TY - JOUR
T1 - IFT-81 and IFT-74 are required for intraflagellar transport in C. elegans
AU - Kobayashi, Tetsuo
AU - Gengyo-ando, Keiko
AU - Ishihara, Takeshi
AU - Katsura, Isao
AU - Mitani, Shohei
PY - 2007/5
Y1 - 2007/5
N2 - Intraflagellar transport (IFT) is essential machinery for biogenesis and maintenance of cilia in many eukaryotic and prokaryotic cells. A large number of polypeptides are known to be involved in IFT, but the physiological role of each component is not fully elucidated. Here, we identified a C. elegans orthologue of a Chlamydomonas reinhardtii IFT component, IFT-81, and found that its loss-of-function mutants show an unusual behavioral property and small body size. IFT-81 is expressed in sensory neurons, and localized at the base of cilia. The similar phenotypes with ift-81 mutants were also observed in several IFT mutants, suggesting these defects are caused by inability of IFT. We also demonstrated that IFT-81 interacts and co-localizes with IFT-74, which is another putative component of IFT. The ift-74 loss-of-function mutants showed phenocopies with ift-81 mutants, suggesting IFT-81 and IFT-74 play comparable functions. Moreover, ift-81 and ift-74 mutants similarly exhibited weak anomalies in cilia formation and obvious disruptions of transport in mature cilia. Thus, we conclude that IFT-81 and IFT-74 coordinately act in IFT in C. elegans sensory cilia.
AB - Intraflagellar transport (IFT) is essential machinery for biogenesis and maintenance of cilia in many eukaryotic and prokaryotic cells. A large number of polypeptides are known to be involved in IFT, but the physiological role of each component is not fully elucidated. Here, we identified a C. elegans orthologue of a Chlamydomonas reinhardtii IFT component, IFT-81, and found that its loss-of-function mutants show an unusual behavioral property and small body size. IFT-81 is expressed in sensory neurons, and localized at the base of cilia. The similar phenotypes with ift-81 mutants were also observed in several IFT mutants, suggesting these defects are caused by inability of IFT. We also demonstrated that IFT-81 interacts and co-localizes with IFT-74, which is another putative component of IFT. The ift-74 loss-of-function mutants showed phenocopies with ift-81 mutants, suggesting IFT-81 and IFT-74 play comparable functions. Moreover, ift-81 and ift-74 mutants similarly exhibited weak anomalies in cilia formation and obvious disruptions of transport in mature cilia. Thus, we conclude that IFT-81 and IFT-74 coordinately act in IFT in C. elegans sensory cilia.
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U2 - 10.1111/j.1365-2443.2007.01076.x
DO - 10.1111/j.1365-2443.2007.01076.x
M3 - Article
C2 - 17535250
AN - SCOPUS:34249653927
SN - 1356-9597
VL - 12
SP - 593
EP - 602
JO - Genes to Cells
JF - Genes to Cells
IS - 5
ER -