Abstract
Intracellular transport, unlike in vitro, is typically bi-directional -- consisting of a series of back and forth movements. Kinesin-1 and cytoplasmic dynein require each other for bi-directional transport of intracellular cargo along microtubules i.e. inhibition or depletion of kinesin-1 abolishes dynein-driven cargo transport, and vice versa. Using Drosophila S2 cells, we demonstrate that replacement of endogenous kinesin-1 or dynein with an unrelated motor of the same directionality, and targeted to peroxisomes, activates peroxisome transport in the opposite direction. However motility-deficient versions of motors, that retain the ability to bind microtubules and hydrolyze ATP, do not activate peroxisome motility. Thus any pair of opposite-polarity motors, provided they move along microtubules, can activate one another. These results demonstrate that mechanical interactions between opposite-polarity motors are necessary and sufficient for bi-directional organelle transport in live cells.
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