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dc.contributor.author | Satoda, Yuuki | en |
dc.contributor.author | Noguchi, Tatsuro | en |
dc.contributor.author | Fujii, Taiju | en |
dc.contributor.author | Taniguchi, Aoi | en |
dc.contributor.author | Katoh, Yohei | en |
dc.contributor.author | Nakayama, Kazuhisa | en |
dc.contributor.alternative | 里田, 裕紀 | ja |
dc.contributor.alternative | 野口, 達郎 | ja |
dc.contributor.alternative | 藤居, 大樹 | ja |
dc.contributor.alternative | 谷口, 葵 | ja |
dc.contributor.alternative | 加藤, 洋平 | ja |
dc.contributor.alternative | 中山, 和久 | ja |
dc.date.accessioned | 2022-10-14T06:50:37Z | - |
dc.date.available | 2022-10-14T06:50:37Z | - |
dc.date.issued | 2022-08 | - |
dc.identifier.uri | http://hdl.handle.net/2433/276722 | - |
dc.description.abstract | Primary cilia are antenna-like organelles that contain specific proteins, and are crucial for tissue morphogenesis. Anterograde and retrograde trafficking of ciliary proteins are mediated by the intraflagellar transport (IFT) machinery. BROMI/TBC1D32 interacts with CCRK/CDK20, which phosphorylates and activates the ICK/CILK1 kinase, to regulate the change in direction of the IFT machinery at the ciliary tip. Mutations in BROMI, CCRK, and ICK in humans cause ciliopathies, and mice defective in these genes are also known to demonstrate ciliopathy phenotypes. We here show that BROMI interacts not only with CCRK but also with CFAP20, an evolutionarily conserved ciliary protein, and with FAM149B1/JBTS36, a protein in which mutations cause Joubert syndrome. In addition, we show that FAM149B1 interacts directly with CCRK as well as with BROMI. Ciliary defects observed in CCRK-knockout (KO), BROMI-KO, and FAM149B1-KO cells, including abnormally long cilia and accumulation of the IFT machinery and ICK at the ciliary tip, resembled one another, and BROMI mutants that are defective in binding to CCRK and CFAP20 were unable to rescue the ciliary defects of BROMI-KO cells. These data indicate that CCRK, BROMI, FAM149B1, and probably CFAP20, all together regulate the IFT turnaround process under the control of ICK. | en |
dc.language.iso | eng | - |
dc.publisher | American Society for Cell Biology (ASCB) | en |
dc.rights | © 2022 Satoda et al. | en |
dc.rights | This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial-Share Alike 4.0 International Creative Commons License | en |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0 | - |
dc.title | BROMI/TBC1D32 together with CCRK/CDK20 and FAM149B1/JBTS36 contributes to intraflagellar transport turnaround involving ICK/CILK1 | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | Molecular Biology of the Cell | en |
dc.identifier.volume | 33 | - |
dc.identifier.issue | 9 | - |
dc.relation.doi | 10.1091/mbc.E22-03-0089 | - |
dc.textversion | publisher | - |
dc.identifier.artnum | ar79 | - |
dc.identifier.pmid | 35609210 | - |
dcterms.accessRights | open access | - |
datacite.awardNumber | 19H00980 | - |
datacite.awardNumber | 20H04904 | - |
datacite.awardNumber | 18H02403 | - |
datacite.awardNumber | 21H02427 | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-19H00980/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/ja/grant/KAKENHI-PUBLICLY-20H04904/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-18H02403/ | - |
datacite.awardNumber.uri | https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-21H02427/ | - |
dc.identifier.eissn | 1939-4586 | - |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.awardTitle | 繊毛内タンパク質輸送複合体の構築様式と機能の相関:繊毛病の分子基盤 | ja |
jpcoar.awardTitle | 繊毛内と細胞質を隔てるトランジション・ゾーンの構築様式と選択的タンパク質透過機構 | ja |
jpcoar.awardTitle | 多角的アプローチによる繊毛内タンパク質輸送システムの解明 | ja |
jpcoar.awardTitle | 多角的な研究手法の組み合わせによる繊毛内タンパク質輸送システムの統合的理解 | ja |
出現コレクション: | 学術雑誌掲載論文等 |
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