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Epigenetic and Post-Transcriptional Regulation of Gene Expression
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Epigenetic and Post-Transcriptional Regulation of Gene Expression

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 4833

Editor

Dr. Lidia Borkiewicz

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, Medical University of Lublin, Aleje Racławickie 1, 20-059 Lublin, Poland
Interests: gene expression regulation; RNA editing; lncRNA; cell signalling; RNA-protein interactions; synthetic biology

Special Issue Information

Dear Colleagues,

Regulation of gene expression is a multilayered process that occurs at the chromatin, transcriptional, post-transcriptional, and post-translational levels. Many molecular mechanisms of epigenetic modulation—including DNA methylation, chromatin remodeling and histone modification, regulation by non-coding RNA, as well as post-transcriptional processes such as alternative splicing, RNA methylation and pseudouridylation, RNA editing, and regulation by microRNA—have been extensively investigated. With the wealth of information now available, it has become clear that these mechanisms can be harvested as tools to modulate gene expression for therapeutic purposes without altering the genome itself.

This Special Issue aims to highlight the latest advances in our understanding of the molecular basis of epigenetic and epitranscriptomic regulation across multiple RNA species, mRNA and ncRNA, including rRNA and tRNA. The focus is on innovative research uncovering the discovery and function of key regulatory players and their applications in cell and developmental biology, stem cell research, tissue engineering, physiology, neuroscience, immunology, oncology, and therapeutics. We invite the submission of original research articles, reviews, and short communications.

Dr. Lidia Borkiewicz
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • epigenome
  • DNA methylation
  • chromatin remodeling
  • histone modifications
  • non-coding RNA
  • epitranscriptome
  • alternative splicing
  • RNA methylation
  • RNA edition

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Published Papers (2 papers)

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Research

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19 pages, 5401 KB  
Article
Suppressed SF3B1 Expression Lowers METTL3 Transcription and m6A RNA Expression
by Namjeong Choi, Hina Ashraf and Haihong Shen
Int. J. Mol. Sci. 2026, 27(12), 5396; https://doi.org/10.3390/ijms27125396 - 15 Jun 2026
Viewed by 491
Abstract
Splicing factor 3b1 (SF3B1), a component of U2 small nuclear ribonucleoprotein (U2 snRNP), has been known for its essential roles in pre-mRNA splicing and alternative splicing. Here we show that knocking down (KD) of SF3B1 broadly induced a significant reduction in mRNA expression [...] Read more.
Splicing factor 3b1 (SF3B1), a component of U2 small nuclear ribonucleoprotein (U2 snRNP), has been known for its essential roles in pre-mRNA splicing and alternative splicing. Here we show that knocking down (KD) of SF3B1 broadly induced a significant reduction in mRNA expression in the genome. One of the genes whose expression is reduced by SF3B1 KD is methyl-transferase-like 3 (METTL3), a writer of N6-methyladenosine (m6A). We demonstrate that expression of both METTL3 mRNA and protein is affected by SF3B1 KD, which further decreases the m6A RNA expression level. m6A-seq indicates that SF3B1 KD affects m6A distribution within multiple genes in the genome. In addition, a high proportion of hypo-methylation events by SF3B1 KD (~70%) are overlapped in METTL3 KD cells, and a conserved m6A motif is observed in the hypo-methylated regions as in SF3B1 KD cells, suggesting the m6A decrease by SF3B1 is a direct effect of the reduced METTL3 expression. Furthermore, RT-qPCR using unlabeled RNA and 5-Bromouridine (BrU)-labeled nascent RNA and actinomycin D treatment demonstrates that transcription of METTL3 is significantly reduced but the mRNA decay rate is not altered, suggesting that METTL3 expression is altered at the transcription level. We further show that SF3B1 interacts with RNA polymerase (Pol) II in the RNA independent manner, further indicating the involvement of SF3B1 in transcription. Lastly, we demonstrate that the transcription inactive H3K27me3 on the METTL3 promoter was significantly increased whereas transcription active H3K4me3 was not changed by SF3B1 KD. Taken together, we conclude that reduced SF3B1 expression suppresses the transcription of METTL3 and inhibits m6A RNA expression. Full article
(This article belongs to the Special Issue Epigenetic and Post-Transcriptional Regulation of Gene Expression)
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Review

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22 pages, 2065 KB  
Review
Evolution of Engineered ADAR-Based RNA Editing Systems
by Lidia Borkiewicz
Int. J. Mol. Sci. 2026, 27(4), 1858; https://doi.org/10.3390/ijms27041858 - 14 Feb 2026
Cited by 1 | Viewed by 1950
Abstract
RNA editing is a way to diversify, regulate expression, and expand the cell transcriptome. The most common RNA editing is the reversible conversion of adenosine (A) to inosine (I) driven by double-stranded RNA-binding adenosine deaminases (ADARs). As inosine is recognized as guanosine (G) [...] Read more.
RNA editing is a way to diversify, regulate expression, and expand the cell transcriptome. The most common RNA editing is the reversible conversion of adenosine (A) to inosine (I) driven by double-stranded RNA-binding adenosine deaminases (ADARs). As inosine is recognized as guanosine (G) during translation, the RNA editing may result in non-synonymous codon changes. For this reason, ADARs have gained attention as promising enzymes to rewrite mRNA. Many efforts were undertaken to engineer a precise, effective, and controllable ADAR-based system to target certain Adenines on RNA to repair pathological mutations. This review summarizes the advances in ADAR-mediated RNA editing, evolving from systems using antisense oligonucleotides as guide RNA to recruit endogenous or overexpressed ADARs, through more complex setups additionally expressing other RNA-binding proteins, to rational designs harnessing ADARs to convert other nucleotides and amplify the low initial signal. Increasing the specificity and yield of RNA editing, expanding the number of targetable sites, and reducing off-target and bystander activity remain key challenges for these technologies. Improving delivery efficiency across a broad range of cell types, as well as optimizing delivery routes in in vivo studies are also critical to harness them as advantageous tools for both research and therapy. Full article
(This article belongs to the Special Issue Epigenetic and Post-Transcriptional Regulation of Gene Expression)
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