Feature Papers in Journal of Developmental Biology

A special issue of Journal of Developmental Biology (ISSN 2221-3759).

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 27835

Special Issue Editors

Department of Pediatrics, Northwestern University and Developmental BIology Program, Stanley Manne Children’s Research Institute, Ann and Robert H. Lurie Children's Hospital, 225 E. Chicago Ave., Chicago, IL 60611, USA
Interests: cell-fate determination; cell lineage; organ development; fibrotic disease; microRNAs
Special Issues, Collections and Topics in MDPI journals
Department of Craniofacial Biology, School of Dental Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA
Interests: neural crest development; craniofacial development; zebrafish
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue “Feature Papers in Journal of Developmental Biology” aims to collect high-quality review articles, research articles and communications on the development of multicellular organisms at the molecule, cell, tissue, organ, and whole organism levels.

We hope this topic is of interest to you and invite you to send a tentative title and short abstract to our editorial office ([email protected]) for evaluation before submission. Please note that selected papers are still subject to thorough peer review, and only invited papers can be published online once accepted in this collection.

Topics include without being limited to the following:

  • Development mechanisms and genetics;
  • Cell differentiation;
  • Embryonic development;
  • Tissue/organism growth;
  • Metamorphosis and regeneration;
  • Genetics/human genetics;
  • Cell biology in development;
  • Development of the nervous system;
  • Evolution of development;
  • Rare developmental disorders;
  • RNA mechanisms in development;
  • Transcriptomics including single cell RNA-Seq to study development

We look forward to receiving your excellent work.

Dr. Robert W. Dettman
Prof. Dr. Kristin Bruk Artinger
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. Journal of Developmental Biology is an international peer-reviewed open access quarterly 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 1800 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.

Published Papers (6 papers)

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Editorial

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2 pages, 145 KiB  
Editorial
Special Issue “Feature Papers in Journal of Developmental Biology”
by Robert W. Dettman
J. Dev. Biol. 2022, 10(1), 5; https://0-doi-org.brum.beds.ac.uk/10.3390/jdb10010005 - 10 Jan 2022
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Abstract
Here, we have assembled five interesting manuscripts that deserve special attention [...] Full article
(This article belongs to the Special Issue Feature Papers in Journal of Developmental Biology)

