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2022•Molecular Biology of the CellOpen access

Molecular basis underlying the ciliary defects caused by IFT52 variations found in skeletal ciliopathies

Yamato Ishida, Koshi Tasaki, Yohei Katoh, Kazuhisa Nakayama

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Abstract

-KO cells expressing an SRPS variant of IFT52, ciliary tip localization of ICK/CILK1 and KIF17, both of which are likely to be transported to the tip via binding to the IFT-B complex, was significantly impaired. Altogether these results indicate that impaired anterograde trafficking caused by a decrease in the ciliary level of IFT-B or in its binding to kinesin-II underlies the ciliary defects found in skeletal ciliopathies caused by IFT52 variations.

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What this paper is about

-KO cells expressing an SRPS variant of IFT52, ciliary tip localization of ICK/CILK1 and KIF17, both of which are likely to be transported to the tip via binding to the IFT-B complex, was significantly impaired. Altogether these results indicate that impaired anterograde trafficking caused by a decrease in the ciliary level of IFT-B or in its binding to kinesin-II underlies the ciliary defects found in skeletal ciliopathies caused by IFT52 variations.

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Available abstract

-KO cells expressing an SRPS variant of IFT52, ciliary tip localization of ICK/CILK1 and KIF17, both of which are likely to be transported to the tip via binding to the IFT-B complex, was significantly impaired. Altogether these results indicate that impaired anterograde trafficking caused by a decrease in the ciliary level of IFT-B or in its binding to kinesin-II underlies the ciliary defects found in skeletal ciliopathies caused by IFT52 variations.

Key concepts: Ciliopathies, Cilium, Intraflagellar transport, Ciliogenesis, Biology, Ciliopathy, Cell biology, Bardet–Biedl syndrome

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Molecular basis underlying the ciliary defects caused by IFT52 variations found in skeletal ciliopathies — Research Paper | ScholarLens