Special Issue "2020 Feature Papers by JDB’ Editorial Board Members"

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

Deadline for manuscript submissions: closed (31 December 2020).

Special Issue Editor

Prof. Dr. Simon J. Conway
E-Mail Website
Guest Editor
Herman B Wells Center for Pediatric Research, 1044 West Walnut Street, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Interests: birth defects; developmental basis of congenital and acquired cardiopulmonary diseases; neonatal lung alveolar septation; transgenic mouse modelling; cell lineage tracing; neural crest; fibroblast-to-myofibroblast transition; extracellular matrix
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Special Issue Information

Dear Colleagues,

This Special Issue of the Journal of Developmental Biology (JDB) represents a collection of papers submitted exclusively by its Editorial Board Members (EBMs), as well as invited papers from relevant experts. By representing different areas of research on developmental biology conducted in the laboratories of its EBMs, this Special Issue introduces JDB as a first-class platform for reporting scientific data.

Authors can submit their manuscripts online by registering and logging in to the following website: https://susy.mdpi.com/user/login. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the Special Issue website.

Prof. Simon J. Conway
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 papers will be 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 1600 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 (8 papers)

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Editorial

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Open AccessEditorial
Developmental Biology: An Introduction and Invitation
J. Dev. Biol. 2020, 8(3), 11; https://doi.org/10.3390/jdb8030011 - 28 Jun 2020
Viewed by 705
(This article belongs to the Special Issue 2020 Feature Papers by JDB’ Editorial Board Members)

