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The spindle assembly checkpoint and the spatial activation of Polo kinase determine the duration of cell division and prevent tumor formation
The maintenance of a restricted pool of asymmetrically dividing stem cells is essential for tissue homeostasis. This process requires the control of mitotic progression that ensures the accurate chromosome segregation. In addition, this event is coupled to the asymmetric distribution of cell fate de...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9009772/ https://www.ncbi.nlm.nih.gov/pubmed/35377889 http://dx.doi.org/10.1371/journal.pgen.1010145 |
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author | Gallaud, Emmanuel Richard-Parpaillon, Laurent Bataillé, Laetitia Pascal, Aude Métivier, Mathieu Archambault, Vincent Giet, Régis |
author_facet | Gallaud, Emmanuel Richard-Parpaillon, Laurent Bataillé, Laetitia Pascal, Aude Métivier, Mathieu Archambault, Vincent Giet, Régis |
author_sort | Gallaud, Emmanuel |
collection | PubMed |
description | The maintenance of a restricted pool of asymmetrically dividing stem cells is essential for tissue homeostasis. This process requires the control of mitotic progression that ensures the accurate chromosome segregation. In addition, this event is coupled to the asymmetric distribution of cell fate determinants in order to prevent stem cell amplification. How this coupling is regulated remains poorly described. Here, using asymmetrically dividing Drosophila neural stem cells (NSCs), we show that Polo kinase activity levels determine timely Cyclin B degradation and mitotic progression independent of the spindle assembly checkpoint (SAC). This event is mediated by the direct phosphorylation of Polo kinase by Aurora A at spindle poles and Aurora B kinases at centromeres. Furthermore, we show that Aurora A-dependent activation of Polo is the major event that promotes NSC polarization and together with the SAC prevents brain tumor growth. Altogether, our results show that an Aurora/Polo kinase module couples NSC mitotic progression and polarization for tissue homeostasis. |
format | Online Article Text |
id | pubmed-9009772 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-90097722022-04-15 The spindle assembly checkpoint and the spatial activation of Polo kinase determine the duration of cell division and prevent tumor formation Gallaud, Emmanuel Richard-Parpaillon, Laurent Bataillé, Laetitia Pascal, Aude Métivier, Mathieu Archambault, Vincent Giet, Régis PLoS Genet Research Article The maintenance of a restricted pool of asymmetrically dividing stem cells is essential for tissue homeostasis. This process requires the control of mitotic progression that ensures the accurate chromosome segregation. In addition, this event is coupled to the asymmetric distribution of cell fate determinants in order to prevent stem cell amplification. How this coupling is regulated remains poorly described. Here, using asymmetrically dividing Drosophila neural stem cells (NSCs), we show that Polo kinase activity levels determine timely Cyclin B degradation and mitotic progression independent of the spindle assembly checkpoint (SAC). This event is mediated by the direct phosphorylation of Polo kinase by Aurora A at spindle poles and Aurora B kinases at centromeres. Furthermore, we show that Aurora A-dependent activation of Polo is the major event that promotes NSC polarization and together with the SAC prevents brain tumor growth. Altogether, our results show that an Aurora/Polo kinase module couples NSC mitotic progression and polarization for tissue homeostasis. Public Library of Science 2022-04-04 /pmc/articles/PMC9009772/ /pubmed/35377889 http://dx.doi.org/10.1371/journal.pgen.1010145 Text en © 2022 Gallaud et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Gallaud, Emmanuel Richard-Parpaillon, Laurent Bataillé, Laetitia Pascal, Aude Métivier, Mathieu Archambault, Vincent Giet, Régis The spindle assembly checkpoint and the spatial activation of Polo kinase determine the duration of cell division and prevent tumor formation |
title | The spindle assembly checkpoint and the spatial activation of Polo kinase determine the duration of cell division and prevent tumor formation |
title_full | The spindle assembly checkpoint and the spatial activation of Polo kinase determine the duration of cell division and prevent tumor formation |
title_fullStr | The spindle assembly checkpoint and the spatial activation of Polo kinase determine the duration of cell division and prevent tumor formation |
title_full_unstemmed | The spindle assembly checkpoint and the spatial activation of Polo kinase determine the duration of cell division and prevent tumor formation |
title_short | The spindle assembly checkpoint and the spatial activation of Polo kinase determine the duration of cell division and prevent tumor formation |
title_sort | spindle assembly checkpoint and the spatial activation of polo kinase determine the duration of cell division and prevent tumor formation |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9009772/ https://www.ncbi.nlm.nih.gov/pubmed/35377889 http://dx.doi.org/10.1371/journal.pgen.1010145 |
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