Chromatin Modifications and RNA-Based Regulation of Gene Expression

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

Deadline for manuscript submissions: 15 October 2026 | Viewed by 545

Special Issue Editor


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Guest Editor
Department of Biotechnology and Chemical Engineering, University of Cambridge, Cambridge, UK
Interests: chromatin biology; intrinsically disordered proteins; genome functionalization

Special Issue Information

Dear Colleagues,

RNA molecules are increasingly recognized as active regulators of transcription, adding new dimensions to classical transcription factor and chromatin-based control. During initiation, nascent RNAs can act as a “trapping mesh”, retaining transcription factors in the vicinity of their DNA binding sites, increasing their binding turnover through a local high concentration effect. Architectural proteins such as CTCF rely on RNA binding to maintain certain chromatin loops, while other transcription factors engage RNA directly through canonical or non-canonical RNA-binding domains. Concurrently, RNA modifications occur co-transcriptionally in chromatin contexts. The m6A writer complex, guided by histone marks such as H3K36me3, deposits methylation on newly synthesized transcripts. These marks, read by nuclear proteins, feed back on chromatin by recruiting histone modifiers, thereby linking RNA methylation with chromatin state and transcriptional output. During elongation, RNA itself modulates the phosphorylation dynamics of RNA polymerase II, influencing the activity of cofactors such as P-TEFb. Transcription-coupled deposition of histone modifications further integrates RNA splicing, as chromatin marks recruit components of the spliceosome, ensuring coordination between RNA processing and elongation. Finally, termination also engages RNA-based mechanisms. RNA helicases help couple RNA modifications with genome stability, while interactions with RNA-binding proteins shape the final stages of transcript maturation. Together, these discoveries establish RNA as an integral partner of chromatin modifications, creating feedback loops that fine-tune gene expression across all stages of transcription.

Dr. Alonso Javier Pardal
Guest Editor

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Keywords

  • chromatin modifications
  • RNA
  • gene expression
  • transcription
  • chromatin boundaries
  • RNA-binding proteins

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Published Papers (1 paper)

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Research

11 pages, 758 KB  
Article
Monocyte Titin Gene Expression as a Biomarker of Left Ventricular Dysfunction in Acute Myocarditis
by Spyridon Maragkoudakis, Aleksi Sallo, Ioanna Kontaraki, Emmanouil Marakas Sideras, Gabriela Lilikaki, Onoufrios Malikidis, Konstantinos Fragkiadakis, Eleutherios Kallergis, Nick Kopidakis, Ioannis Kopidakis, Evangelos Zacharis, Vasiliki Katsi, Emmanouil Kampanieris, George Kochiadakis, Emmanouil Simantirakis and Maria Marketou
Genes 2026, 17(3), 268; https://doi.org/10.3390/genes17030268 - 26 Feb 2026
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Abstract
Background: Titin (TTN), a giant structural and signaling protein of striated muscle, participates in intracellular signaling networks and cytoskeletal organization, potentially influencing cell activation, trafficking, and interactions with other tissues, including the heart. Methods: In this pilot study, 29 patients with acute myocarditis [...] Read more.
Background: Titin (TTN), a giant structural and signaling protein of striated muscle, participates in intracellular signaling networks and cytoskeletal organization, potentially influencing cell activation, trafficking, and interactions with other tissues, including the heart. Methods: In this pilot study, 29 patients with acute myocarditis and 10 healthy individuals were prospectively enrolled. Peripheral blood was obtained on the first day of hospital admission, total RNA was isolated from peripheral blood mononuclear cells (PBMCs), and TTN mRNA expression was quantified. Results: TTN expression in PBMCs was significantly higher in patients with acute myocarditis compared with healthy controls (p = 0.015), corresponding to a 2.8-fold median increase. Moreover, TTN expression showed a strong positive correlation with global longitudinal strain impairment (Spearman’s r = 0.576, p < 0.001), a moderate positive correlation with peak hs-cTnI levels (r = 0.435, p = 0.021; and a moderate inverse correlation with baseline LVEF (r = −0.421, p = 0.025). Conclusions: These findings support a pathophysiological link between TTN-related pathways in peripheral immune cells and myocardial injury in acute myocarditis and raise the hypothesis that TTN expression in PBMCs may serve as a novel biomarker of disease severity and long-term ventricular remodeling. Further studies in larger cohorts are warranted to validate these results and to elucidate the mechanistic role of titin in immune–cardiac cross-talk. Full article
(This article belongs to the Special Issue Chromatin Modifications and RNA-Based Regulation of Gene Expression)
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