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Microtubules are key structural elements of living cells that are crucial forcell division, intracellular transport and motility. Recent experiments haveshown that microtubule severing proteins and molecular motors stimulate thedirect and localized incorporation of free tubulin into the shaft. However, amechanistic picture how microtubule associated proteins affect the lattice iscompletely missing. Here we theoretically explore a potential mechanism oflattice turnover stimulated by processive molecular motors in which a weaktransient destabilization of the lattice by the motor stepping promotes theformation of mobile vacancies. In the absence of free tubulin the defectrapidly propagates leading to a complete fracture. In the presence of freetubulin, the motor walk induces a vacancy drift in the direction opposite ofthe motor walk. The drift is accompanied by the direct and localizedincorporation of free tubulin along the trajectory of the vacancy. Our resultsare consistent with experiments and strongly suggest that a weak lattice-motorinteraction is responsible for an augmented microtubule shaft plasticity.

Molecular motors enhance microtubule lattice plasticity