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Developmental Biology: Computational and Experimental Approaches, 3rd Edition

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: 31 August 2026 | Viewed by 1482

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Novosibirsk State University; Institute of Cytology and Genetics, Novosibirsk, Russia
Interests: DNA sequence analysis; mutation; single-nucleotide polymorphism (SNP); quantitative sequence-activity relationships; DNA-protein affinity; TATA-binding protein binding site (TATA box); genome-wide prediction in silico; experimental verification; in vitro; in vivo; hereditary disease
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Special Issue Information

Dear Colleague,

Developmental biology investigates ontogenesis,  the step-by-step process through which single cells (e.g., animal zygotes) turn into multicellular organisms of proper shape, size and structure, providing all functions during whole life cycle. Molecular mechanisms of both signal transduction and gene regulation networks provide an elementary basis for ontogenesis within the biological organization hierarchy, where they interfere with each other in varied ways, ranging from cellular processes (e.g., differentiation and migration) through morphogenesis to whole life cycle. As for embryogenesis, among the top achievements of both experimental and computational approaches, which mutually enrich one another to reconstruct the Drosophila segment polarity gene network, it is a well-established molecular mechanism of the fruit fly initializing segmentation over 3 hours just after fertilization until creating an embryo of 14 para-segmental units. Regarding morphogenesis, one of the breakthroughs achieved through combined experimental–computational techniques focused on the gene networks of the synthesis, diffusion, and active transport of auxin in Arabidopsis, from the high-resolution 3D mapping of cell cycle stages from the root meristem to layers of completely differentiated cells. Regarding life cycle, among the greatest successes achieved through computational models using the experimental signaling network for all 959 cells, including all 302 nerve cells, of Caenorhabditis elegans is the development of a real-time in silico simulator of how nematodes find food and avoid obstacles. Regarding evolutionary limitations within developmental biology, the recent cross-kingdom comparison between animals, plants and fungi integrated the developmental hourglass concept into a modern paradigm of transcriptome ontogenetic switches. During normal development, everything develops normally, whereas developmental abnormalities, such as premature aging, neurodegeneration, tumorigenesis, induced pluripotent cells, wound healing, post-traumatic repair, regeneration, assisted reproductive technologies, and stress-induced epigenetic reprogramming, which pose challenges for the post-genome experimental–computational biology, must be overcome through predictive preventive personalized participatory (4P) medicine. 

Dr. Mikhail P. Ponomarenko
Guest Editor

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Keywords

  • animal
  • plant
  • fungus
  • biological organization hierarchy
  • evolutionary limitations
  • fertilization
  • zygote
  • cell cycle
  • stem cell
  • meristem
  • cell layer
  • tissue
  • embryo
  • multicellular organism
  • ontogenesis
  • morphogenesis
  • life cycle
  • molecular mechanism
  • signal transduction
  • gene regulation
  • gene networks
  • cellular process
  • differentiation
  • migration
  • segmentation
  • high-resolution 3D-map
  • real-time in silico simulator
  • developmental hourglass
  • transcriptome ontogenetic switch
  • developmental abnormality
  • premature aging
  • neurodegeneration
  • tumorigenesis
  • atherogenesis
  • autoimmunity
  • induced pluripotent cell
  • wound healing
  • regeneration
  • assisted reproductive technologies
  • epigenetic reprogramming
  • predictive preventive personalized participatory (4P) medicine

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Published Papers (2 papers)

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Research

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17 pages, 3209 KB  
Article
Morphological Features and HIF1-Dependent Processes in the Brain of Progeny of Female Rats Exposed to Maternal Hypoxia
by Sofiya Potapova, Elizaveta Zugan, Yan Isakov, Ekaterina Tyulkova and Oleg Vetrovoy
Int. J. Mol. Sci. 2026, 27(8), 3421; https://doi.org/10.3390/ijms27083421 - 10 Apr 2026
Viewed by 405
Abstract
Fetal hypoxia and maternal stress during pregnancy are major risk factors for neurological disorders. The effects of maternal hypoxia may be transmitted to the next generation through persistent alterations in maternal endocrine and metabolic regulation. In this study, using immunohistochemistry, quantitative RT-PCR, and [...] Read more.
Fetal hypoxia and maternal stress during pregnancy are major risk factors for neurological disorders. The effects of maternal hypoxia may be transmitted to the next generation through persistent alterations in maternal endocrine and metabolic regulation. In this study, using immunohistochemistry, quantitative RT-PCR, and Western blotting, we assessed morphological features and HIF1-dependent processes in the fetal and adult brains of progeny of female rats exposed to maternal hypoxia (PMH). We identified a delay in progenitor cell differentiation into neurons at embryonic day 14, a decreased number of neurons in the hippocampus, an increased number of astrocytes in the prefrontal cortex, and a decreased number of astrocytes in the raphe nuclei of the PMH rats. However, no significant changes were observed in HIF1α protein levels or in the protein levels of HIF1-dependent gene products in the examined brain structures. Thus, the transgenerational effect of maternal hypoxia is manifested as structural disturbances of brain development but is not accompanied by changes in HIF1-dependent metabolism. Full article
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Review

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42 pages, 4401 KB  
Review
Glucocorticoid Receptor Signaling: Multilevel Organization, Roles in Fetal Development, and Postnatal Outcomes
by Sofiya Potapova, Yan Isakov, Ekaterina Tyulkova and Oleg Vetrovoy
Int. J. Mol. Sci. 2026, 27(6), 2873; https://doi.org/10.3390/ijms27062873 - 22 Mar 2026
Viewed by 683
Abstract
The hypothalamic–pituitary–adrenal (HPA) axis coordinates metabolic, immune, and behavioral responses to a changing environment. Its molecular effectors are the nuclear receptors for glucocorticoids and mineralocorticoids (the GRs/MRs), encoded by nr3c1/nr3c2. The MR serves as the high-affinity sensor of basal hormone [...] Read more.
The hypothalamic–pituitary–adrenal (HPA) axis coordinates metabolic, immune, and behavioral responses to a changing environment. Its molecular effectors are the nuclear receptors for glucocorticoids and mineralocorticoids (the GRs/MRs), encoded by nr3c1/nr3c2. The MR serves as the high-affinity sensor of basal hormone concentrations, whereas the GR amplifies the stress response and mediates negative feedback. Despite their shared domain architecture, the receptors have diverged functionally: isoform composition, post-translational modifications, and the complement of co-regulators together determine which genes are activated or repressed in a given tissue at a given time. The regulation of the HPA axis activity is a major determinant of embryonic development. Pregnancy adds a placental control layer that meters maternal signals: 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in the syncytiotrophoblast inactivates cortisol, whereas 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) can regenerate it, and systemic buffering by transcortin (cortisol-binding globulin, CBG) limits the free hormone fraction. Under stress, inflammation, or hypoxia, this barrier weakens, exposing the fetus to stronger glucocorticoid pulses during windows of heightened vulnerability for brain and immune development. Such overexposure not only reshapes ongoing transcription but is also epigenetically inscribed: the methylation of alternative nr3c1 promoters, the remodeling of histones, and the shifts in ncRNA profiles recalibrate the axis sensitivity for the long term. At the phenotypic level, this manifests as variability in stress reactivity, cognitive and affective trajectories, and an immune and metabolic risk across later ontogeny. In this review, we integrate evidence on the structure and functions of the GR, the mechanisms of its post-translational and epigenetic regulation, and the role of the placenta, to provide a coherent framework for understanding the multifaceted consequences of prenatal stress and to identify potential targets for early prevention. Full article
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