Microtubules are key structural elements of living cells that are crucial for cell division, intracellular transport and motility. Recent experiments have shown that microtubule severing proteins and molecular motors stimulate the direct and localized incorporation of free tubulin into the shaft. However, a mechanistic picture how microtubule associated proteins affect the lattice is completely missing. Here we theoretically explore a potential mechanism of lattice turnover stimulated by processive molecular motors in which a weak transient destabilization of the lattice by the motor stepping promotes the formation of mobile vacancies. In the absence of free tubulin the defect rapidly propagates leading to a complete fracture. In the presence of free tubulin, the motor walk induces a vacancy drift in the direction opposite of the motor walk. The drift is accompanied by the direct and localized incorporation of free tubulin along the trajectory of the vacancy. Our results are consistent with experiments and strongly suggest that a weak lattice-motor interaction is responsible for an augmented microtubule shaft plasticity.