Published online 9 August 2004. doi:10.1083/jcb1664iti3
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 166, Number 4, 443-443
Kif2a cures monopolar disorder
| |
Bipolar spindles form in cells lacking Kif2a if MCAK is also inhibited.
|
|
The Eg5 kinesin helps build a bipolar spindle by sliding microtubules past each other at the spindle midzone. On page 473, Ganem and Compton show that bipolarity requires another kinesin, called Kif2a, that localizes to spindle poles.
Kif2a is strongly expressed in neuronal cells and is a member of a class of kinesins that depolymerize microtubules instead of stepping along their surface. The authors find that Kif2a is also present in several other vertebrate cell types and that reduction in Kif2a activity resulted in monopolar spindles.
Rescue experiments demonstrate that bipolar spindles fail to form following Kif2a inhibition because kinetochores chew up microtubule plus ends and pull spindle poles together. Bipolar spindles were restored if microtubule plus ends were stabilized at kinetochores by inhibition of another depolymerizing kinesin, called MCAK.
MCAK is needed to correct spindle attachment errors. Proper bipolar attachment generates tension that is thought to turn off the depolymerizing activity of MCAK. The work by Ganem and Compton suggests that Kif2a activity is also needed to create tension by lopping off tubulin subunits from the minus ends of spindle microtubules and thus initiating poleward microtubule flux. Slack microtubules resulting from the absence of Kif2a would thus lead to strong kinetochore activity and spindle collapse. 
Nicole LeBrasseur
lebrasn{at}rockefeller.edu
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
