Environmental Genomics and Low-Dose Induced Adaptive Response: Underlying Mechanisms from Cells to Organisms

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Genes & Environments".

Deadline for manuscript submissions: 20 July 2026 | Viewed by 735

Special Issue Editors


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Guest Editor
Institute of Biodiversity and Ecosystem Research, Bulgarian Academy of Sciences, Sofia, Bulgaria
Interests: low-dose adaptive response (AR); the contribution of DNA repair; antioxidant and chaperone systems for the formation of an AR; genotypes and induced resistance; screening of genotoxics; mutagenic effects of environmental pollutants; lower eukaryotes; higher plants; anti-mutagenesis

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Guest Editor
Institute of Biodiversity and Ecosystem Research, Bulgarian Academy of Sciences, Sofia, Bulgaria
Interests: small mammals; eco-toxicology; eco-physiology; adaptive responses at different levels of biological organization to various environmental pollutants

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Guest Editor
Institute of Biodiversity and Ecosystem Research, Bulgarian Academy of Sciences, 1113 Sofia, Bulgaria
Interests: mutagenesis/antimutagenesis; anticarcinogenesis; oxidative stress; natural products; low-dose adaptive response; mechanisms of DSBs induction and repair; Ty1 retrotransposition; genome stability
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Special Issue Information

Dear Colleagues,

We are pleased to announce the launch of the Special Issue "Environmental Genomics and Low-Dose Induced Adaptive Response: Underlying Mechanisms from Cells to Organisms". This Special Issue calls for original research and reviews that explore the genomic and molecular foundations of adaptive responses triggered by low-dose exposure to environmental stressors, including radiation and genotoxic chemicals. The central focus is on the phenomenon of induced resistance (the adaptive response), a critical radio-protective mechanism formally recognized by the International Atomic Energy Agency and the World Health Organization for its implications in human and environmental health. We welcome contributions that use cutting-edge environmental genomics, mutagenesis screening, epigenomics, and molecular techniques to decipher the signaling pathways that enable this protection—from activation of DNA repair, as well as antioxidant and chaperone defenses, to systemic organismal resilience. At higher levels of biological organization, the submission of eco-toxicological research is encouraged, particularly research focused on how low-dose environmental stressors shape whole organisms’ physiology, fitness, and adaptive resilience in natural or experimental populations. This collection aims to synthesize knowledge about the dual aspects of environmental mutagenesis and the low-dose induced adaptive response, ultimately improving our understanding of the mechanisms of biological defense and informing environmental risk assessment and public health strategies.

Prof. Dr. Stephka Chankova
Prof. Dr. Michaela Beltcheva
Dr. Teodora Todorova
Guest Editors

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Keywords

  • environmental genomics
  • ecotoxicology
  • low-dose induced adaptive response
  • low-dose radiation
  • genomic instability
  • environmental mutagenesis
  • DNA repair
  • radio-protection
  • stress response
  • toxicogenomics
  • antioxidant system
  • chaperone system

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Published Papers (1 paper)

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Research

20 pages, 2441 KB  
Article
Identification of Radiation-Induced Injury Pathways and Hub Genes from RNA-Seq Data Based on Integrative Bioinformatics Approach
by Khalish Arsy Al Khairy Siregar, Chi-Ho Lee, Jong-Jin Kim, Dong-Jo Chang and Seung-Hyun Jeong
Genes 2026, 17(4), 377; https://doi.org/10.3390/genes17040377 - 27 Mar 2026
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Abstract
Background: Ionizing radiation (IR) induces profound bone marrow (BM) injury by disrupting hematopoietic stem cell (HSC) homeostasis, leading to acute myelosuppression and long-term hematopoietic dysfunction. Although transcriptome-wide analyses have advanced our understanding of radiation responses, the key molecular networks and hub genes governing [...] Read more.
Background: Ionizing radiation (IR) induces profound bone marrow (BM) injury by disrupting hematopoietic stem cell (HSC) homeostasis, leading to acute myelosuppression and long-term hematopoietic dysfunction. Although transcriptome-wide analyses have advanced our understanding of radiation responses, the key molecular networks and hub genes governing post-irradiation BM injury remain incompletely defined. Methods: This study aimed to systematically identify radiation-responsive pathways and central genes in BM after irradiation through an integrative bioinformatics approach based on RNA sequencing (RNA-seq). Public RNA-seq data from mouse BM HSCs collected 3 days after whole-body irradiation were analyzed. Differentially expressed genes (DEGs) were identified using two independent statistical frameworks to improve the robustness of the results. Functional analysis was performed through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA). Protein–protein interaction (PPI) networks were constructed using STRING, and hub genes were identified using network topology parameters. Results: Both analysis pathways consistently demonstrated extensive transcriptome reprogramming after irradiation. DEGs were primarily enriched in processes related to cytokine signaling, hematopoietic lineage regulation, immune response, and extracellular matrix remodeling. KEGG analysis highlighted cytokine–cytokine receptor interaction, hematopoietic cell lineage, JAK-STAT signaling, and PI3K-Akt signaling as key molecular axes. GSEA further supported coordinated changes in pathways related to inflammatory response, stress response, and metabolic reprogramming. PPI network analysis identified four consensus hub genes, namely Il6, Cd34, Gypa, and Pdgfrb, which are related to inflammatory signaling, hematopoietic regulation, erythroid dynamics, and microenvironmental remodeling, respectively. Conclusion: This integrative bioinformatics study demonstrates that radiation-induced BM injury is associated with coordinated activation of inflammatory cytokine networks, alterations in the hematopoietic program, and microenvironmental restructuring. The hub genes identified in this study may represent candidate regulatory genes or molecular indicators potentially involved in the response to radiation-induced hematopoietic damage. Full article
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