Research

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18 pages, 2873 KiB  
Article
Gbx2 Is Required for the Migration and Survival of a Subpopulation of Trigeminal Cranial Neural Crest Cells
by David A. Roeseler, Lona Strader, Matthew J. Anderson and Samuel T. Waters
J. Dev. Biol. 2020, 8(4), 33; https://0-doi-org.brum.beds.ac.uk/10.3390/jdb8040033 - 11 Dec 2020
Cited by 3 | Viewed by 2852
Abstract
The development of key structures within the mature vertebrate hindbrain requires the migration of neural crest (NC) cells and motor neurons to their appropriate target sites. Functional analyses in multiple species have revealed a requirement for the transcription factor gastrulation-brain-homeobox 2 (Gbx2) in [...] Read more.
The development of key structures within the mature vertebrate hindbrain requires the migration of neural crest (NC) cells and motor neurons to their appropriate target sites. Functional analyses in multiple species have revealed a requirement for the transcription factor gastrulation-brain-homeobox 2 (Gbx2) in NC cell migration and positioning of motor neurons in the developing hindbrain. In addition, loss of Gbx2 function studies in mutant mouse embryos, Gbx2neo, demonstrate a requirement for Gbx2 for the development of NC-derived sensory neurons and axons constituting the mandibular branch of the trigeminal nerve (CNV). Our recent GBX2 target gene identification study identified multiple genes required for the migration and survival of NC cells (e.g., Robo1, Slit3, Nrp1). In this report, we performed loss-of-function analyses using Gbx2neo mutant embryos, to improve our understanding of the molecular and genetic mechanisms regulated by Gbx2 during anterior hindbrain and CNV development. Analysis of Tbx20 expression in the hindbrain of Gbx2neo homozygotes revealed a severely truncated rhombomere (r)2. Our data also provide evidence demonstrating a requirement for Gbx2 in the temporal regulation of Krox20 expression in r3. Lastly, we show that Gbx2 is required for the expression of Nrp1 in a subpopulation of trigeminal NC cells, and correct migration and survival of cranial NC cells that populate the trigeminal ganglion. Taken together, these findings provide additional insight into molecular and genetic mechanisms regulated by Gbx2 that underlie NC migration, trigeminal ganglion assembly, and, more broadly, anterior hindbrain development. Full article
(This article belongs to the Special Issue Feature Papers in Journal of Developmental Biology)
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19 pages, 3418 KiB  
Article
Exploring the Expression of Cardiac Regulators in a Vertebrate Extremophile: The Cichlid Fish Oreochromis (Alcolapia) alcalica
by Gemma Sutton, Lewis J. White, Antonia G.P. Ford, Asilatu Shechonge, Julia J. Day, Kanchon K. Dasmahapatra and Mary E. Pownall
J. Dev. Biol. 2020, 8(4), 22; https://0-doi-org.brum.beds.ac.uk/10.3390/jdb8040022 - 04 Oct 2020
Cited by 2 | Viewed by 3698
Abstract
Although it is widely accepted that the cellular and molecular mechanisms of vertebrate cardiac development are evolutionarily conserved, this is on the basis of data from only a few model organisms suited to laboratory studies. Here, we investigate gene expression during cardiac development [...] Read more.
Although it is widely accepted that the cellular and molecular mechanisms of vertebrate cardiac development are evolutionarily conserved, this is on the basis of data from only a few model organisms suited to laboratory studies. Here, we investigate gene expression during cardiac development in the extremophile, non-model fish species, Oreochromis (Alcolapia) alcalica. We first characterise the early development of O. alcalica and observe extensive vascularisation across the yolk prior to hatching. We further investigate heart development by identifying and cloning O. alcalica orthologues of conserved cardiac transcription factors gata4, tbx5, and mef2c for analysis by in situ hybridisation. Expression of these three key cardiac developmental regulators also reveals other aspects of O. alcalica development, as these genes are expressed in developing blood, limb, eyes, and muscle, as well as the heart. Our data support the notion that O. alcalica is a direct-developing vertebrate that shares the highly conserved molecular regulation of the vertebrate body plan. However, the expression of gata4 in O. alcalica reveals interesting differences in the development of the circulatory system distinct from that of the well-studied zebrafish. Understanding the development of O. alcalica embryos is an important step towards providing a model for future research into the adaptation to extreme conditions; this is particularly relevant given that anthropogenic-driven climate change will likely result in more freshwater organisms being exposed to less favourable conditions. Full article
(This article belongs to the Special Issue Feature Papers in Journal of Developmental Biology)
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16 pages, 3292 KiB  
Article
Cerebellar Morphology and Behavioral Profiles in Mice Lacking Heparan Sulfate Ndst Gene Function
by Lars Lewejohann, Srinivas R. Pallerla, Rebecca S. Schreiber, Joanna Gerula and Kay Grobe
J. Dev. Biol. 2020, 8(3), 13; https://0-doi-org.brum.beds.ac.uk/10.3390/jdb8030013 - 11 Jul 2020
Cited by 4 | Viewed by 2929
Abstract
Disruption of the Heparan sulfate (HS)-biosynthetic gene N-acetylglucosamine N-Deacetylase/N-sulfotransferase 1 (Ndst1) during nervous system development causes malformations that are composites of those caused by mutations of multiple HS binding growth factors and morphogens. However, the role of Ndst function in adult [...] Read more.
Disruption of the Heparan sulfate (HS)-biosynthetic gene N-acetylglucosamine N-Deacetylase/N-sulfotransferase 1 (Ndst1) during nervous system development causes malformations that are composites of those caused by mutations of multiple HS binding growth factors and morphogens. However, the role of Ndst function in adult brain physiology is less explored. Therefore, we generated mice bearing a Purkinje-cell-specific deletion in Ndst1 gene function by using Cre/loxP technology under the control of the Purkinje cell protein 2 (Pcp2/L7) promotor, which results in HS undersulfation. We observed that mutant mice did not show overt changes in the density or organization of Purkinje cells in the adult cerebellum, and behavioral tests also demonstrated normal cerebellar function. This suggested that postnatal Purkinje cell development and homeostasis are independent of Ndst1 function, or that impaired HS sulfation upon deletion of Ndst1 function may be compensated for by other Purkinje cell-expressed Ndst isoforms. To test the latter possibility, we additionally deleted the second Purkinje-cell expressed Ndst family member, Ndst2. This selectively abolished reproductive capacity of compound mutant female, but not male, mice, suggesting that ovulation, gestation, or female reproductive behavior specifically depends on Ndst-dependent HS sulfation in cells types that express Cre under Pcp2/L7 promotor control. Full article
(This article belongs to the Special Issue Feature Papers in Journal of Developmental Biology)
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23 pages, 4592 KiB  
Article
A Synthetic Peptide, CK2.3, Inhibits RANKL-Induced Osteoclastogenesis through BMPRIa and ERK Signaling Pathway
by John Nguyen, Semaj Kelly, Ryan Wood, Brian Heubel and Anja Nohe
J. Dev. Biol. 2020, 8(3), 12; https://0-doi-org.brum.beds.ac.uk/10.3390/jdb8030012 - 09 Jul 2020
Cited by 6 | Viewed by 3261
Abstract
The skeletal system plays an important role in the development and maturation process. Through the bone remodeling process, 10% of the skeletal system is renewed every year. Osteoblasts and osteoclasts are two major bone cells that are involved in the development of the [...] Read more.
The skeletal system plays an important role in the development and maturation process. Through the bone remodeling process, 10% of the skeletal system is renewed every year. Osteoblasts and osteoclasts are two major bone cells that are involved in the development of the skeletal system, and their activity is kept in balance. An imbalance between their activities can lead to diseases such as osteoporosis that are characterized by significant bone loss due to the overactivity of bone-resorbing osteoclasts. Our laboratory has developed a novel peptide, CK2.3, which works as both an anabolic and anti-resorptive agent to induce bone formation and prevent bone loss. We previously reported that CK2.3 mediated mineralization and osteoblast development through the SMAD, ERK, and AKT signaling pathways. In this study, we demonstrated the mechanism by which CK2.3 inhibits osteoclast development. We showed that the inhibition of MEK by the U0126 inhibitor rescued the osteoclast development of RAW264.7 induced by RANKL in a co-culture system with CK2.3. We observed that CK2.3 induced ERK activation and BMPRIa expression on Day 1 after stimulation with CK2.3. While CK2.3 was previously reported to induce the SMAD signaling pathway in osteoblast development, we did not observe any changes in SMAD activation in osteoclast development with CK2.3 stimulation. Understanding the mechanism by which CK2.3 inhibits osteoclast development will allow CK2.3 to be developed as a new treatment for osteoporosis. Full article
(This article belongs to the Special Issue Feature Papers in Journal of Developmental Biology)
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Review

