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Current Genetic Insights in Organ Development
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Current Genetic Insights in Organ Development

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 July 2022) | Viewed by 13291

Special Issue Editor

Dr. Vasilios Tsarouhas

E-Mail Website
Guest Editor
Molecular Biosciences, (MBW), Stockholm University, Stockholm, Sweden
Interests: genetics; developmental biology; organogenesis; cell biology; membrane traficking; cytoskeleton; live imaging

Special Issue Information

Dear Colleagues, 

Organ development involves a synchronized series of morphological and biochemical transformations that are precisely controlled to ensure normal organ growth and function. We now know many genes that drive tissue remodeling during organogenesis, but we still do not fully understand the underlying mechanisms that regulate organogenesis on the genetic, transcriptomic, and epigenetic level. It is still unclear, for example, how organ size is regulated or how an organ becomes functional.

Much of the progress made in unraveling the responsible genetic networks in organ development has come from research in model organisms. Recent developments in gene editing methods, advanced microscopy, and transcriptomics technologies have started to rapidly enhance our understanding in the field. This Special Issue aims at exploring recent and novel insights in the genetics of organ development using a range of model systems and approaches to consolidate frontline research across model organs in one place and stimulate a flow of ideas for future studies. Researchers are invited to contribute original articles or short reports or new methods or reviews or commentaries that address current advances in genetics of organ development on the model organism they study. A particular focus will be on (but not limited to) mutational analysis of previously uncharacterized genes, gene interactions, epigenetic modifications, and gene expression patterns that affect organ development. We further aim at reporting on the cellular and molecular mechanisms through which gene mutations result in developmental aberrations, and how these genes are regulated or dysregulated. 

Dr. Vasilios Tsarouhas
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. Genes 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 2600 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

  • Organ development 
  • Genes 
  • Mutations 
  • Gene expression 
  • Cell signaling 
  • Genomics 
  • Transcriptome 
  • Epigenetics 
  • Cellular mechanism 
  • Gene editing–CRISPR

Published Papers (4 papers)

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Research

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15 pages, 6216 KiB  
Article
Dynamic Spatiotemporal Expression Changes in Connexins of the Developing Primate’s Cochlea
by Makoto Hosoya, Masato Fujioka, Ayako Y. Murayama, Kaoru Ogawa, Hideyuki Okano and Hiroyuki Ozawa
Genes 2021, 12(7), 1082; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12071082 - 16 Jul 2021
Cited by 9 | Viewed by 2218
Abstract
Connexins are gap junction components that are essential for acquiring normal hearing ability. Up to 50% of congenital, autosomal-recessive, non-syndromic deafness can be attributed to variants in GJB2, the gene that encodes connexin 26. Gene therapies modifying the expression of connexins are [...] Read more.
Connexins are gap junction components that are essential for acquiring normal hearing ability. Up to 50% of congenital, autosomal-recessive, non-syndromic deafness can be attributed to variants in GJB2, the gene that encodes connexin 26. Gene therapies modifying the expression of connexins are a feasible treatment option for some patients with genetic hearing losses. However, the expression patterns of these proteins in the human fetus are not fully understood due to ethical concerns. Recently, the common marmoset was used as a primate animal model for the human fetus. In this study, we examined the expression patterns of connexin 26 and connexin 30 in the developing cochlea of this primate. Primate-specific spatiotemporal expression changes were revealed, which suggest the existence of primate-specific control of connexin expression patterns and specific functions of these gap junction proteins. Moreover, our results indicate that treatments for connexin-related hearing loss established in rodent models may not be appropriate for human patients, underscoring the importance of testing these treatments in primate models before applying them in human clinical trials. Full article
(This article belongs to the Special Issue Current Genetic Insights in Organ Development)
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15 pages, 4951 KiB  
Article
MiR-92 Family Members Form a Cluster Required for Notochord Tubulogenesis in Urochordate Ciona savignyi
by Libo Yang, Xiaoming Zhang, Chengzhang Liu, Jin Zhang and Bo Dong
Genes 2021, 12(3), 406; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12030406 - 12 Mar 2021
Cited by 2 | Viewed by 2045
Abstract
MicroRNAs are frequently clustered in the genome and polycistronically transcribed, regulating targeted genes in diverse signaling pathways. The miR-17-92 cluster is a typical miRNA cluster, playing crucial roles in the organogenesis and homeostasis of physiological processes in vertebrates. Here, we identified three miRNAs [...] Read more.
MicroRNAs are frequently clustered in the genome and polycistronically transcribed, regulating targeted genes in diverse signaling pathways. The miR-17-92 cluster is a typical miRNA cluster, playing crucial roles in the organogenesis and homeostasis of physiological processes in vertebrates. Here, we identified three miRNAs (csa-miR-92a, csa-miR-92b, and csa-miR-92c) that belonged to the miR-92 family and formed a miRNA cluster in the genome of a urochordate marine ascidian Ciona savignyi. Except for miR-92a and miR-92b, other homologs of the vertebrate miR-17-92 cluster members could not be identified in the Ciona genome. We further found that the mature sequences of urochordate miR-92 family members were highly conserved compared with the vertebrate species. The expression pattern revealed that three miR-92 family members had consistent expression levels in adult tissues and were predominantly expressed in heart and muscle tissue. We further showed that, at the embryonic and larval stages, csa-miR-92c was expressed in the notochord of embryos during 18–31 h post fertilization (hpf) by in situ hybridization. Knockout of csa-miR-92c resulted in the disorganization of notochord cells and the block of lumen coalescence in the notochord. Fibroblast growth factor (FGF), mitogen-activated protein kinase (MAPK), and wingless/integrated (Wnt)/planar cell polarity (PCP) signaling pathways might be involved in the regulatory processes, since a large number of core genes of these pathways were the predicted target genes of the miR-92 family. Taken together, we identified a miR-92 cluster in urochordate Ciona and revealed the expression patterns and the regulatory roles of its members in organogenesis. Our results provide expression and phylogenetic data on the understanding of the miR-92 miRNA cluster’s function during evolution. Full article
(This article belongs to the Special Issue Current Genetic Insights in Organ Development)
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Review

