Submit to Cells Review for Cells Propose a Special Issue

Journal Browser

10th Anniversary of Cells—Advances in Cell Cycle

Special Issue Editors
Special Issue Information
Published Papers

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Proliferation and Division".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 47943

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special issue 10th Anniversary of Cells—Advances in Cell Cycle book cover image

Share This Special Issue

Special Issue Editor

Prof. Dr. Zhixiang Wang

E-Mail Website
Guest Editor

Signal Transduction Research Group, Department of Medical Genetics, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB T6G 2H7, Canada
Interests: receptor tyrosine kinases; EGFR; signal transduction; cancer therapy; breast cancer treatment; targeted therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

2021 marks the 10th anniversary of the publication of Cells. We are delighted and proud to celebrate with a series of Special Issues and events. To date, the journal has published more than 4000 papers, and the journal website attracts more than 50,000 monthly page views. We would like to express our sincerest thanks to our readers, innumerable authors, anonymous peer reviewers, editors, and all the people working in some way for the journal who have made substantial contributions for years. Without your support, we would never have made it.

To mark this important milestone, a Special Issue entitled “10th Anniversary of Cells—Advances in Cell Cycle” is being launched. This Special Issue will collect, research articles, and high-quality review papers in the Cell Cycle research fields. We kindly encourage all research groups working in Cell Cycle areas to make contributions to this Special Issue.

This scientific journal is the collaborative achievement of many scientists from all over the world, and we would like to thank all our authors and reviewers who have contributed to this Special Issue. In recognition of our authors’ continued support, Cells is pleased to announce that the Cells Best Paper Awards for Anniversary Special Issues will be launched and granted to the best papers published in the Anniversary Special Issues. See the details at the following link:

https://0-www-mdpi-com.brum.beds.ac.uk/journal/cells/awards

Prof. Zhixiang Wang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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.

Published Papers (11 papers)

Download All Papers

Editorial

Jump to: Research, Review

4 pages, 213 KiB

Open AccessEditorial

Editorial to Summarize the Papers Published in the Special Issue “10th Anniversary of Cells—Advances in Cell Cycle”

by Zhixiang Wang

Cells 2022, 11(15), 2437; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11152437 - 05 Aug 2022

Viewed by 1051

Abstract

To celebrate its 10th anniversary, the prestigious journal Cells launched a series of Special Issues in 2021 [...] Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

Research

Jump to: Editorial, Review

19 pages, 3717 KiB

Open AccessCommunication

A Novel Hyperactive Nud1 Mitotic Exit Network Scaffold Causes Spindle Position Checkpoint Bypass in Budding Yeast

by Michael Vannini, Victoria R. Mingione, Ashleigh Meyer, Courtney Sniffen, Jenna Whalen and Anupama Seshan

Cells 2022, 11(1), 46; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11010046 - 24 Dec 2021

Cited by 1 | Viewed by 3041

Abstract

Mitotic exit is a critical cell cycle transition that requires the careful coordination of nuclear positioning and cyclin B destruction in budding yeast for the maintenance of genome integrity. The mitotic exit network (MEN) is a Ras-like signal transduction pathway that promotes this process during anaphase. A crucial step in MEN activation occurs when the Dbf2-Mob1 protein kinase complex associates with the Nud1 scaffold protein at the yeast spindle pole bodies (SPBs; centrosome equivalents) and thereby becomes activated. This requires prior priming phosphorylation of Nud1 by Cdc15 at SPBs. Cdc15 activation, in turn, requires both the Tem1 GTPase and the Polo kinase Cdc5, but how Cdc15 associates with SPBs is not well understood. We have identified a hyperactive allele of NUD1, nud1-A308T, that recruits Cdc15 to SPBs in all stages of the cell cycle in a CDC5-independent manner. This allele leads to early recruitment of Dbf2-Mob1 during metaphase and requires known Cdc15 phospho-sites on Nud1. The presence of nud1-A308T leads to loss of coupling between nuclear position and mitotic exit in cells with mispositioned spindles. Our findings highlight the importance of scaffold regulation in signaling pathways to prevent improper activation. Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

► Show Figures

Figure 1

21 pages, 9221 KiB

Open AccessFeature PaperArticle

Effects of Dithiothreitol on Fertilization and Early Development in Sea Urchin

by Nunzia Limatola, Jong Tai Chun, Sawsen Cherraben, Jean-Louis Schmitt, Jean-Marie Lehn and Luigia Santella

Cells 2021, 10(12), 3573; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10123573 - 17 Dec 2021

