The selective continued linkage of centromeres from mitosis to interphase in the absence of mammalian separase

Separase is an evolutionarily conserved protease that is essential for chromosome segregation and cleaves cohesin Scc1/Rad21, which joins the sister chromatids together. Although mammalian separase also functions in chromosome segregation, our understanding of this process in mammals is still incomp...

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Autores principales: Kumada, Kazuki, Yao, Ryoji, Kawaguchi, Tokuichi, Karasawa, Mika, Hoshikawa, Yutaka, Ichikawa, Koji, Sugitani, Yoshinobu, Imoto, Issei, Inazawa, Johji, Sugawara, Minoru, Yanagida, Mitsuhiro, Noda, Tetsuo
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2006
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2063728/
https://www.ncbi.nlm.nih.gov/pubmed/16533944
http://dx.doi.org/10.1083/jcb.200511126
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author Kumada, Kazuki
Yao, Ryoji
Kawaguchi, Tokuichi
Karasawa, Mika
Hoshikawa, Yutaka
Ichikawa, Koji
Sugitani, Yoshinobu
Imoto, Issei
Inazawa, Johji
Sugawara, Minoru
Yanagida, Mitsuhiro
Noda, Tetsuo
author_facet Kumada, Kazuki
Yao, Ryoji
Kawaguchi, Tokuichi
Karasawa, Mika
Hoshikawa, Yutaka
Ichikawa, Koji
Sugitani, Yoshinobu
Imoto, Issei
Inazawa, Johji
Sugawara, Minoru
Yanagida, Mitsuhiro
Noda, Tetsuo
author_sort Kumada, Kazuki
collection PubMed
description Separase is an evolutionarily conserved protease that is essential for chromosome segregation and cleaves cohesin Scc1/Rad21, which joins the sister chromatids together. Although mammalian separase also functions in chromosome segregation, our understanding of this process in mammals is still incomplete. We generated separase knockout mice, reporting an essential function for mammalian separase. Separase-deficient mouse embryonic fibroblasts exhibited severely restrained increases in cell number, polyploid chromosomes, and amplified centrosomes. Chromosome spreads demonstrated that multiple chromosomes connected to a centromeric region. Live observation demonstrated that the chromosomes of separase-deficient cells condensed, but failed to segregate, although subsequent cytokinesis and chromosome decondensation proceeded normally. These results establish that mammalian separase is essential for the separation of centromeres, but not of the arm regions of chromosomes. Other cell cycle events, such as mitotic exit, DNA replication, and centrosome duplication appear to occur normally. We also demonstrated that heterozygous separase-deficient cells exhibited severely restrained increases in cell number with apparently normal mitosis in the absence of securin, which is an inhibitory partner of separase.
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spelling pubmed-20637282007-11-29 The selective continued linkage of centromeres from mitosis to interphase in the absence of mammalian separase Kumada, Kazuki Yao, Ryoji Kawaguchi, Tokuichi Karasawa, Mika Hoshikawa, Yutaka Ichikawa, Koji Sugitani, Yoshinobu Imoto, Issei Inazawa, Johji Sugawara, Minoru Yanagida, Mitsuhiro Noda, Tetsuo J Cell Biol Research Articles Separase is an evolutionarily conserved protease that is essential for chromosome segregation and cleaves cohesin Scc1/Rad21, which joins the sister chromatids together. Although mammalian separase also functions in chromosome segregation, our understanding of this process in mammals is still incomplete. We generated separase knockout mice, reporting an essential function for mammalian separase. Separase-deficient mouse embryonic fibroblasts exhibited severely restrained increases in cell number, polyploid chromosomes, and amplified centrosomes. Chromosome spreads demonstrated that multiple chromosomes connected to a centromeric region. Live observation demonstrated that the chromosomes of separase-deficient cells condensed, but failed to segregate, although subsequent cytokinesis and chromosome decondensation proceeded normally. These results establish that mammalian separase is essential for the separation of centromeres, but not of the arm regions of chromosomes. Other cell cycle events, such as mitotic exit, DNA replication, and centrosome duplication appear to occur normally. We also demonstrated that heterozygous separase-deficient cells exhibited severely restrained increases in cell number with apparently normal mitosis in the absence of securin, which is an inhibitory partner of separase. The Rockefeller University Press 2006-03-13 /pmc/articles/PMC2063728/ /pubmed/16533944 http://dx.doi.org/10.1083/jcb.200511126 Text en Copyright © 2006, The Rockefeller University Press 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 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Research Articles
Kumada, Kazuki
Yao, Ryoji
Kawaguchi, Tokuichi
Karasawa, Mika
Hoshikawa, Yutaka
Ichikawa, Koji
Sugitani, Yoshinobu
Imoto, Issei
Inazawa, Johji
Sugawara, Minoru
Yanagida, Mitsuhiro
Noda, Tetsuo
The selective continued linkage of centromeres from mitosis to interphase in the absence of mammalian separase
title The selective continued linkage of centromeres from mitosis to interphase in the absence of mammalian separase
title_full The selective continued linkage of centromeres from mitosis to interphase in the absence of mammalian separase
title_fullStr The selective continued linkage of centromeres from mitosis to interphase in the absence of mammalian separase
title_full_unstemmed The selective continued linkage of centromeres from mitosis to interphase in the absence of mammalian separase
title_short The selective continued linkage of centromeres from mitosis to interphase in the absence of mammalian separase
title_sort selective continued linkage of centromeres from mitosis to interphase in the absence of mammalian separase
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2063728/
https://www.ncbi.nlm.nih.gov/pubmed/16533944
http://dx.doi.org/10.1083/jcb.200511126
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