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15th Anniversary of Genes: Feature Papers in the “Molecular...
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15th Anniversary of Genes: Feature Papers in the “Molecular Genetics and Genomics” Section

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: 15 July 2025 | Viewed by 1214

Special Issue Editors

Dr. Paolo Cinelli

E-Mail Website
Guest Editor
Center for Clinical Research, Clinic for Trauma Surgery, University Hospital Zurich, Sternwartstrasse 14, CH-8091 Zurich, Switzerland
Interests: transcriptomics; microarrays; gene expression analysis; genotyping; molecular genetics; mouse genetics; transgenic technologies; embryonic stem cells; pluripotency
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Albert Jeltsch

E-Mail Website
Guest Editor
Institute of Biochemistry and Technical Biochemistry, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
Interests: DNA methyltransferases; DNA methylation; protein methyltransferases; protein methylation; reading domains; molecular epigenetics; synthetic biology; molecular enzymology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, “15th Anniversary of Genes: Feature Papers in the “Molecular Genetics and Genomics” Section”, will gather high-quality research articles, reviews, and communications on advances in research in molecular genetics and genomics. This Special Issue will celebrate the 15th anniversary of Genes and the 10th anniversary of the journal receiving its first impact factor. As our aim for this Special Issue is to illustrate, through selected works, frontier research in the field of molecular genetics and genomics, we encourage Editorial Board Members for the “Molecular Genetics and Genomics” Section to contribute feature papers reflecting the latest progress in their research field or to invite relevant senior experts and colleagues to contribute to this Special Issue. We aim to showcase our Section as an attractive open access publishing platform for molecular genetics research.

Possible topics include, but are not limited to, the following:

  • Chromatin remodeling and dynamics;
  • Epigenetics, DNA methylation, histone modification, and histone codes;
  • DNA replication, repair, and recombination, mobile DNA, and mitochondrial DNA;
  • RNA biology;
  • Cell signaling, signal transduction, cell cycle, cell death, and stem cells;
  • The post-transcriptional regulation of gene expression;
  • Developmental genetics;
  • The molecular basis of diseases.

Dr. Paolo Cinelli
Prof. Dr. Albert Jeltsch
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. Genes is an international peer-reviewed open access monthly 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 2600 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

  • chromatin remodeling and dynamics
  • epigenetics, DNA methylation, histone modification, and histone codes
  • DNA replication, repair, and recombination, mobile DNA, and mitochondrial DNA
  • RNA biology

