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Cells
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Cell Biology: State-of-the-Art and Perspectives in Spain
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Cell Biology: State-of-the-Art and Perspectives in Spain

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 12897

Special Issue Editors

Dr. Miguel Vicente Manzanares

E-Mail Website
Guest Editor
Instituto de Biología Molecular y Celular del Cáncer USAL-CSIC, 37007 Salamanca, Spain
Interests: cytoskeleton; mechanobiology; actin; myosin; chemotaxis; signaling; Rho GTPases; microenvironment; immunosuppression
Prof. Dr. José M. Fuentes

E-Mail Website1 Website2
Guest Editor
Departamento de Bioquímica y Biología Molecular y Genética, Facultad de Enfermería y Terapia Ocupacional, Universidad de Extremadura, Cáceres, Spain
Interests: metabolism; natural compounds; metabolic changes; neural cells
Special Issues, Collections and Topics in MDPI journals
Dr. Elena Llano

E-Mail Website
Guest Editor
Departamento de Fisiología y Farmacalogía. Centro de Investigación del Cancer, Universidad de Salamanca, Salamanca, Spain
Interests: meiosis; chromosome segregation; spermatogenesis; oogenesis; aneuploidy; cohesins
Prof. Dr. Pablo Martín-Vasallo

E-Mail Website
Guest Editor
Departament of Biochemistry, Microbiology, Cell Biology and Genetics, University of La Laguna, Av Astrofisico Fco Sanchez s/n, 38206 La Laguna, Tenerife, Spain
Interests: stem cells; gene expression; regeneration; cancer research; cancer stem cells; stem cell differentiation; tumor angiogenesis; tumor stem cells; neural development, tumor microenvironment, glioblastoma, colorectal cancer; Na,K‐ATPase
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to provide a comprehensive overview of state-of-the-art of cell biology in Spain. We invite research papers that will consolidate our understanding in this area. The Special Issue will publish full research articles and comprehensive reviews. Potential topics include but are not limited to the following research areas:

  • OMICS: transcriptomics, genomics, proteomics, metabolomics, glycomics, lipidomics, interactomics, fluxomics, and biomics;
  • Cell structure: organelles, cytoskeleton, cell membrane, capsule, flagella, etc.;
  • Cell physiology: cell growth, metabolism, protein synthesis, division, movement of proteins, active/passive transport, intra- and extracellular signaling, adhesion, DNA repair, etc.;
  • Cell movement and motility;
  • Autophagy;
  • Apoptosis;
  • Cell aging;
  • Cell techniques: cell and tissue culture, isolation and fractionation of cells, immunocytochemistry (ICC), in situ hybridization (ISH), transfection, and optogenetics;
  • Cell growth and differentiation;
  • Hematopoiesis and stem cells;
  • Cancer stem cells;
  • Genetic disorders;
  • CAR-T cell research.

Dr. Miguel Vicente Manzanares
Prof. Dr. José Fuentes
Dr. Elena Llano
Prof. Pablo Martín-Vasallo
Guest Editors

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 (5 papers)

