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Cells
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Molecular Mechanisms of Cell Division and Chromosome Segregation: What Can...
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Molecular Mechanisms of Cell Division and Chromosome Segregation: What Can Go Wrong?

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Nuclei: Function, Transport and Receptors".

Deadline for manuscript submissions: 31 January 2025 | Viewed by 9505

Special Issue Editors

Prof. Dr. Patrizio Dimitri

E-Mail Website
Guest Editor
Department of Biology and Biotechnology “Charles Darwin”, Laboratory of Epigenetics, “Sapienza” University of Rome, Rome, Italy
Interests: chromosome biology; genome evolution; heterochromatin; epigenetics; chromatin remodeling; cytokinesis; drosophila
Special Issues, Collections and Topics in MDPI journals
Dr. Giovanni Messina

E-Mail Website
Guest Editor
1. Department of Biology and Biotechnology “Charles Darwin”, Sapienza University of Rome, 00185 Rome, Italy
2. Pasteur Institute, Fondazione Cenci-Bolognetti, 00161 Rome, Italy
Interests: epigenetics and chromatin remodeling; mechanisms of mitosis in drosophila melanogaster and human; meiosis and spermiogenesis in drosophila melanogaster; cytokinesis; floating-harbor syndrome and tubulinopathies
Special Issues, Collections and Topics in MDPI journals
Yuri Prozzillo

E-Mail Website
Guest Editor Assistant
1. Department of Biology and Biotechnology “Charles Darwin”, Sapienza University of Rome, 00185 Rome, Italy
2. Pasteur Institute of Italy, Roma, Italy
Interests: cell cycle and cell division in Drosophila melanogaster and humans; protein phosphorylation; protein degradation technologies; Chromatin remodeling; gametogenesis in Drosophila melanogaster; tubulinopathies and ciliopathies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Cell division consists of a series of tightly controlled events which lead a cell to segregate its genetic material, equally balanced into two daughter cells. The failure of cell division and the resulting generation of genetic instability (including both numerical and structural chromosomal abnormalities) lead to an unstable state, hence activating tumorigenic transformation. Cancer cells strive to elude the surveillance systems that monitor genome stability, such as those coordinated by the transcriptional regulator p53. Therefore, understanding how genetic stability is transmitted through cell division and how uncorrected mitotic errors can originate genetically unbalanced cells is of primary importance to cancer research.

Thus, this Special Issue entitled ‘Molecular Mechanisms of Cell Division and Chromosome Segregation: What Can Go Wrong?’ will discuss how the deregulation of molecular aspects of cell division can generate an unbalanced distribution of chromosomes and in turn contribute to cancer onset and progression. Both original research and review articles are welcome.

Prof. Dr. Patrizio Dimitri
Dr. Giovanni Messina
Guest Editors
Yuri Prozzillo 
Guest Editor Assistant

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitosis
  • cell division
  • genetic instability
  • aneuploidy
  • lagging chromosomes
  • chrosomomes misalignment
  • mitotic checkpoint
  • microtubules attachment
  • kinetochores
  • microtubules dynamics

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Published Papers (4 papers)

