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Abnormal centrosomal structure and duplication in Cep135-deficient vertebrate cells
Centrosomes are key microtubule-organizing centers that contain a pair of centrioles, conserved cylindrical, microtubule-based structures. Centrosome duplication occurs once per cell cycle and relies on templated centriole assembly. In many animal cells this process starts with the formation of a ra...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The American Society for Cell Biology
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756917/ https://www.ncbi.nlm.nih.gov/pubmed/23864714 http://dx.doi.org/10.1091/mbc.E13-03-0149 |
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author | Inanç, Burcu Pütz, Monika Lalor, Pierce Dockery, Peter Kuriyama, Ryoko Gergely, Fanni Morrison, Ciaran G. |
author_facet | Inanç, Burcu Pütz, Monika Lalor, Pierce Dockery, Peter Kuriyama, Ryoko Gergely, Fanni Morrison, Ciaran G. |
author_sort | Inanç, Burcu |
collection | PubMed |
description | Centrosomes are key microtubule-organizing centers that contain a pair of centrioles, conserved cylindrical, microtubule-based structures. Centrosome duplication occurs once per cell cycle and relies on templated centriole assembly. In many animal cells this process starts with the formation of a radially symmetrical cartwheel structure. The centrosomal protein Cep135 localizes to this cartwheel, but its role in vertebrates is not well understood. Here we examine the involvement of Cep135 in centriole function by disrupting the Cep135 gene in the DT40 chicken B-cell line. DT40 cells that lack Cep135 are viable and show no major defects in centrosome composition or function, although we note a small decrease in centriole numbers and a concomitant increase in the frequency of monopolar spindles. Furthermore, electron microscopy reveals an atypical structure in the lumen of Cep135-deficient centrioles. Centrosome amplification after hydroxyurea treatment increases significantly in Cep135-deficient cells, suggesting an inhibitory role for the protein in centrosome reduplication during S-phase delay. We propose that Cep135 is required for the structural integrity of centrioles in proliferating vertebrate cells, a role that also limits centrosome amplification in S-phase–arrested cells. |
format | Online Article Text |
id | pubmed-3756917 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | The American Society for Cell Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-37569172013-11-16 Abnormal centrosomal structure and duplication in Cep135-deficient vertebrate cells Inanç, Burcu Pütz, Monika Lalor, Pierce Dockery, Peter Kuriyama, Ryoko Gergely, Fanni Morrison, Ciaran G. Mol Biol Cell Articles Centrosomes are key microtubule-organizing centers that contain a pair of centrioles, conserved cylindrical, microtubule-based structures. Centrosome duplication occurs once per cell cycle and relies on templated centriole assembly. In many animal cells this process starts with the formation of a radially symmetrical cartwheel structure. The centrosomal protein Cep135 localizes to this cartwheel, but its role in vertebrates is not well understood. Here we examine the involvement of Cep135 in centriole function by disrupting the Cep135 gene in the DT40 chicken B-cell line. DT40 cells that lack Cep135 are viable and show no major defects in centrosome composition or function, although we note a small decrease in centriole numbers and a concomitant increase in the frequency of monopolar spindles. Furthermore, electron microscopy reveals an atypical structure in the lumen of Cep135-deficient centrioles. Centrosome amplification after hydroxyurea treatment increases significantly in Cep135-deficient cells, suggesting an inhibitory role for the protein in centrosome reduplication during S-phase delay. We propose that Cep135 is required for the structural integrity of centrioles in proliferating vertebrate cells, a role that also limits centrosome amplification in S-phase–arrested cells. The American Society for Cell Biology 2013-09-01 /pmc/articles/PMC3756917/ /pubmed/23864714 http://dx.doi.org/10.1091/mbc.E13-03-0149 Text en © 2013 Inanç et al. 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 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society of Cell Biology. |
spellingShingle | Articles Inanç, Burcu Pütz, Monika Lalor, Pierce Dockery, Peter Kuriyama, Ryoko Gergely, Fanni Morrison, Ciaran G. Abnormal centrosomal structure and duplication in Cep135-deficient vertebrate cells |
title | Abnormal centrosomal structure and duplication in Cep135-deficient vertebrate cells |
title_full | Abnormal centrosomal structure and duplication in Cep135-deficient vertebrate cells |
title_fullStr | Abnormal centrosomal structure and duplication in Cep135-deficient vertebrate cells |
title_full_unstemmed | Abnormal centrosomal structure and duplication in Cep135-deficient vertebrate cells |
title_short | Abnormal centrosomal structure and duplication in Cep135-deficient vertebrate cells |
title_sort | abnormal centrosomal structure and duplication in cep135-deficient vertebrate cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756917/ https://www.ncbi.nlm.nih.gov/pubmed/23864714 http://dx.doi.org/10.1091/mbc.E13-03-0149 |
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