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18 pages, 1062 KiB  
Review
Current Epigenetic Insights in Kidney Development
by Katrina Chan and Xiaogang Li
Genes 2021, 12(8), 1281; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12081281 - 21 Aug 2021
Cited by 5 | Viewed by 5451
Abstract
The kidney is among the best characterized developing tissues, with the genes and signaling pathways that regulate embryonic and adult kidney patterning and development having been extensively identified. It is now widely understood that DNA methylation and histone modification patterns are imprinted during [...] Read more.
The kidney is among the best characterized developing tissues, with the genes and signaling pathways that regulate embryonic and adult kidney patterning and development having been extensively identified. It is now widely understood that DNA methylation and histone modification patterns are imprinted during embryonic development and must be maintained in adult cells for appropriate gene transcription and phenotypic stability. A compelling question then is how these epigenetic mechanisms play a role in kidney development. In this review, we describe the major genes and pathways that have been linked to epigenetic mechanisms in kidney development. We also discuss recent applications of single-cell RNA sequencing (scRNA-seq) techniques in the study of kidney development. Additionally, we summarize the techniques of single-cell epigenomics, which can potentially be used to characterize epigenomes at single-cell resolution in embryonic and adult kidneys. The combination of scRNA-seq and single-cell epigenomics will help facilitate the further understanding of early cell lineage specification at the level of epigenetic modifications in embryonic and adult kidney development, which may also be used to investigate epigenetic mechanisms in kidney diseases. Full article
(This article belongs to the Special Issue Current Genetic Insights in Organ Development)
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Other

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16 pages, 9919 KiB  
Case Report
Skeletal Deformities in Osterix-Cre;Tgfbr2f/f Mice May Cause Postnatal Death
by Kara Corps, Monica Stanwick, Juliann Rectenwald, Andrew Kruggel and Sarah B. Peters
Genes 2021, 12(7), 975; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12070975 - 25 Jun 2021
Cited by 5 | Viewed by 2536
Abstract
Transforming growth factor β (TGFβ) signaling plays an important role in skeletal development. We previously demonstrated that the loss of TGFβ receptor II (Tgfbr2) in Osterix-Cre-expressing mesenchyme results in defects in bones and teeth due to reduced proliferation and differentiation in pre-osteoblasts and [...] Read more.
Transforming growth factor β (TGFβ) signaling plays an important role in skeletal development. We previously demonstrated that the loss of TGFβ receptor II (Tgfbr2) in Osterix-Cre-expressing mesenchyme results in defects in bones and teeth due to reduced proliferation and differentiation in pre-osteoblasts and pre-odontoblasts. These Osterix-Cre;Tgfbr2f/f mice typically die within approximately four weeks for unknown reasons. To investigate the cause of death, we performed extensive pathological analysis on Osterix-Cre- (Cre-), Osterix-Cre+;Tgfbr2f/wt (HET), and Osterix-Cre+;Tgfbr2f/f (CKO) mice. We also crossed Osterix-Cre mice with the ROSA26mTmG reporter line to identify potential off-target Cre expression. The findings recapitulated published skeletal and tooth abnormalities and revealed previously unreported osteochondral dysplasia throughout both the appendicular and axial skeletons in the CKO mice, including the calvaria. Alterations to the nasal area and teeth suggest a potentially reduced capacity to sense and process food, while off-target Cre expression in the gastrointestinal tract may indicate an inability to absorb nutrients. Additionally, altered nasal passages and unexplained changes in diaphragmatic muscle support the possibility of hypoxia. We conclude that these mice likely died due to a combination of breathing difficulties, malnutrition, and starvation resulting primarily from skeletal deformities that decreased their ability to sense, gather, and process food. Full article
(This article belongs to the Special Issue Current Genetic Insights in Organ Development)
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