Type-1 mutations in the head domain of KIF5A have defects in the binding of the protein to tubulin.

Type-1 mutations in the head domain of KIF5A have defects in the binding of the protein to tubulin. How would weakened binding to tubulin be expected to affect the function of kinesin and the transport of vesicles in neurons? How would overly strong binding to tubulin be expected to affect the function of kinesin? Please limit your answer to the lines below