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30 pages, 1951 KiB  
Review
Bone Morphogenetic Protein-2 in Development and Bone Homeostasis
by Daniel Halloran, Hilary W. Durbano and Anja Nohe
J. Dev. Biol. 2020, 8(3), 19; https://0-doi-org.brum.beds.ac.uk/10.3390/jdb8030019 - 13 Sep 2020
Cited by 124 | Viewed by 12407
Abstract
Bone morphogenetic proteins (BMPs) are multi-functional growth factors belonging to the Transforming Growth Factor-Beta (TGF-β) superfamily. These proteins are essential to many developmental processes, including cardiogenesis, neurogenesis, and osteogenesis. Specifically, within the BMP family, Bone Morphogenetic Protein-2 (BMP-2) was the first BMP to [...] Read more.
Bone morphogenetic proteins (BMPs) are multi-functional growth factors belonging to the Transforming Growth Factor-Beta (TGF-β) superfamily. These proteins are essential to many developmental processes, including cardiogenesis, neurogenesis, and osteogenesis. Specifically, within the BMP family, Bone Morphogenetic Protein-2 (BMP-2) was the first BMP to be characterized and has been well-studied. BMP-2 has important roles during embryonic development, as well as bone remodeling and homeostasis in adulthood. Some of its specific functions include digit formation and activating osteogenic genes, such as Runt-Related Transcription Factor 2 (RUNX2). Because of its diverse functions and osteogenic potential, the Food and Drug Administration (FDA) approved usage of recombinant human BMP-2 (rhBMP-2) during spinal fusion surgery, tibial shaft repair, and maxillary sinus reconstructive surgery. However, shortly after initial injections of rhBMP-2, several adverse complications were reported, and alternative therapeutics have been developed to limit these side-effects. As the clinical application of BMP-2 is largely implicated in bone, we focus primarily on its role in bone. However, we also describe briefly the role of BMP-2 in development. We then focus on the structure of BMP-2, its activation and regulation signaling pathways, BMP-2 clinical applications, and limitations of using BMP-2 as a therapeutic. Further, this review explores other potential treatments that may be useful in treating bone disorders. Full article
(This article belongs to the Special Issue Feature Papers in Journal of Developmental Biology)
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