Num1 versus NuMA: insights from two functionally homologous proteins.

In both animals and fungi, spindle positioning is dependent upon pulling forces generated by cortically anchored dynein. In animals, cortical anchoring is accomplished by a ternary complex containing the dynein-binding protein NuMA and its cortical attachment machinery. The same function is accomplished by Num1 in budding yeast.

Cortical dynein pulling mechanism is regulated by differentially targeted attachment molecule Num1.

Cortical dynein generates pulling forces via microtubule (MT) end capture-shrinkage and lateral MT sliding mechanisms. In , the dynein attachment molecule Num1 interacts with endoplasmic reticulum (ER) and mitochondria to facilitate spindle positioning across the mother-bud neck, but direct evidence for how these cortical contacts regulate dynein-dependent pulling forces is lacking. We show that loss of Scs2/Scs22, ER tethering proteins, resulted in defective Num1 distribution and loss of dynein-dependent MT sliding, the hallmark of dynein function.