Abstract
Anaphase B spindle elongation is characterized by the sliding apart of overlapping antiparallel interpolar (ip) microtubules (MTs) as the two opposite spindle poles separate, pulling along disjoined sister chromatids, thereby contributing to chromosome segregation and the propagation of all cellular life. The major biochemical “modules” that cooperate to mediate pole–pole separation include: (i) midzone pushing or (ii) braking by MT crosslinkers, such as kinesin-5 motors, which facilitate or restrict the outward sliding of antiparallel interpolar MTs (ipMTs); (iii) cortical pulling by disassembling astral MTs (aMTs) and/or dynein motors that pull aMTs outwards; (iv) ipMT plus end dynamics, notably net polymerization; and (v) ipMT minus end depolymerization manifest as poleward flux. The differential combination of these modules in different cell types produces diversity in the anaphase B mechanism. Combinations of antagonist modules can create a force balance that maintains the dynamic pre-anaphase B spindle at constant length. Tipping such a force balance at anaphase B onset can initiate and control the rate of spindle elongation. The activities of the basic motor filament components of the anaphase B machinery are controlled by a network of non-motor MT-associated proteins (MAPs), for example the key MT cross-linker, Ase1p/PRC1, and various cell-cycle kinases, phosphatases, and proteases. This review focuses on the molecular mechanisms of anaphase B spindle elongation in eukaryotic cells and briefly mentions bacterial DNA segregation systems that operate by spindle elongation.
Highlights
Anaphase B spindle elongation appears to be broadly deployed among eukaryotes and in some systems, e.g., S. cerevisiae cells and early C. elegans embryos, it is the major mechanism of chromosome segregation [8,9]
Underscoring the significance of the process, anaphase B spindle elongation contributes to the correction of mitotic chromosome attachment errors [11,12,13] and defects in the anaphase B component of chromosome segregation may contribute to human disease—for example a prolonged anaphase B in lymphocytes appears to correlate with an increased risk of cancer [14]
While a significant body of evidence supports such a midzone pushing model, other work has poles by motors located on the cell cortex can provide an alternative or complementary mechanism to shown that the pulling apart of the spindle poles by motors located on the cell cortex can provide an accomplish midzonal MT-MT sliding and anaphase B spindle elongation [38,39,40,41]
Summary
Chromosomes are physically separated on the pre-assembled mitotic spindle machinery by a cell type-specific combination of (i) chromosome-to-pole motility (anaphase A). The inhibition of isolated diatom spindle elongation by a pan-kinesin peptide a kinesin motor drives anaphase B [36], a hypothesis supported by the characterization of purified antibody suggested that a kinesin motor drives anaphase B [36], a hypothesis supported by the kinesin-5 motors with the potential to act like miniature myosin filaments that could cross-link and characterization of purified kinesin-5 motors with the potential to act like miniature myosin slide apart antiparallel ipMTs in the spindle midzone [28,37]. While a significant body of evidence supports such a midzone pushing model, other work has poles by motors located on the cell cortex can provide an alternative or complementary mechanism to shown that the pulling apart of the spindle poles by motors located on the cell cortex can provide an accomplish midzonal MT-MT sliding and anaphase B spindle elongation [38,39,40,41]. In Biology 2016, 5, and 51 all other figures, arrows depict direction of movement of ipMTs and aMTs
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
