Abstract
Intracellular bidirectional transport of cargo on Microtubule filaments is achieved by the collective action of oppositely directed dynein and kinesin motors. Experimental investigations probing the nature of bidirectional transport have found that in certain cases, inhibiting the activity of one type of motor results in an overall decline in the motility of the cellular cargo in both directions. This somewhat counter-intuitive observation, referred to as paradox of codependence is inconsistent with the existing paradigm of a mechanistic tug-of-war between oppositely directed motors. Existing theoretical models do not take into account a key difference in the functionality of kinesin and dynein. Unlike kinesin, dynein motors exhibit catchbonding, wherein the unbinding rates of these motors from the filaments are seen to decrease with increasing force on them. Incorporating this catchbonding behavior of dynein in a theoretical model and using experimentally relevant measures characterizing cargo transport, we show that the functional divergence of the two motors species manifests itself as an internal regulatory mechanism for bidirectional transport and resolves the paradox of codependence. Our model reproduces the key experimental features in appropriate parameter regimes and provides an unifying framework for bidirectional cargo transport.
