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The Mitotic Apparatus and Kinetochores in Microcephaly and Neurodevelopmental Diseases

Regulators of mitotic division, when dysfunctional or expressed in a deregulated manner (over- or underexpressed) in somatic cells, cause chromosome instability, which is a predisposing condition to cancer that is associated with unrestricted proliferation. Genes encoding mitotic regulators are grow...

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Detalles Bibliográficos
Autores principales: Degrassi, Francesca, Damizia, Michela, Lavia, Patrizia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7016623/
https://www.ncbi.nlm.nih.gov/pubmed/31878213
http://dx.doi.org/10.3390/cells9010049
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author Degrassi, Francesca
Damizia, Michela
Lavia, Patrizia
author_facet Degrassi, Francesca
Damizia, Michela
Lavia, Patrizia
author_sort Degrassi, Francesca
collection PubMed
description Regulators of mitotic division, when dysfunctional or expressed in a deregulated manner (over- or underexpressed) in somatic cells, cause chromosome instability, which is a predisposing condition to cancer that is associated with unrestricted proliferation. Genes encoding mitotic regulators are growingly implicated in neurodevelopmental diseases. Here, we briefly summarize existing knowledge on how microcephaly-related mitotic genes operate in the control of chromosome segregation during mitosis in somatic cells, with a special focus on the role of kinetochore factors. Then, we review evidence implicating mitotic apparatus- and kinetochore-resident factors in the origin of congenital microcephaly. We discuss data emerging from these works, which suggest a critical role of correct mitotic division in controlling neuronal cell proliferation and shaping the architecture of the central nervous system.
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spelling pubmed-70166232020-03-04 The Mitotic Apparatus and Kinetochores in Microcephaly and Neurodevelopmental Diseases Degrassi, Francesca Damizia, Michela Lavia, Patrizia Cells Review Regulators of mitotic division, when dysfunctional or expressed in a deregulated manner (over- or underexpressed) in somatic cells, cause chromosome instability, which is a predisposing condition to cancer that is associated with unrestricted proliferation. Genes encoding mitotic regulators are growingly implicated in neurodevelopmental diseases. Here, we briefly summarize existing knowledge on how microcephaly-related mitotic genes operate in the control of chromosome segregation during mitosis in somatic cells, with a special focus on the role of kinetochore factors. Then, we review evidence implicating mitotic apparatus- and kinetochore-resident factors in the origin of congenital microcephaly. We discuss data emerging from these works, which suggest a critical role of correct mitotic division in controlling neuronal cell proliferation and shaping the architecture of the central nervous system. MDPI 2019-12-24 /pmc/articles/PMC7016623/ /pubmed/31878213 http://dx.doi.org/10.3390/cells9010049 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Degrassi, Francesca
Damizia, Michela
Lavia, Patrizia
The Mitotic Apparatus and Kinetochores in Microcephaly and Neurodevelopmental Diseases
title The Mitotic Apparatus and Kinetochores in Microcephaly and Neurodevelopmental Diseases
title_full The Mitotic Apparatus and Kinetochores in Microcephaly and Neurodevelopmental Diseases
title_fullStr The Mitotic Apparatus and Kinetochores in Microcephaly and Neurodevelopmental Diseases
title_full_unstemmed The Mitotic Apparatus and Kinetochores in Microcephaly and Neurodevelopmental Diseases
title_short The Mitotic Apparatus and Kinetochores in Microcephaly and Neurodevelopmental Diseases
title_sort mitotic apparatus and kinetochores in microcephaly and neurodevelopmental diseases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7016623/
https://www.ncbi.nlm.nih.gov/pubmed/31878213
http://dx.doi.org/10.3390/cells9010049
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