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Research

Jump to: Review

13 pages, 8260 KiB  
Article
Knockdown of DOM/Tip60 Complex Subunits Impairs Male Meiosis of Drosophila melanogaster
by Yuri Prozzillo, Gaia Fattorini, Diego Ferreri, Manuela Leo, Patrizio Dimitri and Giovanni Messina
Cells 2023, 12(10), 1348; https://doi.org/10.3390/cells12101348 - 9 May 2023
Cited by 3 | Viewed by 2131
Abstract
ATP-dependent chromatin remodeling complexes are involved in nucleosome sliding and eviction and/or the incorporation of histone variants into chromatin to facilitate several cellular and biological processes, including DNA transcription, replication and repair. The DOM/TIP60 chromatin remodeling complex of Drosophila melanogaster contains 18 subunits, [...] Read more.
ATP-dependent chromatin remodeling complexes are involved in nucleosome sliding and eviction and/or the incorporation of histone variants into chromatin to facilitate several cellular and biological processes, including DNA transcription, replication and repair. The DOM/TIP60 chromatin remodeling complex of Drosophila melanogaster contains 18 subunits, including the DOMINO (DOM), an ATPase that catalyzes the exchange of the canonical H2A with its variant (H2A.V), and TIP60, a lysine-acetyltransferase that acetylates H4, H2A and H2A.V histones. In recent decades, experimental evidence has shown that ATP-dependent chromatin remodeling factors, in addition to their role in chromatin organization, have a functional relevance in cell division. In particular, emerging studies suggested the direct roles of ATP-dependent chromatin remodeling complex subunits in controlling mitosis and cytokinesis in both humans and D. melanogaster. However, little is known about their possible involvement during meiosis. The results of this work show that the knockdown of 12 of DOM/TIP60 complex subunits generates cell division defects that, in turn, cause total/partial sterility in Drosophila males, providing new insights into the functions of chromatin remodelers in cell division control during gametogenesis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cell Division and Chromosome Segregation: What Can Go Wrong?)
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19 pages, 2847 KiB  
Article
Aurora B SUMOylation Is Restricted to Centromeres in Early Mitosis and Requires RANBP2
by Erica Di Cesare, Sara Moroni, Jessica Bartoli, Michela Damizia, Maria Giubettini, Carolin Koerner, Veronica Krenn, Andrea Musacchio and Patrizia Lavia
Cells 2023, 12(3), 372; https://doi.org/10.3390/cells12030372 - 19 Jan 2023
Cited by 5 | Viewed by 2704
Abstract
Conjugation with the small ubiquitin-like modifier (SUMO) modulates protein interactions and localisation. The kinase Aurora B, a key regulator of mitosis, was previously identified as a SUMOylation target in vitro and in assays with overexpressed components. However, where and when this modification genuinely [...] Read more.
Conjugation with the small ubiquitin-like modifier (SUMO) modulates protein interactions and localisation. The kinase Aurora B, a key regulator of mitosis, was previously identified as a SUMOylation target in vitro and in assays with overexpressed components. However, where and when this modification genuinely occurs in human cells was not ascertained. Here, we have developed intramolecular Proximity Ligation Assays (PLA) to visualise SUMO-conjugated Aurora B in human cells in situ. We visualised Aurora B-SUMO products at centromeres in prometaphase and metaphase, which declined from anaphase onwards and became virtually undetectable at cytokinesis. In the mitotic window in which Aurora B/SUMO products are abundant, Aurora B co-localised and interacted with NUP358/RANBP2, a nucleoporin with SUMO ligase and SUMO-stabilising activity. Indeed, in addition to the requirement for the previously identified PIAS3 SUMO ligase, we found that NUP358/RANBP2 is also implicated in Aurora B-SUMO PLA product formation and centromere localisation. In summary, SUMOylation marks a distinctive window of Aurora B functions at centromeres in prometaphase and metaphase while being dispensable for functions exerted in cytokinesis, and RANBP2 contributes to this control, adding a novel layer to modulation of Aurora B functions during mitosis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cell Division and Chromosome Segregation: What Can Go Wrong?)
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Review

