Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface

Abstract

How mutations in β3-tubulin cause axonal growth defects in congenital fibrosis of the extraocular muscles type 3 remains elusive. Minoura et al. develop a model system using recombinant human tubulin that demonstrates a link between tubulin mutation, impaired kinesin motility and axonal growth defects.