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Published April 20, 1998 | Published
Journal Article Open

Kinesin Light Chains Are Essential for Axonal Transport in Drosophila


Kinesin is a heterotetramer composed of two 115-kD heavy chains and two 58-kD light chains. The microtubule motor activity of kinesin is performed by the heavy chains, but the functions of the light chains are poorly understood. Mutations were generated in the Drosophila gene Kinesin light chain (Klc), and the phenotypic consequences of loss of Klc function were analyzed at the behavioral and cellular levels. Loss of Klc function results in progressive lethargy, crawling defects, and paralysis followed by death at the end of the second larval instar. Klc mutant axons contain large aggregates of membranous organelles in segmental nerve axons. These aggregates, or organelle jams (Hurd, D.D., and W.M. Saxton. 1996. Genetics. 144: 1075-1085), contain synaptic vesicle precursors as well as organelles that may be transported by kinesin, kinesin-like protein 68D, and cytoplasmic dynein, thus providing evidence that the loss of Klc function blocks multiple pathways of axonal transport. The similarity of the Klc and Khc ((Saxton et al. Cell 64:1093-1102; Hurd, D.D., and W.M. Saxton. 1996. Genetics 144: 1075-1085) mutant phenotypes indicates that KLC is essential for kinesin function, perhaps by tethering KHC to intracellular cargos or by activating the kinesin motor.

Additional Information

RUP grants the public the nonexclusive right to copy, distribute, or display the Work under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/ and http://creativecommons.org/licenses/by-nc-sa/3.0/legalcode. Received for publication 23 December 1997 and in revised form 24 February 1998. We would like to thank Kathy Matthews and the Indiana Stock Center for providing fly stocks, Maria Dolph and Jenny Xu for technical assistance; Bill Saxton, Mary Ann Martin, and Daryl Hurd for valuable advice and communicating results before publication; Tom Hays, J. Troy Littleton, Bill Saxton, and Konrad Zinsmaier for generously providing antibodies; Bill Harris and Bill Hagar for providing equipment for video microscopy and imaging; and members of the Goldstein lab, especially Nelson Barton and Roman Sakowicz, for advice and invigorating discussions. This research was supported by National Institutes of Health grants to L.S.B. Goldstein and K. Zinn. L.SB. Goldstein is an investigator of the Howard Hughes Medical Institute. J.G. Gindhart was supported by a National Institutes of Health postdoctoral fellowship. C.J. Desai was supported by an American Cancer Society postdoctoral fellowship.

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August 19, 2023
October 19, 2023