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15 pages, 1486 KiB  
Review
Contribution of AurkA/TPX2 Overexpression to Chromosomal Imbalances and Cancer
by Federica Polverino, Anna Mastrangelo and Giulia Guarguaglini
Cells 2024, 13(16), 1397; https://doi.org/10.3390/cells13161397 - 22 Aug 2024
Viewed by 1072
Abstract
The AurkA serine/threonine kinase is a key regulator of cell division controlling mitotic entry, centrosome maturation, and chromosome segregation. The microtubule-associated protein TPX2 controls spindle assembly and is the main AurkA regulator, contributing to AurkA activation, localisation, and stabilisation. Since their identification, AurkA [...] Read more.
The AurkA serine/threonine kinase is a key regulator of cell division controlling mitotic entry, centrosome maturation, and chromosome segregation. The microtubule-associated protein TPX2 controls spindle assembly and is the main AurkA regulator, contributing to AurkA activation, localisation, and stabilisation. Since their identification, AurkA and TPX2 have been described as being overexpressed in cancer, with a significant correlation with highly proliferative and aneuploid tumours. Despite the frequent occurrence of AurkA/TPX2 co-overexpression in cancer, the investigation of their involvement in tumorigenesis and cancer therapy resistance mostly arises from studies focusing only on one at the time. Here, we review the existing literature and discuss the mitotic phenotypes described under conditions of AurkA, TPX2, or AurkA/TPX2 overexpression, to build a picture that may help clarify their oncogenic potential through the induction of chromosome instability. We highlight the relevance of the AurkA/TPX2 complex as an oncogenic unit, based on which we discuss recent strategies under development that aim at disrupting the complex as a promising therapeutic perspective. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cell Division and Chromosome Segregation: What Can Go Wrong?)
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17 pages, 917 KiB  
Review
The Multiple Mitotic Roles of the ASPM Orthologous Proteins: Insight into the Etiology of ASPM-Dependent Microcephaly
by Alyona V. Razuvaeva, Lucia Graziadio, Valeria Palumbo, Gera A. Pavlova, Julia V. Popova, Alexey V. Pindyurin, Silvia Bonaccorsi, Maria Patrizia Somma and Maurizio Gatti
Cells 2023, 12(6), 922; https://doi.org/10.3390/cells12060922 - 16 Mar 2023
Cited by 6 | Viewed by 2582
Abstract
The Drosophila abnormal spindle (asp) gene was discovered about 40 years ago and shown to be required for both mitotic and meiotic cell division. Subsequent studies showed that asp is highly conserved and that mutations in its human ortholog ASPM ( [...] Read more.
The Drosophila abnormal spindle (asp) gene was discovered about 40 years ago and shown to be required for both mitotic and meiotic cell division. Subsequent studies showed that asp is highly conserved and that mutations in its human ortholog ASPM (Abnormal Spindle-like Microcephaly-associated; or MCPH5) are the most common cause of autosomal recessive primary microcephaly. This finding greatly stimulated research on ASPM and its fly and mouse (Aspm) orthologs. The three Asp orthologous proteins bind the microtubules (MTs) minus ends during cell division and also function in interphase nuclei. Investigations on different cell types showed that Asp/Aspm/ASPM depletion disrupts one or more of the following mitotic processes: aster formation, spindle pole focusing, centrosome-spindle coupling, spindle orientation, metaphase-to-anaphase progression, chromosome segregation, and cytokinesis. In addition, ASPM physically interacts with components of the DNA repair and replication machineries and is required for the maintenance of chromosomal DNA stability. We propose the working hypothesis that the asp/Aspm/ASPM genes play the same conserved functions in Drosophila, mouse, and human cells. Human microcephaly is a genetically heterogeneous disorder caused by mutations in 30 different genes that play a variety of functions required for cell division and chromosomal DNA integrity. Our hypothesis postulates that ASPM recapitulates the functions of most human microcephaly genes and provides a justification for why ASPM is the most frequently mutated gene in autosomal recessive primary microcephaly. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cell Division and Chromosome Segregation: What Can Go Wrong?)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Contribution of AurkA/TPX2 overexpression to chromosomal imbalances and cancer
Authors: Federica Polverino; Anna Mastrangelo; Giulia Guarguaglini
Affiliation: Institute of Molecular Biology and Pathology, CNR
Abstract: The AurkA serine/threonine kinase is a key regulator of cell division controlling mitotic entry, centrosome maturation and chromosome segregation. The microtubule-associated protein TPX2 controls spindle assembly and is the main AurkA regulator, contributing to AurkA activation, localisation and stabilisation. Since their identification AurkA and TPX2 have been described as overexpressed in cancer, with significant correlation with highly proliferative and aneuploid tumours. Despite the frequency of AurkA/TPX2 co-overexpression in cancer, investigation of their involvement in tumorigenesis and cancer therapy resistance mostly arises from studies focusing only on one or the other. Here we review the existing literature and discuss the mitotic phenotypes described under AurkA, TPX2 or AurkA/TPX2 overexpression conditions, to build a picture that may help clarify their oncogenic potential through induction of chromosome instability. We highlight the relevance of the AurkA/TPX2 complex as an oncogenic unit, based on which we discuss results of the most recent strategies under development that aim at disrupting the complex as a promising therapeutic perspective.

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