KLP64D and KLP68D are members of the kinesin-II family of proteins in Drosophila. Immunostaining for KLP68D and ribonucleic acid in situ hybridization for KLP64D demonstrated their preferential expression in cholinergic neurons. KLP68D was also found to accumulate in cholinergic neurons in axonal obstructions caused by the loss of kinesin light chain. Mutations in the KLP64D gene cause uncoordinated sluggish movement and death, and reduce transport of choline acetyltransferase from cell bodies to the synapse. The inviability of KLP64D mutations can be rescued by expression of mammalian KIF3A. Together, these data suggest that kinesin-II is required for the axonal transport of a soluble enzyme, choline acetyltransferase, in a specific subset of neurons in Drosophila. Furthermore, the data lead to the conclusion that the cargo transport requirements of different classes of neurons may lead to upregulation of specific pathways of axonal transport.
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1 November 1999
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November 01 1999
Kinesin-II Is Required for Axonal Transport of Choline Acetyltransferase in Drosophila
Krishanu Ray,
Krishanu Ray
aHoward Hughes Medical Institute, Department of Cellular and Molecular Medicine, Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0683
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Sharon E. Perez,
Sharon E. Perez
bHoward Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
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Zhaohuai Yang,
Zhaohuai Yang
aHoward Hughes Medical Institute, Department of Cellular and Molecular Medicine, Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0683
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Jenny Xu,
Jenny Xu
aHoward Hughes Medical Institute, Department of Cellular and Molecular Medicine, Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0683
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Bruce W. Ritchings,
Bruce W. Ritchings
aHoward Hughes Medical Institute, Department of Cellular and Molecular Medicine, Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0683
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Hermann Steller,
Hermann Steller
bHoward Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
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Lawrence S.B. Goldstein
Lawrence S.B. Goldstein
aHoward Hughes Medical Institute, Department of Cellular and Molecular Medicine, Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0683
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Krishanu Ray
aHoward Hughes Medical Institute, Department of Cellular and Molecular Medicine, Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0683
Sharon E. Perez
bHoward Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
Zhaohuai Yang
aHoward Hughes Medical Institute, Department of Cellular and Molecular Medicine, Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0683
Jenny Xu
aHoward Hughes Medical Institute, Department of Cellular and Molecular Medicine, Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0683
Bruce W. Ritchings
aHoward Hughes Medical Institute, Department of Cellular and Molecular Medicine, Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0683
Hermann Steller
bHoward Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
Lawrence S.B. Goldstein
aHoward Hughes Medical Institute, Department of Cellular and Molecular Medicine, Department of Pharmacology, University of California, San Diego, La Jolla, California 92093-0683
1.used in this paper: aa, amino acid(s); ChAT, choline acetyltransferase; CNS, central nervous system; CSP, cysteine string protein; EMS, ethyl methanesulphonate; KHC, kinesin heavy chain; nAChR, nicotinic acetylcholine receptor(s); PNS, peripheral nervous system; SYT, synaptotagmin
S. Perez's present address is Division of Biology, California Institute of Technology, Pasadena, CA 91125.
Received:
February 16 1999
Revision Requested:
August 24 1999
Accepted:
September 13 1999
Online ISSN: 1540-8140
Print ISSN: 0021-9525
© 1999 The Rockefeller University Press
1999
The Rockefeller University Press
J Cell Biol (1999) 147 (3): 507–518.
Article history
Received:
February 16 1999
Revision Requested:
August 24 1999
Accepted:
September 13 1999
Citation
Krishanu Ray, Sharon E. Perez, Zhaohuai Yang, Jenny Xu, Bruce W. Ritchings, Hermann Steller, Lawrence S.B. Goldstein; Kinesin-II Is Required for Axonal Transport of Choline Acetyltransferase in Drosophila. J Cell Biol 1 November 1999; 147 (3): 507–518. doi: https://doi.org/10.1083/jcb.147.3.507
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