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Cooperation of the IFT-A complex with the IFT-B complex is required for ciliary retrograde protein trafficking and GPCR import by Takuya Kobayashi; Yamato Ishida; Tomoaki Hirano; Yohei Katoh; Kazuhisa Nakayama is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

What is Cooperation of the IFT-A complex with the IFT-B complex is required for ciliary retrograde protein trafficking and GPCR import about?

Cilia sense and transduce extracellular signals via specific receptors. The intraflagellar transport (IFT) machinery mediates not only bidirectional protein trafficking within cilia but also the import/export of ciliary proteins across the ciliary gate. The IFT machinery is known to comprise two multisubunit complexes, namely, IFT-A and IFT-B; however, little is known about how the two complexes cooperate to mediate ciliary protein trafficking. We here show that IFT144–IFT122 from IFT-A and IFT88–IFT52 from IFT-B make major contributions to the interface between the two complexes. Exogenous expression of the IFT88(Δα) mutant, which has decreased binding to IFT-A, partially restores the ciliogenesis defect of __IFT88__-knockout (KO) cells. However, IFT88(Δα)-expressing __IFT88__-KO cells demonstrate a defect in IFT-A entry into cilia, aberrant accumulation of IFT-B proteins at the bulged ciliary tips, and impaired import of ciliary G protein–coupled receptors (GPCRs). Furthermore, overaccumulated IFT proteins at the bulged tips appeared to be released as extracellular vesicles. These phenotypes of IFT88(Δα)-expressing __IFT88__-KO cells resembled those of __IFT144__-KO cells. These

Who reads Cooperation of the IFT-A complex with the IFT-B complex is required for ciliary retrograde protein trafficking and GPCR import?

Author

Takuya Kobayashi; Yamato Ishida; Tomoaki Hirano; Yohei Katoh; Kazuhisa Nakayama

Publisher

The American Society for Cell Biology

Published

2021

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)