Cited by 7 | Viewed by 2713

Abstract

The vitelline layer (VL) of a sea urchin egg is an intricate meshwork of glycoproteins that intimately ensheathes the plasma membrane. During fertilization, the VL plays important roles. Firstly, the receptors for sperm reside on the VL. Secondly, following cortical granule exocytosis, the VL is elevated and transformed into the fertilization envelope (FE), owing to the assembly and crosslinking of the extruded materials. As these two crucial stages involve the VL, its alteration was expected to affect the fertilization process. In the present study, we addressed this question by mildly treating the eggs with a reducing agent, dithiothreitol (DTT). A brief pretreatment with DTT resulted in partial disruption of the VL, as judged by electron microscopy and by a novel fluorescent polyamine probe that selectively labelled the VL. The DTT-pretreated eggs did not elevate the FE but were mostly monospermic at fertilization. These eggs also manifested certain anomalies at fertilization: (i) compromised Ca²⁺ signaling, (ii) blocked translocation of cortical actin filaments, and (iii) impaired cleavage. Some of these phenotypic changes were reversed by restoring the DTT-exposed eggs in normal seawater prior to fertilization. Our findings suggest that the FE is not the decisive factor preventing polyspermy and that the integrity of the VL is nonetheless crucial to the egg’s fertilization response. Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

► Show Figures

Figure 1

13 pages, 2188 KiB

Open AccessArticle

M2 Muscarinic Receptor Activation Impairs Mitotic Progression and Bipolar Mitotic Spindle Formation in Human Glioblastoma Cell Lines

by Maria Di Bari, Vanessa Tombolillo, Francesco Alessandrini, Claudia Guerriero, Mario Fiore, Italia Anna Asteriti, Emilia Castigli, Miriam Sciaccaluga, Giulia Guarguaglini, Francesca Degrassi and Ada Maria Tata

Cells 2021, 10(7), 1727; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10071727 - 08 Jul 2021

Cited by 6 | Viewed by 2162

Abstract

Background: Glioblastoma multiforme (GBM) is characterized by several genetic abnormalities, leading to cell cycle deregulation and abnormal mitosis caused by a defective checkpoint. We previously demonstrated that arecaidine propargyl ester (APE), an orthosteric agonist of M2 muscarinic acetylcholine receptors (mAChRs), arrests the cell cycle of glioblastoma (GB) cells, reducing their survival. The aim of this work was to better characterize the molecular mechanisms responsible for this cell cycle arrest. Methods: The arrest of cell proliferation was evaluated by flow cytometry analysis. Using immunocytochemistry and time-lapse analysis, the percentage of abnormal mitosis and aberrant mitotic spindles were assessed in both cell lines. Western blot analysis was used to evaluate the modulation of Sirtuin2 and acetylated tubulin—factors involved in the control of cell cycle progression. Results: APE treatment caused arrest in the M phase, as indicated by the increase in p-HH3 (ser10)-positive cells. By immunocytochemistry, we found a significant increase in abnormal mitoses and multipolar mitotic spindle formation after APE treatment. Time-lapse analysis confirmed that the APE-treated GB cells were unable to correctly complete the mitosis. The modulated expression of SIRT2 and acetylated tubulin in APE-treated cells provides new insights into the mechanisms of altered mitotic progression in both GB cell lines. Conclusions: Our data show that the M2 agonist increases aberrant mitosis in GB cell lines. These results strengthen the idea of considering M2 acetylcholine receptors a novel promising therapeutic target for the glioblastoma treatment. Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

► Show Figures

Figure 1

21 pages, 4307 KiB

Open AccessArticle

Comparing Biochemical and Raman Microscopy Analyses of Starch, Lipids, Polyphosphate, and Guanine Pools during the Cell Cycle of Desmodesmus quadricauda

by Šárka Moudříková, Ivan Nedyalkov Ivanov, Milada Vítová, Ladislav Nedbal, Vilém Zachleder, Peter Mojzeš and Kateřina Bišová

Cells 2021, 10(1), 62; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10010062 - 03 Jan 2021

