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Trichoplein and Aurora A block aberrant primary cilia assembly in proliferating cells
The primary cilium is an antenna-like organelle that modulates differentiation, sensory functions, and signal transduction. After cilia are disassembled at the G0/G1 transition, formation of cilia is strictly inhibited in proliferating cells. However, the mechanisms of this inhibition are unknown. I...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341160/ https://www.ncbi.nlm.nih.gov/pubmed/22529102 http://dx.doi.org/10.1083/jcb.201106101 |
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author | Inoko, Akihito Matsuyama, Makoto Goto, Hidemasa Ohmuro-Matsuyama, Yuki Hayashi, Yuko Enomoto, Masato Ibi, Miho Urano, Takeshi Yonemura, Shigenobu Kiyono, Tohru Izawa, Ichiro Inagaki, Masaki |
author_facet | Inoko, Akihito Matsuyama, Makoto Goto, Hidemasa Ohmuro-Matsuyama, Yuki Hayashi, Yuko Enomoto, Masato Ibi, Miho Urano, Takeshi Yonemura, Shigenobu Kiyono, Tohru Izawa, Ichiro Inagaki, Masaki |
author_sort | Inoko, Akihito |
collection | PubMed |
description | The primary cilium is an antenna-like organelle that modulates differentiation, sensory functions, and signal transduction. After cilia are disassembled at the G0/G1 transition, formation of cilia is strictly inhibited in proliferating cells. However, the mechanisms of this inhibition are unknown. In this paper, we show that trichoplein disappeared from the basal body in quiescent cells, whereas it localized to mother and daughter centrioles in proliferating cells. Exogenous expression of trichoplein inhibited primary cilia assembly in serum-starved cells, whereas ribonucleic acid interference–mediated depletion induced primary cilia assembly upon cultivation with serum. Trichoplein controlled Aurora A (AurA) activation at the centrioles predominantly in G1 phase. In vitro analyses confirmed that trichoplein bound and activated AurA directly. Using trichoplein mutants, we demonstrate that the suppression of primary cilia assembly by trichoplein required its ability not only to localize to centrioles but also to bind and activate AurA. Trichoplein or AurA knockdown also induced G0/G1 arrest, but this phenotype was reversed when cilia formation was prevented by simultaneous knockdown of IFT-20. These data suggest that the trichoplein–AurA pathway is required for G1 progression through a key role in the continuous suppression of primary cilia assembly. |
format | Online Article Text |
id | pubmed-3341160 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-33411602012-10-30 Trichoplein and Aurora A block aberrant primary cilia assembly in proliferating cells Inoko, Akihito Matsuyama, Makoto Goto, Hidemasa Ohmuro-Matsuyama, Yuki Hayashi, Yuko Enomoto, Masato Ibi, Miho Urano, Takeshi Yonemura, Shigenobu Kiyono, Tohru Izawa, Ichiro Inagaki, Masaki J Cell Biol Research Articles The primary cilium is an antenna-like organelle that modulates differentiation, sensory functions, and signal transduction. After cilia are disassembled at the G0/G1 transition, formation of cilia is strictly inhibited in proliferating cells. However, the mechanisms of this inhibition are unknown. In this paper, we show that trichoplein disappeared from the basal body in quiescent cells, whereas it localized to mother and daughter centrioles in proliferating cells. Exogenous expression of trichoplein inhibited primary cilia assembly in serum-starved cells, whereas ribonucleic acid interference–mediated depletion induced primary cilia assembly upon cultivation with serum. Trichoplein controlled Aurora A (AurA) activation at the centrioles predominantly in G1 phase. In vitro analyses confirmed that trichoplein bound and activated AurA directly. Using trichoplein mutants, we demonstrate that the suppression of primary cilia assembly by trichoplein required its ability not only to localize to centrioles but also to bind and activate AurA. Trichoplein or AurA knockdown also induced G0/G1 arrest, but this phenotype was reversed when cilia formation was prevented by simultaneous knockdown of IFT-20. These data suggest that the trichoplein–AurA pathway is required for G1 progression through a key role in the continuous suppression of primary cilia assembly. The Rockefeller University Press 2012-04-30 /pmc/articles/PMC3341160/ /pubmed/22529102 http://dx.doi.org/10.1083/jcb.201106101 Text en © 2012 Inoko et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | Research Articles Inoko, Akihito Matsuyama, Makoto Goto, Hidemasa Ohmuro-Matsuyama, Yuki Hayashi, Yuko Enomoto, Masato Ibi, Miho Urano, Takeshi Yonemura, Shigenobu Kiyono, Tohru Izawa, Ichiro Inagaki, Masaki Trichoplein and Aurora A block aberrant primary cilia assembly in proliferating cells |
title | Trichoplein and Aurora A block aberrant primary cilia assembly in proliferating cells |
title_full | Trichoplein and Aurora A block aberrant primary cilia assembly in proliferating cells |
title_fullStr | Trichoplein and Aurora A block aberrant primary cilia assembly in proliferating cells |
title_full_unstemmed | Trichoplein and Aurora A block aberrant primary cilia assembly in proliferating cells |
title_short | Trichoplein and Aurora A block aberrant primary cilia assembly in proliferating cells |
title_sort | trichoplein and aurora a block aberrant primary cilia assembly in proliferating cells |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341160/ https://www.ncbi.nlm.nih.gov/pubmed/22529102 http://dx.doi.org/10.1083/jcb.201106101 |
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