Clonal tests of conventional kinesin function during cell proliferation and differentiation

Null mutations in the Drosophila Kinesin heavy chain gene (Khc), which are lethal during the second larval instar, have shown that conventional kinesi n is critical for fast axonal transport in neurons, but its functions elsew here are uncertain. To test other tissues, single imaginal cells in young l arvae were rendered null for Khc by mitotic recombination. Surprisingly, th e null cells produced large clones of adult tissue. The rates of cell proli feration were not reduced, indicating that conventional kinesin is not esse ntial for cell growth or division. This suggests that in undifferentiated c ells vesicle transport from the Golgi to either the endoplasmic reticulum o r the plasma membrane can proceed at normal rates without conventional kine sin. In adult eye clones produced by null founder cells, there were some de fects in differentiation that caused mild ultrastructural changes, but they were not consistent with serious problems in the positioning or transport of endoplasmic reticulum, mitochondria, or vesicles. In contrast, defective cuticle deposition by highly elongated Khc null bristle shafts suggests th at conventional kinesin is critical for proper secretory vesicle transport in some cell types, particularly ones that must build and maintain long cyt oplasmic extensions. The ubiquity and evolutionary conservation of kinesin heavy chain argue for functions in all cells. We suggest interphase organel le movements away from the cell center are driven by multilayered transport mechanisms; that is, individual organelles can use kinesin-related protein s and myosins, as well as conventional kinesin, to move toward the cell per iphery. In this case, other motors can compensate for the loss of conventio nal kinesin except in cells that have extremely long transport tracks.