A protein complex anchors dynein during mitosis but doesn’t help the motor protein pull, Kotak et al. show.
The location of the mitotic spindle determines where animal cells divide and thereby decides the developmental fate of the resulting daughter cells. Proper spindle positioning requires a ternary complex of proteins that is thought to anchor dynein to the cortex beneath the cell membrane, where the molecular motor can maneuver the spindle into position. But previous research hadn’t confirmed that dynein works at the cell membrane or determined whether the ternary complex serves as more than an anchor for dynein and has a more direct role in positioning the spindle.
HeLa cells overexpressing one ternary complex component, Gαi1, recruited extra dynein to the cell cortex, resulting in exaggerated spindle movements. Cells expressing a version of Gαi1 unable to bind to the membrane, however, lacked cortical dynein and carried misplaced spindles that barely moved, suggesting that membrane-anchored dynein is necessary for positioning the spindle.
To determine if cortical dynein is sufficient to orient the spindle, the researchers directed dynein to the plasma membrane by expressing the dynein-interacting portion of the ternary complex protein NuMA fused to a membrane-targeting motif. Cells expressing this construct showed excess spindle movements even in the absence of the ternary complex, suggesting that cortical dynein can adjust the spindle’s location and that the ternary complex’s primary function is to localize dynein to the right place at the right time.
