Volume 1 Supplement 1

Proceedings of the First International Cilia in Development and Disease Scientific Conference (2012)

Open Access

The GMAP210 homologue SQL 1 modulates intraflagellar transport in C. elegans

Cilia20121(Suppl 1):P40

DOI: 10.1186/2046-2530-1-S1-P40

Published: 16 November 2012

The development and function of cilia require a specialised transport process, called Intraflagellar Transport (IFT). In amphid cilia of C. elegans this process uses two kinesins, kinesin II and OSM-3, which are loaded with complex A and B particle proteins and cargo molecules. We have previously shown that expression of a dominant active G-protein (GPA-3QL) in amphid channel neurons affects the coordination of OSM-3 and kinesin-II and results in shorter cilia. We performed a genetic screen to identify mutants that suppress the gpa-3QL cilia length defect and identified sql-1 (supressor of gpa-3QL), which encodes the homologue of the mammalian Golgi protein GMAP210. GMAP210 has been shown to play a role in vesicular transport from the Golgi apparatus to the cilium. SQL-1 is ubiquitously expressed in C. elegans and localizes to the Golgi. sql-1 loss of function (lf) mutants show wildtype length cilia, while animals overexpressing SQL-1 have longer cilia. Speed measurements in sql-1(lf) animals showed that OSM-3 moves faster and kinesin II moves slower, suggesting that the two kinesins are partially uncoupled. Complex A and B proteins move at the same speed as OSM-3, suggesting that IFT is predominantly mediated by OSM-3 kinesin. Interestingly, in the gpa-3QL; sql-1(lf) double mutants the speed of OSM-3 is decreased. We hypothesize that SQL-1 plays a role in routing or post translational modifications of proteins that are required in the cilium for proper IFT.

Authors’ Affiliations

(1)
Erasmus Medical Center Rotterdam
(2)
Biozentrum, University Basel

Copyright

© Rademakers et al; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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