Cited by 11 | Viewed by 3192

Abstract

Photosynthetic energy conversion and the resulting photoautotrophic growth of green algae can only occur in daylight, but DNA replication, nuclear and cellular divisions occur often during the night. With such a light/dark regime, an algal culture becomes synchronized. In this study, using synchronized cultures of the green alga Desmodesmus quadricauda, the dynamics of starch, lipid, polyphosphate, and guanine pools were investigated during the cell cycle by two independent methodologies; conventional biochemical analyzes of cell suspensions and confocal Raman microscopy of single algal cells. Raman microscopy reports not only on mean concentrations, but also on the distribution of pools within cells. This is more sensitive in detecting lipids than biochemical analysis, but both methods—as well as conventional fluorescence microscopy—were comparable in detecting polyphosphates. Discrepancies in the detection of starch by Raman microscopy are discussed. The power of Raman microscopy was proven to be particularly valuable in the detection of guanine, which was traceable by its unique vibrational signature. Guanine microcrystals occurred specifically at around the time of DNA replication and prior to nuclear division. Interestingly, guanine crystals co-localized with polyphosphates in the vicinity of nuclei around the time of nuclear division. Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

► Show Figures

Figure 1

Review

Jump to: Editorial, Research

14 pages, 1197 KiB

Open AccessReview

Advances in the Current Understanding of How Low-Dose Radiation Affects the Cell Cycle

by Md Gulam Musawwir Khan and Yi Wang

Cells 2022, 11(3), 356; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11030356 - 21 Jan 2022

Cited by 18 | Viewed by 5338

Abstract

Cells exposed to ionizing radiation undergo a series of complex responses, including DNA damage, reproductive cell death, and altered proliferation states, which are all linked to cell cycle dynamics. For many years, a great deal of research has been conducted on cell cycle checkpoints and their regulators in mammalian cells in response to high-dose exposures to ionizing radiation. However, it is unclear how low-dose ionizing radiation (LDIR) regulates the cell cycle progression. A growing body of evidence demonstrates that LDIR may have profound effects on cellular functions. In this review, we summarize the current understanding of how LDIR (of up to 200 mGy) regulates the cell cycle and cell-cycle-associated proteins in various cellular settings. In light of current findings, we also illustrate the conceptual function and possible dichotomous role of p21^Waf1, a transcriptional target of p53, in response to LDIR. Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

► Show Figures

Graphical abstract

18 pages, 1464 KiB

Open AccessReview

Cyclin-Dependent Kinases and CTD Phosphatases in Cell Cycle Transcriptional Control: Conservation across Eukaryotic Kingdoms and Uniqueness to Plants

by Zhi-Liang Zheng

Cells 2022, 11(2), 279; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11020279 - 14 Jan 2022

Cited by 10 | Viewed by 3276

Abstract

Cell cycle control is vital for cell proliferation in all eukaryotic organisms. The entire cell cycle can be conceptually separated into four distinct phases, Gap 1 (G1), DNA synthesis (S), G2, and mitosis (M), which progress sequentially. The precise control of transcription, in particular, at the G1 to S and G2 to M transitions, is crucial for the synthesis of many phase-specific proteins, to ensure orderly progression throughout the cell cycle. This mini-review highlights highly conserved transcriptional regulators that are shared in budding yeast (Saccharomyces cerevisiae), Arabidopsis thaliana model plant, and humans, which have been separated for more than a billion years of evolution. These include structurally and/or functionally conserved regulators cyclin-dependent kinases (CDKs), RNA polymerase II C-terminal domain (CTD) phosphatases, and the classical versus shortcut models of Pol II transcriptional control. A few of CDKs and CTD phosphatases counteract to control the Pol II CTD Ser phosphorylation codes and are considered critical regulators of Pol II transcriptional process from initiation to elongation and termination. The functions of plant-unique CDKs and CTD phosphatases in relation to cell division are also briefly summarized. Future studies towards testing a cooperative transcriptional mechanism, which is proposed here and involves sequence-specific transcription factors and the shortcut model of Pol II CTD code modulation, across the three eukaryotic kingdoms will reveal how individual organisms achieve the most productive, large-scale transcription of phase-specific genes required for orderly progression throughout the entire cell cycle. Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

► Show Figures

Graphical abstract

16 pages, 968 KiB

Open AccessReview

Cell Cycle Regulation by Heat Shock Transcription Factors

by Yasuko Tokunaga, Ken-Ichiro Otsuyama and Naoki Hayashida

Cells 2022, 11(2), 203; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11020203 - 08 Jan 2022

Cited by 6 | Viewed by 3549

Abstract

Cell division and cell cycle mechanism has been studied for 70 years. This research has revealed that the cell cycle is regulated by many factors, including cyclins and cyclin-dependent kinases (CDKs). Heat shock transcription factors (HSFs) have been noted as critical proteins for cell survival against various stresses; however, recent studies suggest that HSFs also have important roles in cell cycle regulation-independent cell-protective functions. During cell cycle progression, HSF1, and HSF2 bind to condensed chromatin to provide immediate precise gene expression after cell division. This review focuses on the function of these HSFs in cell cycle progression, cell cycle arrest, gene bookmarking, mitosis and meiosis. Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

