small GTPases ARL-13 and ARL-3 coordinate intraflagellar transport and ciliogenesis

Intraflagellar transport (IFT) machinery mediates the bidirectional movement of cargos that are required for the assembly and maintenance of cilia. However, little is known about how IFT is regulated in vivo. In this study, we show that the small guanosine triphosphatase (GTPase) adenosine diphospha...

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Bibliographic Details
Published in:The Journal of cell biology 2010-06, Vol.189 (6), p.1039-1051
Main Authors: Li, Yujie, Wei, Qing, Zhang, Yuxia, Ling, Kun, Hu, Jinghua
Format: Article
Language:English
Subjects:
Animals
Animals, Genetically Modified
Biochemistry
Biological Transport - physiology
Caenorhabditis elegans - cytology
Caenorhabditis elegans - physiology
Caenorhabditis elegans Proteins - genetics
Caenorhabditis elegans Proteins - metabolism
Cells
Cilia
Cilia - physiology
Cilia - ultrastructure
Flagella - metabolism
Flagella - ultrastructure
Gene expression regulation
Genes
Histone Deacetylases - genetics
Histone Deacetylases - metabolism
Humans
Kinesin - metabolism
Microtubules
Monomeric GTP-Binding Proteins - genetics
Monomeric GTP-Binding Proteins - metabolism
Mutation
Neurons
Phenotypes
Photoreceptors
Polycystic kidney diseases
Proteins
Recombinant Fusion Proteins - genetics
Recombinant Fusion Proteins - metabolism
Truncation
Velocity
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Summary:Intraflagellar transport (IFT) machinery mediates the bidirectional movement of cargos that are required for the assembly and maintenance of cilia. However, little is known about how IFT is regulated in vivo. In this study, we show that the small guanosine triphosphatase (GTPase) adenosine diphosphate ribosylation factor-like protein 13 (ARL-13) encoded by the Caenorhabditis elegans homologue of the human Joubert syndrome causal gene ARL13B, localizes exclusively to the doublet segment of the cilium. arl-13 mutants have shortened cilia with various ultrastructural deformities and a disrupted association between IFT subcomplexes A and B. Intriguingly, depletion of ARL-3, another ciliary small GTPase, partially suppresses ciliogenesis defects in arl-13 mutants by indirectly restoring binding between IFT subcomplexes A and B. Rescue of arl-13 mutants by ARL-3 depletion is mediated by an HDAC6 deacetylase-dependent pathway. Thus, we propose that two conserved small GTPases, ARL-13 and ARL-3, coordinate to regulate IFT and that perturbing this balance results in cilia deformation.
ISSN:0021-9525
1540-8140
DOI:10.1083/jcb.200912001