Changing Mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis I.

The spindle assembly checkpoint (SAC) ensures correct separation of sister chromatids in somatic cells and provokes a cell cycle arrest in metaphase if one chromatid is not correctly attached to the bipolar spindle. Prolonged metaphase arrest due to overexpression of Mad2 has been shown to be delete...

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Autores principales:	Théodora Niault, Khaled Hached, Rocío Sotillo, Peter K Sorger, Bernard Maro, Robert Benezra, Katja Wassmann
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2007
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/8bd4d848e5924c1cad0b23413be343a5
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spelling	oai:doaj.org-article:8bd4d848e5924c1cad0b23413be343a52021-11-25T06:13:48ZChanging Mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis I.1932-620310.1371/journal.pone.0001165https://doaj.org/article/8bd4d848e5924c1cad0b23413be343a52007-11-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0001165https://doaj.org/toc/1932-6203The spindle assembly checkpoint (SAC) ensures correct separation of sister chromatids in somatic cells and provokes a cell cycle arrest in metaphase if one chromatid is not correctly attached to the bipolar spindle. Prolonged metaphase arrest due to overexpression of Mad2 has been shown to be deleterious to the ensuing anaphase, leading to the generation of aneuploidies and tumorigenesis. Additionally, some SAC components are essential for correct timing of prometaphase. In meiosis, we and others have shown previously that the Mad2-dependent SAC is functional during the first meiotic division in mouse oocytes. Expression of a dominant-negative form of Mad2 interferes with the SAC in metaphase I, and a knock-down approach using RNA interference accelerates anaphase onset in meiosis I. To prove unambigiously the importance of SAC control for mammalian female meiosis I we analyzed oocyte maturation in Mad2 heterozygote mice, and in oocytes overexpressing a GFP-tagged version of Mad2. In this study we show for the first time that loss of one Mad2 allele, as well as overexpression of Mad2 lead to chromosome missegregation events in meiosis I, and therefore the generation of aneuploid metaphase II oocytes. Furthermore, SAC control is impaired in mad2+/- oocytes, also leading to the generation of aneuploidies in meiosis I.Théodora NiaultKhaled HachedRocío SotilloPeter K SorgerBernard MaroRobert BenezraKatja WassmannPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 2, Iss 11, p e1165 (2007)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Théodora Niault Khaled Hached Rocío Sotillo Peter K Sorger Bernard Maro Robert Benezra Katja Wassmann Changing Mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis I.
description	The spindle assembly checkpoint (SAC) ensures correct separation of sister chromatids in somatic cells and provokes a cell cycle arrest in metaphase if one chromatid is not correctly attached to the bipolar spindle. Prolonged metaphase arrest due to overexpression of Mad2 has been shown to be deleterious to the ensuing anaphase, leading to the generation of aneuploidies and tumorigenesis. Additionally, some SAC components are essential for correct timing of prometaphase. In meiosis, we and others have shown previously that the Mad2-dependent SAC is functional during the first meiotic division in mouse oocytes. Expression of a dominant-negative form of Mad2 interferes with the SAC in metaphase I, and a knock-down approach using RNA interference accelerates anaphase onset in meiosis I. To prove unambigiously the importance of SAC control for mammalian female meiosis I we analyzed oocyte maturation in Mad2 heterozygote mice, and in oocytes overexpressing a GFP-tagged version of Mad2. In this study we show for the first time that loss of one Mad2 allele, as well as overexpression of Mad2 lead to chromosome missegregation events in meiosis I, and therefore the generation of aneuploid metaphase II oocytes. Furthermore, SAC control is impaired in mad2+/- oocytes, also leading to the generation of aneuploidies in meiosis I.
format	article
author	Théodora Niault Khaled Hached Rocío Sotillo Peter K Sorger Bernard Maro Robert Benezra Katja Wassmann
author_facet	Théodora Niault Khaled Hached Rocío Sotillo Peter K Sorger Bernard Maro Robert Benezra Katja Wassmann
author_sort	Théodora Niault
title	Changing Mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis I.
title_short	Changing Mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis I.
title_full	Changing Mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis I.
title_fullStr	Changing Mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis I.
title_full_unstemmed	Changing Mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis I.
title_sort	changing mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis i.
publisher	Public Library of Science (PLoS)
publishDate	2007
url	https://doaj.org/article/8bd4d848e5924c1cad0b23413be343a5
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Changing Mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis I.

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