This conclusion is supported by differences in morphological changes during cytokinesis in the mutant cell lines.
Key words: Cellular slime mold, Myosin II, AmiA, Coronin, GFP-histone H1
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