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Biology
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Molecular Regulation during Embryo Development
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Molecular Regulation during Embryo Development

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Developmental Biology".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 4327

Special Issue Editors

Prof. Dr. Beate Brand-Saberi

E-Mail Website
Guest Editor
Department of Anatomy and Molecular Embryology, Medical Faculty, Ruhr University Bochum, 44801 Bochum, Germany
Interests: myogenesis; stem cells; morphogenesis; cell migration; bHLH transcription factors
Dr. Godwin Sokpor

E-Mail Website
Guest Editor
Lincoln Medical School, College of Science, University of Lincoln, Lincoln, UK
Interests: development and patterning of the brain

Special Issue Information

Dear Colleagues,

Embryonic development is a fascinating process which is controlled by extrinsic signals during cellular interactions, as well as intrinsic processes that occur spontaneously at the cellular level known as self-organization. Both aspects have received great attention as researchers are trying to understand the underlying molecular regulation. The rapid progress of stem cell biology has led to the generation of 3D in vitro models, such as organoids and embryoids, from which we can get unprecedented insights into morphogenesis and patterning of vertebrates, including humans.

The Special Issue “Molecular Regulation during Embryo Development” welcomes manuscripts on current topics of genetic hierarchies, as well as signalling pathways governing embryonic development. Additionally, cellular mechanisms, such as proliferation and growth control, autophagy, and epithelial-to-mesenchymal transition in vertebrate model organisms are within the range of interest. A special focus will be given to stem cell-based modelling of human development.

This Special Issue aims to contribute to the following topics:

  • Modelling human development;
  • Fine-tuning embryonic growth;
  • The control of cell fate decisions;
  • Cellular mechanisms governing morphogenesis.

Prof. Dr. Beate Brand-Saberi
Dr. Godwin Sokpor
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • embryoids
  • gastruloids
  • morphogenesis
  • brain development
  • epigenetic modifications
  • intercellular signalling
  • embryogenesis

Published Papers (3 papers)

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Research

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13 pages, 7219 KiB  
Article
Using i-GONAD for Cell-Type-Specific and Systematic Analysis of Developmental Transcription Factors In Vivo
by Christoph Wiegreffe, Simon Ehricke, Luisa Schmid, Jacqueline Andratschke and Stefan Britsch
Biology 2023, 12(9), 1236; https://doi.org/10.3390/biology12091236 - 13 Sep 2023
Cited by 2 | Viewed by 893
Abstract
Transcription factors (TFs) regulate gene expression via direct DNA binding together with cofactors and in chromatin remodeling complexes. Their function is thus regulated in a spatiotemporal and cell-type-specific manner. To analyze the functions of TFs in a cell-type-specific context, genome-wide DNA binding, as [...] Read more.
Transcription factors (TFs) regulate gene expression via direct DNA binding together with cofactors and in chromatin remodeling complexes. Their function is thus regulated in a spatiotemporal and cell-type-specific manner. To analyze the functions of TFs in a cell-type-specific context, genome-wide DNA binding, as well as the identification of interacting proteins, is required. We used i-GONAD (improved genome editing via oviductal nucleic acids delivery) in mice to genetically modify TFs by adding fluorescent reporter and affinity tags that can be exploited for the imaging and enrichment of target cells as well as chromatin immunoprecipitation and pull-down assays. As proof-of-principle, we showed the functional genetic modification of the closely related developmental TFs, Bcl11a and Bcl11b, in defined cell types of newborn mice. i-GONAD is a highly efficient procedure for modifying TF-encoding genes via the integration of small insertions, such as reporter and affinity tags. The novel Bcl11a and Bcl11b mouse lines, described in this study, will be used to improve our understanding of the Bcl11 family’s function in neurodevelopment and associated disease. Full article
(This article belongs to the Special Issue Molecular Regulation during Embryo Development)
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18 pages, 5190 KiB  
Article
Systemic Prenatal Stress Exposure through Corticosterone Application Adversely Affects Avian Embryonic Skin Development
by Morris Gellisch, Martin Bablok, Satya Srirama Karthik Divvela, Gabriela Morosan-Puopolo and Beate Brand-Saberi
Biology 2023, 12(5), 656; https://doi.org/10.3390/biology12050656 - 26 Apr 2023
Viewed by 1393
Abstract
Prenatal stress exposure is considered a risk factor for developmental deficits and postnatal behavioral disorders. While the effect of glucocorticoid-associated prenatal stress exposure has been comprehensively studied in many organ systems, there is a lack of in-depth embryological investigations regarding the effects of [...] Read more.
Prenatal stress exposure is considered a risk factor for developmental deficits and postnatal behavioral disorders. While the effect of glucocorticoid-associated prenatal stress exposure has been comprehensively studied in many organ systems, there is a lack of in-depth embryological investigations regarding the effects of stress on the integumentary system. To approach this, we employed the avian embryo as a model organism and investigated the effects of systemic pathologically-elevated glucocorticoid exposure on the development of the integumentary system. After standardized corticosterone injections on embryonic day 6, we compared the stress-exposed embryos with a control cohort, using histological and immunohistochemical analyses as well as in situ hybridization. The overarching developmental deficits observed in the stress-exposed embryos were reflected through downregulation of both vimentin as well as fibronectin. In addition, a deficient composition in the different skin layers became apparent, which could be linked to a reduced expression of Dermo-1 along with significantly reduced proliferation rates. An impairment of skin appendage formation could be demonstrated by diminished expression of Sonic hedgehog. These results contribute to a more profound understanding of prenatal stress causing severe deficits in the integumentary system of developing organisms. Full article
(This article belongs to the Special Issue Molecular Regulation during Embryo Development)
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Review

