Kinesin-like motor protein involved in the control of the oriented deposition of cellulose microfibrils (PubMed:12468730, Ref.6). Its motor activity is directed toward the microtubule's plus end. It possesses the potential to drive long-distance transport of cargo along cortical microtubules (PubMed:21914648, PubMed:25646318). Regulates cell wall mechanics during cell elongation, by the regulation of primary and secondary walls deposition (Ref.6, PubMed:25600279, PubMed:25646318). Contributes to cortical microtubule-mediated trafficking of cell wall components (PubMed:25646318). Homodimer. Concentrated around the periphery of the cytoplasm. Expressed in stems and flowers (PubMed:12468730). Detected in cells undergoing secondary wall deposition including developing interfascicular fibers and xylem cells, but also in dividing cells and expanding/elongating parenchyma cells (Ref.6). Composed of an N-terminal domain which is responsible for the motor activity of kinesin (it hydrolyzes ATP and binds microtubule) and a central to C-terminal alpha-helical coiled coil domain that mediates the heavy chain dimerization. Reduced length of roots and inflorescence stems. Altered orientation of cellulose microfibrils in fiber walls leading to dramatic reduction in fiber mechanical strength. No apparent alteration in cell wall composition. Lower expansion rate of the inflorescence stem along with the reduced thickness of both primary and secondary cell walls leading to mechanically weaker stems (PubMed:25646318). Overexpression of KIN4A/FRA1 caused a severe reduction in the thickness of secondary walls in interfascicular fibers and deformation of vessels, an increase in the number of secondary wall layers, which are accompanied with a marked decrease in stem strength. Belongs to the TRAFAC class myosin-kinesin ATPase superfamily. Kinesin family. KIN-4 subfamily.