Molecular and Cellular Mechanisms of Brain Development and Neurodevelopmental Disorders

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 539

Special Issue Editor


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Guest Editor
Department of Biochemistry and Medical Genetics, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R3E 0J9, Canada
Interests: epigenetics; DNA methylation; transcriptional control; gene regulation; drug repurposing; neural stem cells; neurodevelopmental disorders; medulloblastoma brain tumor
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Special Issue Information

Dear Collogues,

Brain development is a complex process that is highly regulated at different cellular and molecular levels. Accordingly, specific regulatory mechanisms are in place to ensure the proper expression of key developmental genes. During development, a population of neuronal progenitor cells known as neural stem cells build the central nervous system through differentiating into specific cell types. These progenitor cells represent fundamental biological systems that can be used to study the mechanisms of cell fate determination in the developing and adult brain. Such systems could include in vitro and in vivo models, benefiting from classical and novel technologies.

This Special Issue welcomes review articles and original research studies that cover relevant research in model systems that investigate different molecular and cellular mechanisms of brain development and their impact in neurodevelopmental disorders. We encourage submissions in different areas of research and disciplines, including embryonic brain development and adult brain function and physiology, the epigenetic basis of brain cell development and their deregulation in neurodevelopmental diseases, cell signaling pathways in brain cells, neural stem cell differentiation and self-renewal, gene regulatory mechanisms in relevant model systems, the molecular and cellular basis of brain diseases, next-generation sequencing and multi-omics studies, and neuroscience.

You may choose our Joint Special Issue in Journal of Developmental Biology.

Prof. Dr. Mojgan Rastegar
Guest Editor

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Keywords

  • brain development
  • neural stem cells
  • neurodevelopmental disorders
  • brain diseases
  • cellular and molecular mechanisms
  • embryonic and adult brain

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Published Papers (1 paper)

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Research

30 pages, 6716 KiB  
Article
Mutation of MeCP2 at T158M Leads to Distinct Molecular and Phenotypic Abnormalities in Male and Female Mice
by Chris-Tiann Roberts, Ashraf Kadar Shahib, Khatereh Saei Arezoumand, Ghanan Bin Akhtar, Kazem Nejati-Koshki, Jessica S. Jarmasz, Seyyed Mohyeddin Ziaee, Marjorie Buist, Nicole Raabe, Abbas Rezaeian Mehrabadi, Carl O. Olson and Mojgan Rastegar
Cells 2025, 14(16), 1286; https://doi.org/10.3390/cells14161286 - 19 Aug 2025
Viewed by 182
Abstract
Methyl CpG-binding protein 2 (MeCP2) is an epigenetic reader of DNA methylation with high abundance in the brain. While genetic mutations occur across different protein domains of MeCP2, the T158M mutation is amongst the most frequent MeCP2 mutations. MeCP2 is encoded by the [...] Read more.
Methyl CpG-binding protein 2 (MeCP2) is an epigenetic reader of DNA methylation with high abundance in the brain. While genetic mutations occur across different protein domains of MeCP2, the T158M mutation is amongst the most frequent MeCP2 mutations. MeCP2 is encoded by the MECP2/Mecp2 gene located on the X chromosome. In humans, MECP2 mutations cause Rett Syndrome, a debilitating neurodevelopmental disorder in females, with very rare cases presenting in males. Despite the generation of different transgenic mouse lines with MeCP2 mutations, the sex-dependent phenotypic and molecular impact of common MeCP2 mutations in mouse models of disease remains largely unexplored. Here, we focus on the MeCP2 T158M mutation using Mecp2tm4.1Bird/J transgenic mice (referred to as Mecp2T158M), and report that Mecp2T158M mutant mice display sex-specific molecular, behavioural, and phenotypic characteristics when compared to wild-type controls. Our data indicates sex- and brain-region-dependent impacts on the expression of MeCP2, synaptic proteins, cytoskeletal markers, and autophagy factors. Our findings demonstrate that the phenotypic and molecular characteristics of this mouse model may relate to the clinical manifestation in human patients with Rett Syndrome. Full article
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