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Research

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11 pages, 1152 KiB  
Communication
Down-Regulation of the Longevity-Associated Protein SIRT1 in Peripheral Blood Mononuclear Cells of Treated HIV Patients
by Aleksandra Gruevska, Ángela B. Moragrega, María J. Galindo, Juan V. Esplugues, Ana Blas-García and Nadezda Apostolova
Cells 2022, 11(3), 348; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11030348 - 20 Jan 2022
Cited by 2 | Viewed by 1766
Abstract
The activity of sirtuin 1 (SIRT1), a class III histone deacetylase with a critical role in several biological functions, decreases with age and its deficiency is associated with many inflammatory and age-related diseases. It also regulates the chronic immune activation and viral latency [...] Read more.
The activity of sirtuin 1 (SIRT1), a class III histone deacetylase with a critical role in several biological functions, decreases with age and its deficiency is associated with many inflammatory and age-related diseases. It also regulates the chronic immune activation and viral latency during an HIV infection. The life-span and particularly the health span of HIV patients are substantially shortened; however, the participation of SIRT1 in these effects is not clear. We performed a prospective cross-sectional monocentric study that included 70 HIV-infected patients and 43 BMI-, age- and sex-matched uninfected individuals. We found that in the PBMCs of the HIV patients, SIRT1 mRNA levels were significantly lower (p < 0.0001). This decrease, which was corroborated at the protein level, occurred irrespectively of the antiretroviral regimen these patients received and was not significantly related to the general, HIV-related or comorbidity-related parameters. The levels of the major mitochondrial sirtuin SIRT3 were not altered. Moreover, the strong correlations of SIRT1 with the leukocyte markers CD8A and CD19 present in the uninfected individuals were absent in the HIV patients. In conclusion, this study showed that the PBMCs of the HIV patients displayed diminished SIRT1 levels and altered correlations of SIRT1 with markers of CD8+ T cells and B cells, findings which may be relevant for understanding the complex pathogenic milieu in HIV patients. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Spain)
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13 pages, 5545 KiB  
Article
Endogenous pH 6.0 β-Galactosidase Activity Is Linked to Neuronal Differentiation in the Olfactory Epithelium
by José Antonio de Mera-Rodríguez, Guadalupe Álvarez-Hernán, Yolanda Gañán, Ana Santos-Almeida, Gervasio Martín-Partido, Joaquín Rodríguez-León and Javier Francisco-Morcillo
Cells 2022, 11(2), 298; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11020298 - 16 Jan 2022
Cited by 6 | Viewed by 2248
Abstract
The histochemical detection of β-galactosidase enzymatic activity at pH 6.0 (β-gal-pH6) is a widely used biomarker of cellular senescence in aging tissues. This histochemical assay also detects the presence of programmed cell senescence during specific time windows in degenerating structures of vertebrate embryos. [...] Read more.
The histochemical detection of β-galactosidase enzymatic activity at pH 6.0 (β-gal-pH6) is a widely used biomarker of cellular senescence in aging tissues. This histochemical assay also detects the presence of programmed cell senescence during specific time windows in degenerating structures of vertebrate embryos. However, it has recently been shown that this enzymatic activity is also enhanced in subpopulations of differentiating neurons in the developing central nervous system in vertebrates. The present study addressed the histochemical detection of β-gal-pH6 enzymatic activity in the developing postnatal olfactory epithelium in the mouse. This activity was detected in the intermediate layer of the olfactory epithelium. As development progressed, the band of β-gal-pH6 labeling in this layer increased in width. Immunohistochemistry and lectin histochemistry showed the β-gal-pH6 staining to be strongly correlated with the immunolabeling of the olfactory marker protein (OMP) that identifies mature olfactory sensory neurons. The cell somata of a subpopulation of differentiated olfactory neurons that were recognized with the Dolichos biflorus agglutinin (DBA) were always located inside this band of β-gal-pH6 staining. However, the β-gal-pH6 histochemical signal was always absent from the apical region where the cytokeratin-8 positive supporting cells were located. Furthermore, no β-gal-pH6 staining was found in the basal region of the olfactory epithelium where PCNA/pHisH3 immunoreactive proliferating progenitor cells, GAP43 positive immature neurons, and cytokeratin-5 positive horizontal basal cells were located. Therefore, β-gal-pH6 seems to be linked to neuronal differentiation and cannot be regarded as a biomarker of cellular senescence during olfactory epithelium development in mice. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Spain)
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17 pages, 2675 KiB  
Article
The N-Terminal Region of the Polo Kinase Cdc5 Is Required for Downregulation of the Meiotic Recombination Checkpoint
by Sara González-Arranz, Isabel Acosta, Jesús A. Carballo, Beatriz Santos and Pedro A. San-Segundo
Cells 2021, 10(10), 2561; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10102561 - 27 Sep 2021
Cited by 1 | Viewed by 2127
Abstract
During meiosis, the budding yeast polo-like kinase Cdc5 is a crucial driver of the prophase I to meiosis I (G2/M) transition. The meiotic recombination checkpoint restrains cell cycle progression in response to defective recombination to ensure proper distribution of intact chromosomes to the [...] Read more.
During meiosis, the budding yeast polo-like kinase Cdc5 is a crucial driver of the prophase I to meiosis I (G2/M) transition. The meiotic recombination checkpoint restrains cell cycle progression in response to defective recombination to ensure proper distribution of intact chromosomes to the gametes. This checkpoint detects unrepaired DSBs and initiates a signaling cascade that ultimately inhibits Ndt80, a transcription factor required for CDC5 gene expression. Previous work revealed that overexpression of CDC5 partially alleviates the checkpoint-imposed meiotic delay in the synaptonemal complex-defective zip1Δ mutant. Here, we show that overproduction of a Cdc5 version (Cdc5-ΔN70), lacking the N-terminal region required for targeted degradation of the protein by the APC/C complex, fails to relieve the zip1Δ-induced meiotic delay, despite being more stable and reaching increased protein levels. However, precise mutation of the consensus motifs for APC/C recognition (D-boxes and KEN) has no effect on Cdc5 stability or function during meiosis. Compared to the zip1Δ single mutant, the zip1Δ cdc5-ΔN70 double mutant exhibits an exacerbated meiotic block and reduced levels of Ndt80 consistent with persistent checkpoint activity. Finally, using a CDC5-inducible system, we demonstrate that the N-terminal region of Cdc5 is essential for its checkpoint erasing function. Thus, our results unveil an additional layer of regulation of polo-like kinase function in meiotic cell cycle control. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Spain)
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23 pages, 12679 KiB  
Article
Epigenetic Dysregulation of Mammalian Male Meiosis Caused by Interference of Recombination and Synapsis
by Roberto de la Fuente, Florencia Pratto, Abrahan Hernández-Hernández, Marcia Manterola, Pablo López-Jiménez, Rocío Gómez, Alberto Viera, María Teresa Parra, Anna Kouznetsova, R. Daniel Camerini-Otero and Jesús Page
Cells 2021, 10(9), 2311; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10092311 - 03 Sep 2021
Cited by 6 | Viewed by 3028
Abstract
Meiosis involves a series of specific chromosome events, namely homologous synapsis, recombination, and segregation. Disruption of either recombination or synapsis in mammals results in the interruption of meiosis progression during the first meiotic prophase. This is usually accompanied by a defective transcriptional inactivation [...] Read more.
Meiosis involves a series of specific chromosome events, namely homologous synapsis, recombination, and segregation. Disruption of either recombination or synapsis in mammals results in the interruption of meiosis progression during the first meiotic prophase. This is usually accompanied by a defective transcriptional inactivation of the X and Y chromosomes, which triggers a meiosis breakdown in many mutant models. However, epigenetic changes and transcriptional regulation are also expected to affect autosomes. In this work, we studied the dynamics of epigenetic markers related to chromatin silencing, transcriptional regulation, and meiotic sex chromosome inactivation throughout meiosis in knockout mice for genes encoding for recombination proteins SPO11, DMC1, HOP2 and MLH1, and the synaptonemal complex proteins SYCP1 and SYCP3. These models are defective in recombination and/or synapsis and promote apoptosis at different stages of progression. Our results indicate that impairment of recombination and synapsis alter the dynamics and localization pattern of epigenetic marks, as well as the transcriptional regulation of both autosomes and sex chromosomes throughout prophase-I progression. We also observed that the morphological progression of spermatocytes throughout meiosis and the dynamics of epigenetic marks are processes that can be desynchronized upon synapsis or recombination alteration. Moreover, we detected an overlap of early and late epigenetic signatures in most mutants, indicating that the normal epigenetic transitions are disrupted. This can alter the transcriptional shift that occurs in spermatocytes in mid prophase-I and suggest that the epigenetic regulation of sex chromosomes, but also of autosomes, is an important factor in the impairment of meiosis progression in mammals. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Spain)
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Review

