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lüll A Kin I-dependent Pacman-flux mechanism for anaphase A Sharp DJ; Rogers GCCell Cycle 2004[Jun]; 3 (6): 707-10Anaphase A chromatid-to-pole motion is fundamental for proper chromosome segregation in most systems. During the past several decades, two models for the mechanism of anaphase A have come to prominence. The Pacman model posits that chromatids induce the depolymerization of microtubule plus-ends embedded in kinetochores, thereby 'chewing' their way poleward. Alternatively, the Poleward-flux model posits that chromatids are 'reeled-in' to poles by the continual depolymerization of the minus-ends of kinetochore-associated microtubules, which are focused at spindle poles. In a recent study, we reported that anaphase A in Drosophila requires the depolymerization of both ends of kinetochore-associated microtubules, simultaneously. This is driven by two members of the Kin I subfamily of kinesins, termed KLP59C and KLP10A, which target specifically to chromatids and spindle poles, respectively. We have termed this hybrid of Pacman and Poleward flux the Kin I-dependent Pacman-flux mechanism for anaphase A. Here, we discuss the implications of these findings and explore potential additional components required to drive chromatid-to-pole motion by such a mechanism.|Anaphase/*physiology[MESH]|Animals[MESH]|Chromatids/enzymology/*metabolism[MESH]|Chromosome Segregation/physiology[MESH]|Kinesins/*physiology[MESH]|Kinetochores/physiology[MESH]|Spindle Apparatus/enzymology/physiology[MESH] |