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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13 pages, 508 KiB  
Article
The rs1403543 Polymorphism of AGTR2, Which Encodes the Type-2 Angiotensin II Receptor, and Left Ventricular Mass in Polish Full-Term Newborns
by Iwona Gorący, Karol Miler, Klaudyna Lewandowska, Monika Rychel, Beata Łoniewska and Andrzej Ciechanowicz
Genes 2025, 16(5), 518; https://doi.org/10.3390/genes16050518 - 29 Apr 2025
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Abstract
Background/Objectives: Left ventricular hypertrophy is a significant independent risk factor for increased cardiovascular morbidity and mortality. There are some reports indicating an association of rs1403543 (1675G>A) polymorphism in the AGTR2 gene, which encodes the type-2 angiotensin II receptor, with left ventricular hypertrophy or [...] Read more.
Background/Objectives: Left ventricular hypertrophy is a significant independent risk factor for increased cardiovascular morbidity and mortality. There are some reports indicating an association of rs1403543 (1675G>A) polymorphism in the AGTR2 gene, which encodes the type-2 angiotensin II receptor, with left ventricular hypertrophy or increased left ventricular mass (LVM) in adults. The aim of this study was to analyze the possible association of the AGTR2:rs1403543 polymorphism with LVM in full-term Polish healthy newborns. Methods: The study group comprised 207 consecutive, full-term, healthy newborns. LVM was assessed, on the 3rd day after birth, from the M-mode echocardiographic measurements of left ventricular dimensions using the Penn convention, with the Huwez et al.-modified equation mode. The AGTR2 polymorphism was identified by PCR-RFLP in genomic DNA extracted from cord blood leukocytes. Results: There were no significant differences in clinical and echocardiographic characteristics of male newborns in regard to the AGTR2:rs1403543 polymorphism. However, the LVM/body mass ratio in female newborns carrying at least one A allele (i.e., with genotype GA or AA) was significantly lower as compared to its value in reference (GG) homozygotes. In addition, in female newborns, the frequency of AGTR2 genotypes with at least one A allele was significantly higher in the lower tertile of LVM/body mass or LVM/body surface area (calculated using the Mosteller formula) ratios as compared with upper tertiles. Conclusions: Our results suggest that the AGTR2:rs1403543 polymorphism may be associated with the physiological variability of cardiac mass in female newborns. Full article
(This article belongs to the Special Issue 15th Anniversary of Genes: Feature Papers in the “Molecular Genetics and Genomics” Section)
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11 pages, 1516 KiB  
Article
Development of a BiAD Sensor for Locus-Specific Detection of Cellular Histone Acetylation Dynamics by Fluorescence Microscopy
by Anja R. Köhler, Nicole Gutekunst, Annika Harsch, Pavel Bashtrykov and Albert Jeltsch
Genes 2025, 16(4), 444; https://doi.org/10.3390/genes16040444 - 10 Apr 2025
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Abstract
Background: Dynamic changes in histone acetylation play crucial roles during cellular differentiation and disease development, but their detection in living cells is still a challenging task. Objectives: Here, we developed a Bimolecular Anchor Detector (BiAD) sensor for the detection of locus-specific changes in [...] Read more.
Background: Dynamic changes in histone acetylation play crucial roles during cellular differentiation and disease development, but their detection in living cells is still a challenging task. Objectives: Here, we developed a Bimolecular Anchor Detector (BiAD) sensor for the detection of locus-specific changes in histone acetylation in living cells by fluorescence microscopy. Methods: We used the BRD9 bromodomain cloned as tandem double domain (2xBRD9-BD) as a reader of histone acetylation. It was integrated into a dual-color BiAD chassis that was previously described by us. Results: We identified the gene body of TTC34 as a potential target for our sensor, because it contains dense histone acetylation and 392 local sequence repeats. Using a binding-deficient mutant of 2xBRD9-BD as a negative control, we established a successful readout of histone acetylation at the TTC34 locus. A single-domain reader did not function, indicating the requirement for the double reader to enhance the affinity and specificity of the chromatin interaction via avidity effects. With this sensor, we could detect dynamic increases in histone acetylation at the TTC34 locus after the treatment of cells with the histone deacetylase inhibitor Trichostatin A for 6 h indicating the applicability of the sensor for single-cell epigenome studies. Conclusions: Our data demonstrate that active chromatin modifications can be detected by BiAD sensors using 2xBRD9-BD as a reader. This complements the toolkit of the available BiAD sensors and documents the modularity of BiAD sensors. Full article
(This article belongs to the Special Issue 15th Anniversary of Genes: Feature Papers in the “Molecular Genetics and Genomics” Section)
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Review

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17 pages, 1225 KiB  
Review
The Role of Non-Coding RNAs in ALS
by Alessandra Falduti, Adele Giovinazzo, Elisa Lo Feudo, Valentina Rocca, Filippo Brighina, Angela Messina, Francesca Luisa Conforti and Rodolfo Iuliano
Genes 2025, 16(6), 623; https://doi.org/10.3390/genes16060623 - 23 May 2025
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Abstract
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects motor neurons, leading to muscle weakness, paralysis, and eventually death. The pathogenesis of ALS is influenced by genetic factors, environmental factors, and age-related dysfunctions. These factors, taken together, are responsible for sporadic [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects motor neurons, leading to muscle weakness, paralysis, and eventually death. The pathogenesis of ALS is influenced by genetic factors, environmental factors, and age-related dysfunctions. These factors, taken together, are responsible for sporadic cases of ALS, which account for approximately 85–90% of ALS cases, while familial ALS accounts for the remaining 10–15% of cases, usually with dominant traits. Despite advances in understanding and studying the disease, the cause of the onset of ALS remains unknown. Emerging evidence suggests that non-coding RNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), play crucial roles in the pathogenesis of the disease. An abnormal expression of these molecules is implicated in various ALS-related processes, including motor neuron survival, protein aggregation, and inflammation. Here, we describe the dysregulation of non-coding RNAs in the pathogenic mechanism of ALS, highlighting the potential roles of miRNAs, lncRNAs, and circRNAs as biomarkers or therapeutic targets to examine the progression of the disease. Full article
(This article belongs to the Special Issue 15th Anniversary of Genes: Feature Papers in the “Molecular Genetics and Genomics” Section)
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