Abstract
Proper transport and positioning of cell organelles often depends on the antagonistic activities of dynein and kinesin-1, two microtubule motors with opposite directionality.1 One of the largest known transport cargoes is the cell nucleus. Both dynein and kinesin-1 participate in positioning of the nucleus through binding to the nuclear envelope (NE).2-9 Surprisingly, both dynein and kinesin-1 can be recruited to the NE through multiple pathways, one involving SUN-KASH domain containing proteins and the other involving nuclear pore complexes (NPCs). Here, we discuss the molecular mechanisms of dynein and kinesin recruitment to the NE through NPCs, as well as the functional implications of dynein and kinesin-1 activity at the NE in mammalian cells. Finally, we discuss how motor activities at the NE might be controlled during the cell cycle.