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Vol. 14, Issue 5, 2057-2070, May 2003
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* Department of Cell Biology, University of Alabama at Birmingham Medical
Center, Birmingham, Alabama 35294;
Department of Genome Sciences, University of Washington, Seattle, Washington
98195; and
¶ Karolinska Institute, Department of Biosciences, Södertörn
University College, Section of Natural Sciences, S-14189 Huddinge,
Sweden
Submitted October 22, 2002;
Revised December 13, 2002;
Accepted December 27, 2002
Monitoring Editor: Mary Beckerle
Intraflagellar transport (IFT) is a process required for flagella and cilia assembly that describes the dynein and kinesin mediated movement of particles along axonemes that consists of an A and a B complex, defects in which disrupt retrograde and anterograde transport, respectively. Herein, we describe a novel Caenorhabditis elegans gene, xbx-1, that is required for retrograde IFT and shares homology with a mammalian dynein light intermediate chain (D2LIC). xbx-1 expression in ciliated sensory neurons is regulated by the transcription factor DAF-19, as demonstrated previously for genes encoding IFT complex B proteins. XBX-1 localizes to the base of the cilia and undergoes anterograde and retrograde movement along the axoneme. Disruption of xbx-1 results in cilia defects and causes behavioral abnormalities observed in other cilia mutants. Analysis of cilia in xbx-1 mutants reveals that they are shortened and have a bulb like structure in which IFT proteins accumulate. The role of XBX-1 in IFT was further confirmed by analyzing the effect that other IFT mutations have on XBX-1 localization and movement. In contrast to other IFT proteins, retrograde XBX-1 movement was detected in complex A mutants. Our results suggest that the DLIC protein XBX-1 functions together with the CHE-3 dynein in retrograde IFT, downstream of the complex A proteins.
Online version of this article contains video materials. Online version is
available at
www.molbiolcell.org.
Both authors contributed equally to this work.
Corresponding authors. E-mail addresses:
Byoder{at}uab.edu;
peter.swoboda{at}biosci.ki.se.
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