► Show Figures

Figure 1

23 pages, 2893 KiB

Open AccessReview

Regulation of Cell Cycle Progression by Growth Factor-Induced Cell Signaling

by Zhixiang Wang

Cells 2021, 10(12), 3327; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10123327 - 26 Nov 2021

Cited by 76 | Viewed by 15861

Abstract

The cell cycle is the series of events that take place in a cell, which drives it to divide and produce two new daughter cells. The typical cell cycle in eukaryotes is composed of the following phases: G1, S, G2, and M phase. Cell cycle progression is mediated by cyclin-dependent kinases (Cdks) and their regulatory cyclin subunits. However, the driving force of cell cycle progression is growth factor-initiated signaling pathways that control the activity of various Cdk–cyclin complexes. While the mechanism underlying the role of growth factor signaling in G1 phase of cell cycle progression has been largely revealed due to early extensive research, little is known regarding the function and mechanism of growth factor signaling in regulating other phases of the cell cycle, including S, G2, and M phase. In this review, we briefly discuss the process of cell cycle progression through various phases, and we focus on the role of signaling pathways activated by growth factors and their receptor (mostly receptor tyrosine kinases) in regulating cell cycle progression through various phases. Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

► Show Figures

Figure 1

15 pages, 1539 KiB

Open AccessReview

Cell Cycle, Telomeres, and Telomerase in Leishmania spp.: What Do We Know So Far?

by Luiz H. C. Assis, Débora Andrade-Silva, Mark E. Shiburah, Beatriz C. D. de Oliveira, Stephany C. Paiva, Bryan E. Abuchery, Yete G. Ferri, Veronica S. Fontes, Leilane S. de Oliveira, Marcelo S. da Silva and Maria Isabel N. Cano

Cells 2021, 10(11), 3195; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10113195 - 16 Nov 2021

Cited by 4 | Viewed by 3465

Abstract

Leishmaniases belong to the inglorious group of neglected tropical diseases, presenting different degrees of manifestations severity. It is caused by the transmission of more than 20 species of parasites of the Leishmania genus. Nevertheless, the disease remains on the priority list for developing new treatments, since it affects millions in a vast geographical area, especially low-income people. Molecular biology studies are pioneers in parasitic research with the aim of discovering potential targets for drug development. Among them are the telomeres, DNA–protein structures that play an important role in the long term in cell cycle/survival. Telomeres are the physical ends of eukaryotic chromosomes. Due to their multiple interactions with different proteins that confer a likewise complex dynamic, they have emerged as objects of interest in many medical studies, including studies on leishmaniases. This review aims to gather information and elucidate what we know about the phenomena behind Leishmania spp. telomere maintenance and how it impacts the parasite’s cell cycle. Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

► Show Figures

Figure 1

15 pages, 2878 KiB

Open AccessReview

Incorporation of 5-Bromo-2′-deoxyuridine into DNA and Proliferative Behavior of Cerebellar Neuroblasts: All That Glitters Is Not Gold

by Joaquín Martí-Clúa

Cells 2021, 10(6), 1453; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10061453 - 10 Jun 2021

Cited by 7 | Viewed by 2754

Abstract

The synthetic halogenated pyrimidine analog, 5-bromo-2′-deoxyuridine (BrdU), is a marker of DNA synthesis. This exogenous nucleoside has generated important insights into the cellular mechanisms of the central nervous system development in a variety of animals including insects, birds, and mammals. Despite this, the detrimental effects of the incorporation of BrdU into DNA on proliferation and viability of different types of cells has been frequently neglected. This review will summarize and present the effects of a pulse of BrdU, at doses ranging from 25 to 300 µg/g, or repeated injections. The latter, following the method of the progressively delayed labeling comprehensive procedure. The prenatal and perinatal development of the cerebellum are studied. These current data have implications for the interpretation of the results obtained by this marker as an index of the generation, migration, and settled pattern of neurons in the developing central nervous system. Caution should be exercised when interpreting the results obtained using BrdU. This is particularly important when high or repeated doses of this agent are injected. I hope that this review sheds light on the effects of this toxic maker. It may be used as a reference for toxicologists and neurobiologists given the broad use of 5-bromo-2′-deoxyuridine to label dividing cells. Full article

(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cell Cycle)

► Show Figures