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Cells
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Molecular and Clinical Advances in Understanding Early Embryo Development—Volume II
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Molecular and Clinical Advances in Understanding Early Embryo Development—Volume II

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Reproductive Cells and Development".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 2242

Special Issue Editor

Dr. Lon J. van Winkle

E-Mail Website
Guest Editor
1. Department of Biochemistry, Midwestern University, Downers Grove, IL 60515, USA
2. Department of Medical Humanities, Rocky Vista University, Parker, CO 80122, USA
Interests: cell physiology; cell metabolism; development; cell differentiation; stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Both maternal and paternal environmental challenges and assisted reproductive technology (ART) can alter early embryo development. These molecular alterations often produce unwanted characteristics in adulthood. Included in the undesirable characteristics are metabolic syndrome, diabetes, hypertension, and other related disorders.  Strikingly, these disorders may, in many cases, exhibit transgenerational expression. A previous Special Issue, entitled "Molecular and Clinical Advances in Understanding Early Embryo Development” was very successful, and comprises 13 papers and reviews concerning various aspects of early embryo development. However,  embryo development is complicated and dynamic, making it difficult to cover in one Special Issue.

Therefore, we aim to work towards creating an additional Special Issue on this topic. In this Special Issue, we aim to explore current research concerning these and related environmental challenges to early embryos and their mothers and fathers. We invite submission of manuscripts concerning, but not limited to, the following keywords regarding early embryo development.

We are pleased to invite you to contribute original articles, reviews, communications, etc. We are looking forward to your contributions to this Special Issue.

Dr. Lon J. van Winkle
Guest Editor

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. Cells is an international peer-reviewed open access semimonthly 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

  • metabolism
  • biomembrane transport
  • genetics
  • epigenetic modifications
  • transgenerational inheritance
  • signaling
  • ART
  • in vitro culture
  • trophectoderm
  • inner cell mass

Related Special Issue

Published Papers (2 papers)

