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Robust interaction of IFT70 with IFT52–IFT88 in the IFT-B complex is required for ciliogenesis
In the intraflagellar transport (IFT) machinery, the IFT-B and IFT-A complexes mediate anterograde and retrograde ciliary protein trafficking, respectively. Among the 16 subunits of the IFT-B complex, several subunits are essential for ciliogenesis, whereas others, which are associated peripherally...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Company of Biologists Ltd
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5992529/ https://www.ncbi.nlm.nih.gov/pubmed/29654116 http://dx.doi.org/10.1242/bio.033241 |
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author | Takei, Ryota Katoh, Yohei Nakayama, Kazuhisa |
author_facet | Takei, Ryota Katoh, Yohei Nakayama, Kazuhisa |
author_sort | Takei, Ryota |
collection | PubMed |
description | In the intraflagellar transport (IFT) machinery, the IFT-B and IFT-A complexes mediate anterograde and retrograde ciliary protein trafficking, respectively. Among the 16 subunits of the IFT-B complex, several subunits are essential for ciliogenesis, whereas others, which are associated peripherally with the complex, are dispensable for ciliogenesis but play a role in protein trafficking. IFT22-knockout (KO) cells established in this study demonstrated no defects in ciliogenesis or ciliary protein trafficking. In stark contrast, IFT70A and IFT70B double-knockout cells did not form cilia, even though IFT70 is associated peripherally with the IFT-B complex via the IFT52–IFT88 dimer, and other IFT-B subunits assembled at the ciliary base in the absence of IFT70. Exogenous expression of either IFT70A or IFT70B restored the ciliogenesis defect of IFT70-KO cells, indicating their redundant roles. IFT70 has 15 consecutive tetratricopeptide repeats (TPRs) followed by a short helix (α36). Deletion of the first TPR or α36 of IFT70A greatly reduced its ability to interact with the IFT52–IFT88 dimer. Exogenous expression of any of the IFT70A deletion mutants in IFT70-KO cells could not restore ciliogenesis. These results show that IFT70 plays an essential role in ciliogenesis, although it is dispensable for assembly of the residual IFT-B subunits. |
format | Online Article Text |
id | pubmed-5992529 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | The Company of Biologists Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-59925292018-06-08 Robust interaction of IFT70 with IFT52–IFT88 in the IFT-B complex is required for ciliogenesis Takei, Ryota Katoh, Yohei Nakayama, Kazuhisa Biol Open Research Article In the intraflagellar transport (IFT) machinery, the IFT-B and IFT-A complexes mediate anterograde and retrograde ciliary protein trafficking, respectively. Among the 16 subunits of the IFT-B complex, several subunits are essential for ciliogenesis, whereas others, which are associated peripherally with the complex, are dispensable for ciliogenesis but play a role in protein trafficking. IFT22-knockout (KO) cells established in this study demonstrated no defects in ciliogenesis or ciliary protein trafficking. In stark contrast, IFT70A and IFT70B double-knockout cells did not form cilia, even though IFT70 is associated peripherally with the IFT-B complex via the IFT52–IFT88 dimer, and other IFT-B subunits assembled at the ciliary base in the absence of IFT70. Exogenous expression of either IFT70A or IFT70B restored the ciliogenesis defect of IFT70-KO cells, indicating their redundant roles. IFT70 has 15 consecutive tetratricopeptide repeats (TPRs) followed by a short helix (α36). Deletion of the first TPR or α36 of IFT70A greatly reduced its ability to interact with the IFT52–IFT88 dimer. Exogenous expression of any of the IFT70A deletion mutants in IFT70-KO cells could not restore ciliogenesis. These results show that IFT70 plays an essential role in ciliogenesis, although it is dispensable for assembly of the residual IFT-B subunits. The Company of Biologists Ltd 2018-04-13 /pmc/articles/PMC5992529/ /pubmed/29654116 http://dx.doi.org/10.1242/bio.033241 Text en © 2018. Published by The Company of Biologists Ltd http://creativecommons.org/licenses/by/3.0This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. |
spellingShingle | Research Article Takei, Ryota Katoh, Yohei Nakayama, Kazuhisa Robust interaction of IFT70 with IFT52–IFT88 in the IFT-B complex is required for ciliogenesis |
title | Robust interaction of IFT70 with IFT52–IFT88 in the IFT-B complex is required for ciliogenesis |
title_full | Robust interaction of IFT70 with IFT52–IFT88 in the IFT-B complex is required for ciliogenesis |
title_fullStr | Robust interaction of IFT70 with IFT52–IFT88 in the IFT-B complex is required for ciliogenesis |
title_full_unstemmed | Robust interaction of IFT70 with IFT52–IFT88 in the IFT-B complex is required for ciliogenesis |
title_short | Robust interaction of IFT70 with IFT52–IFT88 in the IFT-B complex is required for ciliogenesis |
title_sort | robust interaction of ift70 with ift52–ift88 in the ift-b complex is required for ciliogenesis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5992529/ https://www.ncbi.nlm.nih.gov/pubmed/29654116 http://dx.doi.org/10.1242/bio.033241 |
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