Mitotic motors and chromosome segregation: the mechanism of anaphase B.

Publisher: Portland Press On The Behalf Of The Biochemical Society Country of Publication: England NLM ID: 7506897 Publication Model: Print Cited Medium: Internet ISSN: 1470-8752 (Electronic) Linking ISSN: 03005127 NLM ISO Abbreviation: Biochem Soc Trans Subsets: MEDLINE

Original Publication: London : Portland Press On The Behalf Of The Biochemical Society

Chromosome Segregation*; Anaphase/*physiology ; Molecular Motor Proteins/*metabolism ; Spindle Apparatus/*metabolism; Animals ; Embryo, Nonmammalian/cytology ; Embryo, Nonmammalian/physiology ; Fungi/cytology ; Fungi/physiology ; Kinesins/metabolism ; Kinetochores/metabolism ; Microtubules/metabolism ; Microtubules/ultrastructure

Anaphase B spindle elongation plays an important role in chromosome segregation. In the present paper, we discuss our model for anaphase B in Drosophila syncytial embryos, in which spindle elongation depends on an ip (interpolar) MT (microtubule) sliding filament mechanism generated by homotetrameric kinesin-5 motors acting in concert with poleward ipMT flux, which acts as an 'on/off' switch. Specifically, the pre-anaphase B spindle is maintained at a steady-state length by the balance between ipMT sliding and ipMT depolymerization at spindle poles, producing poleward flux. Cyclin B degradation at anaphase B onset triggers: (i) an MT catastrophe gradient causing ipMT plus ends to invade the overlap zone where ipMT sliding forces are generated; and (ii) the inhibition of ipMT minus-end depolymerization so flux is turned 'off', tipping the balance of forces to allow outward ipMT sliding to push apart the spindle poles. We briefly comment on the relationship of this model to anaphase B in other systems.

GM55507 United States GM NIGMS NIH HHS

0 (Molecular Motor Proteins)
EC 3.6.4.4 (Kinesins)

Date Created: 20110923 Date Completed: 20120117 Latest Revision: 20211203

20221213

10.1042/BST0391149

21936780