Research

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Open AccessArticle
Genome-Wide Binding Analyses of HOXB1 Revealed a Novel DNA Binding Motif Associated with Gene Repression
J. Dev. Biol. 2021, 9(1), 6; https://doi.org/10.3390/jdb9010006 - 03 Feb 2021
Viewed by 481
Abstract
Knowledge of the diverse DNA binding specificities of transcription factors is important for understanding their specific regulatory functions in animal development and evolution. We have examined the genome-wide binding properties of the mouse HOXB1 protein in embryonic stem cells differentiated into neural fates. [...] Read more.
Knowledge of the diverse DNA binding specificities of transcription factors is important for understanding their specific regulatory functions in animal development and evolution. We have examined the genome-wide binding properties of the mouse HOXB1 protein in embryonic stem cells differentiated into neural fates. Unexpectedly, only a small number of HOXB1 bound regions (7%) correlate with binding of the known HOX cofactors PBX and MEIS. In contrast, 22% of the HOXB1 binding peaks display co-occupancy with the transcriptional repressor REST. Analyses revealed that co-binding of HOXB1 with PBX correlates with active histone marks and high levels of expression, while co-occupancy with REST correlates with repressive histone marks and repression of the target genes. Analysis of HOXB1 bound regions uncovered enrichment of a novel 15 base pair HOXB1 binding motif HB1RE (HOXB1 response element). In vitro template binding assays showed that HOXB1, PBX1, and MEIS can bind to this motif. In vivo, this motif is sufficient for direct expression of a reporter gene and over-expression of HOXB1 selectively represses this activity. Our analyses suggest that HOXB1 has evolved an association with REST in gene regulation and the novel HB1RE motif contributes to HOXB1 function in part through a repressive role in gene expression. Full article
(This article belongs to the Special Issue 2020 Feature Papers by JDB’ Editorial Board Members)
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Open AccessArticle
Mud Loss Restricts Yki-Dependent Hyperplasia in Drosophila Epithelia
J. Dev. Biol. 2020, 8(4), 34; https://doi.org/10.3390/jdb8040034 - 13 Dec 2020
Viewed by 716
Abstract
Tissue development demands precise control of cell proliferation and organization, which is achieved through multiple conserved signaling pathways and protein complexes in multicellular animals. Epithelia are a ubiquitous tissue type that provide diverse functions including physical protection, barrier formation, chemical exchange, and secretory [...] Read more.
Tissue development demands precise control of cell proliferation and organization, which is achieved through multiple conserved signaling pathways and protein complexes in multicellular animals. Epithelia are a ubiquitous tissue type that provide diverse functions including physical protection, barrier formation, chemical exchange, and secretory activity. However, epithelial cells are also a common driver of tumorigenesis; thus, understanding the molecular mechanisms that control their growth dynamics is important in understanding not only developmental mechanisms but also disease. One prominent pathway that regulates epithelial growth is the conserved Hippo/Warts/Yorkie network. Hippo/Warts inactivation, or activating mutations in Yorkie that prevent its phosphorylation (e.g., YkiS168A), drive hyperplastic tissue growth. We recently reported that loss of Mushroom body defect (Mud), a microtubule-associated protein that contributes to mitotic spindle function, restricts YkiS168A-mediated growth in Drosophila imaginal wing disc epithelia. Here we show that Mud loss alters cell cycle progression and triggers apoptosis with accompanying Jun kinase (JNK) activation in YkiS168A-expressing discs. To identify additional molecular insights, we performed RNAseq and differential gene expression profiling. This analysis revealed that Mud knockdown in YkiS168A-expressing discs resulted in a significant downregulation in expression of core basement membrane (BM) and extracellular matrix (ECM) genes, including the type IV collagen gene viking. Furthermore, we found that YkiS168A-expressing discs accumulated increased collagen protein, which was reduced following Mud knockdown. Our results suggest that ECM/BM remodeling can limit untoward growth initiated by an important driver of tumor growth and highlight a potential regulatory link with cytoskeleton-associated genes. Full article
(This article belongs to the Special Issue 2020 Feature Papers by JDB’ Editorial Board Members)
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Open AccessArticle
Evolution of Developmental GATA Factors in Nematodes
J. Dev. Biol. 2020, 8(4), 27; https://doi.org/10.3390/jdb8040027 - 16 Nov 2020
Viewed by 796
Abstract
GATA transcription factors are found in animals, plants, and fungi. In animals, they have important developmental roles in controlling specification of cell identities and executing tissue-specific differentiation. The Phylum Nematoda is a diverse group of vermiform animals that inhabit ecological niches all over [...] Read more.
GATA transcription factors are found in animals, plants, and fungi. In animals, they have important developmental roles in controlling specification of cell identities and executing tissue-specific differentiation. The Phylum Nematoda is a diverse group of vermiform animals that inhabit ecological niches all over the world. Both free-living and parasitic species are known, including those that cause human infectious disease. To date, GATA factors in nematodes have been studied almost exclusively in the model system C. elegans and its close relatives. In this study, we use newly available sequences to identify GATA factors across the nematode phylum. We find that most species have fewer than six GATA factors, but some species have 10 or more. Comparisons of gene and protein structure suggest that there were at most two GATA factors at the base of the phylum, which expanded by duplication and modification to result in a core set of four factors. The high degree of structural similarity with the corresponding orthologues in C. elegans suggests that the nematode GATA factors share similar functions in development. Full article
(This article belongs to the Special Issue 2020 Feature Papers by JDB’ Editorial Board Members)
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Open AccessArticle
Cracd Marks the First Wave of Meiosis during Spermatogenesis and Is Mis-Expressed in Azoospermia Mice
J. Dev. Biol. 2020, 8(3), 21; https://doi.org/10.3390/jdb8030021 - 18 Sep 2020
Viewed by 641
Abstract
Testicular development starts in utero and maturation continues postnatally, requiring a cascade of gene activation and differentiation into different cell types, with each cell type having its own specific function. As we had previously reported that the Capping protein inhibiting regulator of actin [...] Read more.
Testicular development starts in utero and maturation continues postnatally, requiring a cascade of gene activation and differentiation into different cell types, with each cell type having its own specific function. As we had previously reported that the Capping protein inhibiting regulator of actin (Cracd) gene was expressed in the adult mouse testis, herein we examine when and where the β-catenin associated Cracd is initially expressed during postnatal testis development. Significantly, Cracd mRNA is present in both the immature postnatal and adult testis in round spermatid cells, with highest level of expression occurring during the first wave of meiosis and spermatogenesis. In the juvenile testes, Cracd is initially expressed within the innermost region but as maturation occurs, Cracd mRNA switches to a more peripheral location. Thereafter, Cracd is downregulated to maintenance levels in the haploid male germ cell lineage. As Cracd mRNA was expressed within developing round spermatids, we tested its effectiveness as a biomarker of non-obstructive azoospermia using transgenic knockout mice models. Meaningfully, Cracd expression was absent in Deleted in azoospermia like (Dazl) null testis, which exhibit a dramatic germ cell loss. Moreover, Cracd was abnormally regulated and ectopically mis-expressed in Polypyrimidine tract binding protein-2 (Ptbp2) conditional germ cell restricted knockout testis, which exhibit a block during spermatid differentiation and a reduction in the number of late stage spermatocytes coincident with reduced β-catenin expression. Combined, these data suggest that Cracd is a useful first wave of spermatogenesis biomarker of azoospermia phenotypes, even prior to an overt phenotype being evident. Full article
(This article belongs to the Special Issue 2020 Feature Papers by JDB’ Editorial Board Members)
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Open AccessArticle
Reelin Mediates Hippocampal Cajal-Retzius Cell Positioning and Infrapyramidal Blade Morphogenesis
J. Dev. Biol. 2020, 8(3), 20; https://doi.org/10.3390/jdb8030020 - 18 Sep 2020
Viewed by 603
Abstract
We have previously described hypomorphic reelin (Reln) mutant mice, RelnCTRdel, in which the morphology of the dentate gyrus is distinct from that seen in reeler mice. In the RelnCTRdel mutant, the infrapyramidal blade of the dentate gyrus fails [...] Read more.
We have previously described hypomorphic reelin (Reln) mutant mice, RelnCTRdel, in which the morphology of the dentate gyrus is distinct from that seen in reeler mice. In the RelnCTRdel mutant, the infrapyramidal blade of the dentate gyrus fails to extend, while the suprapyramidal blade forms with a relatively compact granule neuron layer. Underlying this defect, we now report several developmental anomalies in the RelnCTRdel dentate gyrus. Most strikingly, the distribution of Cajal-Retzius cells was aberrant; Cajal-Retzius neurons were increased in the suprapyramidal blade, but were greatly reduced along the subpial surface of the prospective infrapyramidal blade. We also observed multiple abnormalities of the fimbriodentate junction. Firstly, progenitor cells were distributed abnormally; the “neurogenic cluster” at the fimbriodentate junction was absent, lacking the normal accumulation of Tbr2-positive intermediate progenitors. However, the number of dividing cells in the dentate gyrus was not generally decreased. Secondly, a defect of secondary glial scaffold formation, limited to the infrapyramidal blade, was observed. The densely radiating glial fibers characteristic of the normal fimbriodentate junction were absent in mutants. These fibers might be required for migration of progenitors, which may account for the failure of neurogenic cluster formation. These findings suggest the importance of the secondary scaffold and neurogenic cluster of the fimbriodentate junction in morphogenesis of the mammalian dentate gyrus. Our study provides direct genetic evidence showing that normal RELN function is required for Cajal-Retzius cell positioning in the dentate gyrus, and for formation of the fimbriodentate junction to promote infrapyramidal blade extension. Full article
(This article belongs to the Special Issue 2020 Feature Papers by JDB’ Editorial Board Members)
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Review

