Genetic and Epigenetic Mechanisms in Gametogenesis and Early Development: Insights from Models, Stem Cells, and Human Disorders

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Department of Biomedical Sciences, Rocky Vista University, Englewood, CO 80112, USA
Interests: psychoneuroimmunology; biomarkers of stress and resilience; trauma surgeon fatigue and performance; cytokine and neuropeptide signatures; stress-induced neuroinflammation
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Special Issue Information

Dear Colleagues,

The successful transmission of genetic information across generations depends on the precise coordination of gametogenesis and the earliest stages of embryonic development. Over the past decade, rapid advances in genetics, epigenomics, single-cell technologies, and imaging have reshaped our understanding of how germ cells are specified, how epigenetic programs are established and reprogrammed, and how these processes collectively influence fertilization, early lineage decisions, and developmental competence.

Gametogenesis is governed by the complex interplay among transcriptional networks, chromatin remodeling, and tightly regulated epigenetic marks. These mechanisms ensure not only the proper formation and maturation of sperm and oocytes but also the establishment of totipotency and developmental potential in the zygote. Meanwhile, early embryo development represents a critical window during which epigenetic asymmetry is resolved, parental genomes undergo extensive reprogramming, and the foundation for embryonic and extraembryonic lineages is laid. Disruptions to these processes can lead to infertility, early pregnancy loss, congenital disorders, or long-term health consequences.

This Special Issue will bring together original research articles, reviews, and perspectives to enhance our understanding of the genetic and epigenetic mechanisms driving gametogenesis and early embryogenesis. Contributions may include, but are not limited to, the following topics:

  • Molecular and cellular regulation of germ cell specification and maturation;
  • Epigenetic reprogramming during fertilization and early cleavage stages;
  • Chromatin architecture, non-coding RNAs, and regulatory networks in early development;
  • Genetic and epigenetic determinants of oocyte and sperm quality;
  • Molecular causes of infertility or early developmental failure;
  • Comparative or evolutionary perspectives on germline and early embryo biology.

We look forward to receiving contributions that will advance this field and help elucidate the fundamental mechanisms underlying successful reproduction and early development.

Prof. Dr. Lon J. van Winkle
Prof. Dr. Philip Iannaccone
Dr. Rebecca Jean Ryznar
Guest Editors

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Keywords

  • gametogenesis
  • germline development
  • early embryogenesis
  • epigenetic regulation
  • chromatin organization
  • cell fate
  • developmental gene regulation
  • embryonic lineage formation
  • evolutionary developmental biology

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Published Papers (1 paper)

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Research

17 pages, 21451 KB  
Article
Compensatory Serotonin Synthesis and Histone H3 Serotonylation in Preimplantation Embryos Exposed to Maternal Fluoxetine or Monoamine Oxidase Blockade
by Veronika S. Frolova and Denis A. Nikishin
J. Dev. Biol. 2026, 14(2), 15; https://doi.org/10.3390/jdb14020015 - 3 Apr 2026
Viewed by 390
Abstract
Serotonin is a critical morphogen in early development, yet the mechanisms regulating its homeostasis in the preimplantation embryo remain unclear, particularly under conditions of maternal antidepressant exposure. Here, we investigated embryonic serotonergic autonomy using mouse models of pharmacological transport blockade (maternal fluoxetine treatment) [...] Read more.
Serotonin is a critical morphogen in early development, yet the mechanisms regulating its homeostasis in the preimplantation embryo remain unclear, particularly under conditions of maternal antidepressant exposure. Here, we investigated embryonic serotonergic autonomy using mouse models of pharmacological transport blockade (maternal fluoxetine treatment) and in vitro treatment with the monoamine oxidase inhibitor pargyline. We employed immunofluorescence, RT-qPCR, and live-cell imaging to assess metabolic flux, gene expression, and physiological health. We demonstrate that monoamine oxidase functions as a metabolic firewall, progressively maturing from zygote to blastocyst to degrade excess amines. Paradoxically, maternal serotonin transporter blockade triggered significant intracellular serotonin hyper-accumulation in blastocysts, associated with a trend toward a compensatory upregulation of the biosynthetic gene Ddc. While this serotonin overload did not compromise morphology, mitochondrial function, or pluripotency marker expression, it induced a robust epigenetic response. Excess serotonin promoted elevated H3Q5ser immunoreactivity in both nuclear and cytoplasmic compartments via a transglutaminase-dependent mechanism. These findings reveal that the preimplantation embryo possesses a resilient, autonomous serotonergic system capable of compensatory synthesis. However, environmental fluctuations are chemically recorded via transglutaminase-mediated serotonylation, representing an epigenetic mark that warrants further long-term study within the Developmental Origins of Health and Disease (DOHaD) framework. Full article
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