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A more recent version of this article appeared on May 1, 2003
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Submitted on October 22, 2002
Revised on December 13, 2002
Accepted on December 27, 2002
1 Department of Cell Biology, University of Alabama at Birmingham Medical Center, Birmingham, Alabama 35294, USA
2 Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA
3 Karolinska Institute, Department of Biosciences, Södertörn University College, Section of Natural Sciences, S-14189 Huddinge, Sweden
* Corresponding author. E-mail address: byoder{at}uab.edu, peter.swoboda{at}biosci.ki.se.
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 C. 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.
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