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15 pages, 5127 KiB  
Review
Cytoskeletal Remodelling as an Achilles’ Heel for Therapy Resistance in Melanoma
by Adrian Barreno and Jose L. Orgaz
Cells 2022, 11(3), 518; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11030518 - 02 Feb 2022
Cited by 1 | Viewed by 2624
Abstract
Melanoma is an aggressive skin cancer with a poor prognosis when diagnosed late. MAPK-targeted therapies and immune checkpoint blockers benefit a subset of melanoma patients; however, acquired therapy resistance inevitably arises within a year. In addition, some patients display intrinsic (primary) resistance and [...] Read more.
Melanoma is an aggressive skin cancer with a poor prognosis when diagnosed late. MAPK-targeted therapies and immune checkpoint blockers benefit a subset of melanoma patients; however, acquired therapy resistance inevitably arises within a year. In addition, some patients display intrinsic (primary) resistance and never respond to therapy. There is mounting evidence that resistant cells adapt to therapy through the rewiring of cytoskeleton regulators, leading to a profound remodelling of the actomyosin cytoskeleton. Importantly, this renders therapy-resistant cells highly dependent on cytoskeletal signalling pathways for sustaining their survival under drug pressure, which becomes a vulnerability that can be exploited therapeutically. Here, we discuss the current knowledge on cytoskeletal pathways involved in mainly targeted therapy resistance and future avenues, as well as potential clinical interventions. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Spain)
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