Epigenetic Programming of Cellular States

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: 31 July 2026 | Viewed by 2220

Special Issue Editor


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Department of Molecular & Cellular Biosciences, Rowan University, 201 Mullica Hill Rd., Glassboro, NJ 08028, USA
Interests: epigenetics; genomics; bioinformatics; antimicrobials
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Special Issue Information

Dear Colleagues,

Within complex multicellular organisms, cells undergo defined transcriptional regulation to differentiate and dedifferentiate into unique and essential cell types. Underlying these transcriptional changes are epigenetic changes including chromatin remodeling, histone modifications, and modulation of DNA methylation and small non-coding RNAs. Recent advances in this field have significantly expanded its potential for artificial reprogramming in regenerative medicine, disease modeling, and drug discovery.

This Special Issue aims to capture studies profiling the associations of epigenetic changes with cellular programming in both in vivo and ex vivo model systems.  Moreover, studies in non-model organisms or development of experimental systems capable of inducing or preventing cellular reprogramming are also welcome. Both research and review articles are welcome.

We look forward to your contributions.

Dr. Benjamin Carone
Guest Editor

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Keywords

  • iPSCs
  • stem cells
  • reprogramming
  • chromatin
  • epigenetics

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Published Papers (2 papers)

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Review

26 pages, 1936 KB  
Review
Germline and Embryonic Mechanisms in the Epigenetic Inheritance of Neurodevelopmental and Cognitive Traits in Mammals
by Mehmet Kizilaslan, Zeynep Kizilaslan and Hasan Khatib
Biomolecules 2026, 16(5), 669; https://doi.org/10.3390/biom16050669 - 1 May 2026
Viewed by 690
Abstract
Epigenetic mechanisms profoundly regulate gene expression, developmental trajectories, and phenotypic variation, extending biological influence beyond DNA sequence alone. A growing body of evidence suggests that environmental exposures, including pollutants, drugs, stress, and diet, can induce germline and early embryonic epimutations that alter developmental [...] Read more.
Epigenetic mechanisms profoundly regulate gene expression, developmental trajectories, and phenotypic variation, extending biological influence beyond DNA sequence alone. A growing body of evidence suggests that environmental exposures, including pollutants, drugs, stress, and diet, can induce germline and early embryonic epimutations that alter developmental programs with lasting consequences for neurodevelopmental and cognitive outcomes. However, the fields most relevant to these processes have largely developed independently. These include germline epigenetics, early embryonic patterning, neurodevelopment and cognitive regulation, and intergenerational or transgenerational inheritance. Each field has its own conceptual frameworks and mechanistic models. This fragmentation obscures the biological reality that these systems are tightly interconnected: environmentally induced epigenetic perturbations in gametes can reshape the epigenetic landscape of the early embryo, influence lineage allocation during gastrulation, and ultimately modify the molecular architecture of the developing central nervous system. A systems–biology perspective capable of linking germline epimutations and early embryonic epigenetic instability to later neurodevelopmental and cognitive phenotypes and their potential inheritance is therefore required. This review synthesizes current evidence across these traditionally isolated domains and proposes a coherent mechanistic framework linking germ cell epimutations and early embryonic epigenetic instability to the emergence of neurodevelopmental and cognitive phenotypes. By bridging these conceptual gaps, we aim to establish a cohesive foundation for understanding how early epigenetic disruptions generate long-lasting and in some cases heritable effects on brain development and cognitive function. Full article
(This article belongs to the Special Issue Epigenetic Programming of Cellular States)
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21 pages, 1686 KB  
Review
Establishment and Maintenance of Repressed Chromatin States on Dosage-Compensated Sex Chromosomes
by Joshua Eduful, Lily LeSarge and Györgyi Csankovszki
Biomolecules 2026, 16(3), 386; https://doi.org/10.3390/biom16030386 - 4 Mar 2026
Viewed by 1030
Abstract
Sex chromosome imbalance is a genetic challenge in species with unequal X-chromosome numbers. Organisms have developed distinct strategies to control this imbalance through a process called dosage compensation. These strategies include X-chromosome inactivation in mammals mediated by the XIST long noncoding RNA and [...] Read more.
Sex chromosome imbalance is a genetic challenge in species with unequal X-chromosome numbers. Organisms have developed distinct strategies to control this imbalance through a process called dosage compensation. These strategies include X-chromosome inactivation in mammals mediated by the XIST long noncoding RNA and proteins recruited by XIST, and X-linked hypertranscription in male Drosophila driven by the Male-Specific Lethal (MSL) complex. In Caenorhabditis elegans, gene expression is downregulated from each of the two X chromosomes of hermaphrodites by half, thereby matching the levels in XO males. This is mediated by a specialized condensin-containing protein complex, the Dosage Compensation Complex (DCC). In all cases, the chromatin states on the sex chromosomes must be first established and then maintained for the entire lifetime of the organism. Although mammals and nematodes both use repression to achieve dosage compensation, the mechanisms are very different. Here, we summarize recent advances on how repressive chromatin states are established and maintained, with a focus on contrasting C. elegans dosage compensation to XIST-mediated X-chromosome inactivation. We review how specialized chromosome topology, repressive chromatin modifications, and higher-order nuclear architecture are established and maintained to achieve sex-specific regulation of the X chromosomes and highlight key outstanding questions and future research directions. Full article
(This article belongs to the Special Issue Epigenetic Programming of Cellular States)
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