A Kin I-dependent Pacman-flux mechanism for anaphase A.
Anaphase 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.
Sharp
David J
DJ
Department of Physiology and Biophysics, Albert Einstein College of Medicine, Bronx, New York 10461, USA. dsharp@aecom.yu.edu
Rogers
Gregory C
GC
D000705:Anaphase / Q000502:physiology*; D000818:Animals; D002842:Chromatids / Q000201:enzymology / Q000378:metabolism*; D020090:Chromosome Segregation / Q000502:physiology; D016547:Kinesins / Q000502:physiology*; D018386:Kinetochores / Q000502:physiology; D008941:Spindle Apparatus / Q000201:enzymology / Q000502:physiology
D016547:Kinesins