Abstract
AbstractBudding yeast must position the mitotic spindle at the mother-bud junction during anaphase to ensure proper chromosome segregation. Pushing and pulling forces on astral microtubules from dynein motors in the cell cortex are crucial for spindle positioning. In some higher eukaryotes and filamentous fungi, dynein also accelerates spindle elongation during anaphase, but in yeast model systems spindle elongation primarily relies on intra-spindle pushing forces from kinesin-5 motors. The pathogenic yeastCandida albicansis unique because its spindle can elongate without a functional kinesin-5. Our study helps explainC. albicans’ diminished kinesin-5 requirement by showing that its dynein, Dyn1, collaborates with its kinesin-5, Kip1, to facilitate spindle elongation. Cells lacking Kip1 activity by eitherKIP1deletion or Kip1 inhibition have more Dyn1 and astral microtubules, indicating spindle elongation happens through enhanced pulling on spindle pole body-bound astral microtubules by cortical Dyn1. When Dyn1 activity is depleted, spindle elongation speed is normal, but anaphase spindles persist for extended periods, and the number and length of astral microtubules increases. Depletion of both motors prevents spindle elongation and is lethal. The significance of astral microtubules in cells lacking either motor is highlighted by the lethal effects of microtubule-destabilizing drugs and exposure to low temperatures (8°C) that compromise microtubule stability. These findings demonstrate thatC. albicansspindle elongation involves cooperative forces from Kip1 and Dyn1 to ensure chromosome separation during cell division and thatC. albicansadapts to changes in abundance of these motors through alterations in their astral microtubule content.
Publisher
Cold Spring Harbor Laboratory