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Research

15 pages, 3633 KiB  
Article
Proline and Proline Analogues Improve Development of Mouse Preimplantation Embryos by Protecting Them against Oxidative Stress
by Madeleine L. M. Hardy, Dheerja Lakhiani, Michael B. Morris and Margot L. Day
Cells 2023, 12(22), 2640; https://doi.org/10.3390/cells12222640 - 16 Nov 2023
Viewed by 887
Abstract
The culture of embryos in the non-essential amino acid L-proline (Pro) or its analogues pipecolic acid (PA) and L-4-thiazolidine carboxylic acid (L4T) improves embryo development, increasing the percentage that develop to the blastocyst stage and hatch. Staining of 2-cell and 4-cell embryos with [...] Read more.
The culture of embryos in the non-essential amino acid L-proline (Pro) or its analogues pipecolic acid (PA) and L-4-thiazolidine carboxylic acid (L4T) improves embryo development, increasing the percentage that develop to the blastocyst stage and hatch. Staining of 2-cell and 4-cell embryos with tetramethylrhodamine methyl ester and 2′,7′-dichlorofluorescein diacetate showed that the culture of embryos in the presence of Pro, or either of these analogues, reduced mitochondrial activity and reactive oxygen species (ROS), respectively, indicating potential mechanisms by which embryo development is improved. Inhibition of the Pro metabolism enzyme, proline oxidase, by tetrahydro-2-furoic-acid prevented these reductions and concomitantly prevented the improved development. The ways in which Pro, PA and L4T reduce mitochondrial activity and ROS appear to differ, despite their structural similarity. Specifically, the results are consistent with Pro reducing ROS by reducing mitochondrial activity while PA and L4T may be acting as ROS scavengers. All three may work to reduce ROS by contributing to the GSH pool. Overall, our results indicate that reduction in mitochondrial activity and oxidative stress are potential mechanisms by which Pro and its analogues act to improve pre-implantation embryo development. Full article
(This article belongs to the Special Issue Molecular and Clinical Advances in Understanding Early Embryo Development—Volume II)
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16 pages, 2034 KiB  
Article
Oocyte-Specific Deletion of Slc6a9 Encoding the GLYT1 Glycine Transporter Eliminates Glycine Transport in Mouse Preimplantation Embryos and Their Ability to Counter Hypertonic Stress
by Allison K. Tscherner, Taylor McClatchie, Gracia Kaboba, Detlev Boison and Jay M. Baltz
Cells 2023, 12(20), 2500; https://doi.org/10.3390/cells12202500 - 21 Oct 2023
Cited by 1 | Viewed by 885
Abstract
Early preimplantation mouse embryos are sensitive to increased osmolarity, which can block their development. To overcome this, they accumulate organic osmolytes to maintain cell volume. The main organic osmolyte used by early mouse embryos is glycine. Glycine is transported during the mature egg [...] Read more.
Early preimplantation mouse embryos are sensitive to increased osmolarity, which can block their development. To overcome this, they accumulate organic osmolytes to maintain cell volume. The main organic osmolyte used by early mouse embryos is glycine. Glycine is transported during the mature egg and 1-cell to 4-cell embryo stages by a transporter identified as GLYT1, encoded by the Slc6a9 gene. Here, we have produced an oocyte-specific knockout of Slc6a9 by crossing mice that have a segment of the gene flanked by LoxP elements with transgenic mice expressing iCre driven by the oocyte-specific Gdf9 promoter. Slc6a9 null oocytes failed to develop glycine transport activity during meiotic maturation. However, females with these oocytes were fertile. When enclosed in their cumulus-oocyte complex, Slc6a9 null oocytes could accumulate glycine via GLYT1 transport in their coupled cumulus cells, which may support female fertility in vivo. In vitro, embryos derived from Slc6a9 null oocytes displayed a clear phenotype. While glycine rescued complete preimplantation development of wild type embryos from increased osmolarity, embryos derived from null oocytes failed to develop past the 2-cell stage even with glycine. Thus, Slc6a9 is required for glycine transport and protection against increased osmolarity in mouse eggs and early embryos. Full article
(This article belongs to the Special Issue Molecular and Clinical Advances in Understanding Early Embryo Development—Volume II)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Keratin 8/18a.1 expression regulates embryonic neural crest cell dynamics and plays a role in postnatal ocular wound healing in zebrafish
Authors: Antionette L. Williams; Brenda L. Bohnsack
Affiliation: Division of Ophthalmology, Ann & Robert H. Lurie Children’s Hospital of Chicago, 225 E. Chicago Ave., Chicago, IL 60611, USA
Abstract: A complete understanding of neural crest cell (NCC) mechanodynamics during ocular development will provide insight into postnatal NCC contributions during ophthalmic injury repair. Herein, single cell RNA sequencing in zebrafish revealed keratin intermediate filament genes krt8 and krt18a.1 as additional factors expressed during early ocular NCC development. In situ hybridization and immunofluorescence microscopy showed krt8 and krt18a.1 expression in the early neural plate border and in migrating NCCs during embryonic development. MO knockdown of K8 and K18a.1 markedly disrupted the migration of NCC subpopulations and decreased NCC marker gene expression in the craniofacial region and eye at 48 hours postfertilization, resulting in severe phenotypic defects reminiscent of neurocristopathies. Interestingly, retinoic acid (RA) regulated the gene expression of K18a.1, but not K8, in the ocular neural crest during embryonic development and in the adult eye. Further, Krt8 and Krt18a.1 expression was detected during postnatal corneal wound healing in adult zebrafish, and the observed corneal regeneration was negatively impacted by changes in RA levels. Altogether, these results suggest that K18a.1 is a downstream target of RA in the cranial neural crest, and both K8 and K18a.1 play roles in the ocular neural crest during embryonic development and postnatal injury repair.

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