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Open AccessReview
Perspective: Controlling Epidermal Terminal Differentiation with Transcriptional Bursting and RNA Bodies
J. Dev. Biol. 2020, 8(4), 29; https://doi.org/10.3390/jdb8040029 - 04 Dec 2020
Viewed by 569
Abstract
The outer layer of the skin, the epidermis, is the principal barrier to the external environment: post-mitotic cells terminally differentiate to form a tough outer cornified layer of enucleate and flattened cells that confer the majority of skin barrier function. Nuclear degradation is [...] Read more.
The outer layer of the skin, the epidermis, is the principal barrier to the external environment: post-mitotic cells terminally differentiate to form a tough outer cornified layer of enucleate and flattened cells that confer the majority of skin barrier function. Nuclear degradation is required for correct cornified envelope formation. This process requires mRNA translation during the process of nuclear destruction. In this review and perspective, we address the biology of transcriptional bursting and the formation of ribonuclear particles in model organisms including mammals, and then examine the evidence that these phenomena occur as part of epidermal terminal differentiation. Full article
(This article belongs to the Special Issue 2020 Feature Papers by JDB’ Editorial Board Members)
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Open AccessReview
Role of Tafazzin in Mitochondrial Function, Development and Disease
J. Dev. Biol. 2020, 8(2), 10; https://doi.org/10.3390/jdb8020010 - 23 May 2020
Viewed by 1057
Abstract
Tafazzin, an enzyme associated with the rare inherited x-linked disorder Barth Syndrome, is a nuclear encoded mitochondrial transacylase that is highly conserved across multiple species and plays an important role in mitochondrial function. Numerous studies have elucidated the mechanisms by which Tafazzin [...] Read more.
Tafazzin, an enzyme associated with the rare inherited x-linked disorder Barth Syndrome, is a nuclear encoded mitochondrial transacylase that is highly conserved across multiple species and plays an important role in mitochondrial function. Numerous studies have elucidated the mechanisms by which Tafazzin affects mitochondrial function, but its effects on development and susceptibility to adult disease are incompletely understood. The purpose of this review is to highlight previous functional studies across a variety of model organisms, introduce recent studies that show an important role in development, and also to provide an update on the role of Tafazzin in human disease. The profound effects of Tafazzin on cardiac development and adult cardiac homeostasis will be emphasized. These studies underscore the importance of mitochondrial function in cardiac development and disease, and also introduce the concept of Tafazzin as a potential therapeutic modality. Full article
(This article belongs to the Special Issue 2020 Feature Papers by JDB’ Editorial Board Members)
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