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17 pages, 1165 KiB  
Review
The Role of Bcl11 Transcription Factors in Neurodevelopmental Disorders
by Franziska Anna Seigfried and Stefan Britsch
Biology 2024, 13(2), 126; https://doi.org/10.3390/biology13020126 - 17 Feb 2024
Viewed by 1339
Abstract
Neurodevelopmental disorders (NDDs) comprise a diverse group of diseases, including developmental delay, autism spectrum disorder (ASD), intellectual disability (ID), and attention-deficit/hyperactivity disorder (ADHD). NDDs are caused by aberrant brain development due to genetic and environmental factors. To establish specific and curative therapeutic approaches, [...] Read more.
Neurodevelopmental disorders (NDDs) comprise a diverse group of diseases, including developmental delay, autism spectrum disorder (ASD), intellectual disability (ID), and attention-deficit/hyperactivity disorder (ADHD). NDDs are caused by aberrant brain development due to genetic and environmental factors. To establish specific and curative therapeutic approaches, it is indispensable to gain precise mechanistic insight into the cellular and molecular pathogenesis of NDDs. Mutations of BCL11A and BCL11B, two closely related, ultra-conserved zinc-finger transcription factors, were recently reported to be associated with NDDs, including developmental delay, ASD, and ID, as well as morphogenic defects such as cerebellar hypoplasia. In mice, Bcl11 transcription factors are well known to orchestrate various cellular processes during brain development, for example, neural progenitor cell proliferation, neuronal migration, and the differentiation as well as integration of neurons into functional circuits. Developmental defects observed in both, mice and humans display striking similarities, suggesting Bcl11 knockout mice provide excellent models for analyzing human disease. This review offers a comprehensive overview of the cellular and molecular functions of Bcl11a and b and links experimental research to the corresponding NDDs observed in humans. Moreover, it outlines trajectories for future translational research that may help to better understand the molecular basis of Bcl11-dependent NDDs as well as to conceive disease-specific therapeutic approaches. Full article
(This article belongs to the Special Issue Molecular Regulation during Embryo Development)
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