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Department of Biology, The Johns Hopkins University, Baltimore, Maryland 21218
Proper positioning of the mitotic spindle is
often essential for cell division and differentiation processes. The asymmetric cell division characteristic of
budding yeast, Saccharomyces cerevisiae, requires that
the spindle be positioned at the mother-bud neck and
oriented along the mother-bud axis. The single dynein
motor encoded by the S. cerevisiae genome performs an
important but nonessential spindle-positioning role.
We demonstrate that kinesin-related Kip3p makes a
major contribution to spindle positioning in the absence of dynein. The elimination of Kip3p function in
dyn1
cells severely compromised spindle movement
to the mother-bud neck. In dyn1 cells that had completed positioning, elimination of Kip3p function
caused spindles to mislocalize to distal positions in
mother cell bodies. We also demonstrate that the spindle-positioning defects exhibited by dyn1 kip3 cells are
caused, to a large extent, by the actions of kinesin-
related Kip2p. Microtubules in kip2 cells were shorter
and more sensitive to benomyl than wild-type, in contrast to the longer and benomyl-resistant microtubules
found in dyn1 and kip3 cells. Most significantly, the
deletion of KIP2 greatly suppressed the spindle localization defect and slow growth exhibited by dyn1 kip3
cells. Likewise, induced expression of KIP2 caused
spindles to mislocalize in cells deficient for dynein and
Kip3p. Our findings indicate that Kip2p participates in
normal spindle positioning but antagonizes a positioning mechanism acting in dyn1 kip3 cells. The observation that deletion of KIP2 could also suppress the inviability of dyn1 kar3 cells suggests that kinesin-related
Kar3p also contributes to spindle positioning.
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