Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.7
2.7
Journals
JDB
Special Issues
Caenorhabditis elegans – a Model for Understanding Development and Disease
share announcement

Caenorhabditis elegans – a Model for Understanding Development and Disease

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

Deadline for manuscript submissions: closed (20 November 2023) | Viewed by 13042

Special Issue Editors

Dr. Ann K. Corsi

E-Mail Website
Guest Editor
Professor, Biology Department, The Catholic University of America, Washington, DC 20064, USA
Interests: transcriptional regulation; mesoderm development; bHLH factors; modeling patient mutations in C. elegans
Dr. Andy Golden

E-Mail Website
Guest Editor
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), Bethesda, MD, USA
Interests: C. elegans; disease gene orthologs; modeling rare diseases

Special Issue Information

Dear Colleagues,

In the intervening time since Sydney Brenner published his seminal paper on isolating the first Caenorhabditis elegans mutants, this tiny nematode has greatly contributed to our understanding of eukaryotic biology. As a classic model organism, the worm’s rapid development, ease of genetic manipulation, and molecular toolbox have revealed many similarities to cellular development in more complicated metazoans. Further, with the advent of CRISPR/Cas9 genome editing it has become possible to use reporter genes that are expressed at physiological levels due to insertion into endogenous genes of interest and, importantly, to more closely mimic the pathology of human diseases by making genomic mutations that take advantage of the amino acid conservation shared between many proteins in humans and C. elegans.

In this Special Issue, we will highlight the many ways C. elegans continues to advance our understanding of development and disease with original research and up-to-date reviews, including a primer directed at general audiences, particularly students, for using C. elegans to understand mechanisms of human disease pathology. We plan to emphasize examples of how human genetic diseases can be modeled in C. elegans. Characterization of mutant phenotypes at the cellular and molecular levels can help to identify the role conserved genes play in cell biology and development. Modifier screens can then be performed to learn more about a given biological process and possibly identify potential targets for future therapies in humans.

We welcome your contributions and look forward to highlighting your work.

Dr. Ann K. Corsi
Dr. Andy Golden
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. 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.

Keywords

  • genetic approaches
  • disease modeling
  • C. elegans development
  • gene editing
  • model organism

Published Papers (6 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review, Other

12 pages, 2696 KiB  
Article
The New Nematicide Cyclobutrifluram Targets the Mitochondrial Succinate Dehydrogenase Complex in Caenorhabditis elegans
by Fariba Heydari, David Rodriguez-Crespo and Chantal Wicky
J. Dev. Biol. 2023, 11(4), 39; https://doi.org/10.3390/jdb11040039 - 19 Oct 2023
Viewed by 2019
Abstract
Today, agriculture around the world is challenged by parasitic nematode infections. Plant-parasitic nematodes (PPNs) can cause significant damage and crop loss and are a threat to food security. For a long time, the management of PPN infection has relied on nematicides that impact [...] Read more.
Today, agriculture around the world is challenged by parasitic nematode infections. Plant-parasitic nematodes (PPNs) can cause significant damage and crop loss and are a threat to food security. For a long time, the management of PPN infection has relied on nematicides that impact not only parasitic nematodes but also other organisms. More recently, new nematicides have been developed that appear to specifically target PPN. Cyclobutrifluram belongs to this new category of nematicides. Using the nematode Caenorhabditis elegans as a model organism, we show here that cyclobutrifluram strongly impacts the survival and fertility rates of the worm by decreasing the number of germ cells. Furthermore, using a genetic approach, we demonstrate that cyclobutrifluram functions by inhibiting the mitochondrial succinate dehydrogenase (SDH) complex. Transcriptomic analysis revealed a strong response to cyclobutrifluram exposure. Among the deregulated genes, we found genes coding for detoxifying proteins, such as cytochrome P450s and UDP-glucuronosyl transferases (UGTs). Overall, our study contributes to the understanding of the molecular mode of action of cyclobutrifluram, to the finding of new approaches against nematicide resistance, and to the discovery of novel nematicides. Furthermore, this study confirms that C. elegans is a suitable model organism to study the mode of action of nematicides. Full article
(This article belongs to the Special Issue Caenorhabditis elegans – a Model for Understanding Development and Disease)
►▼ Show Figures

Figure 1

23 pages, 5207 KiB  
Article
Attenuation of Dopaminergic Neurodegeneration in a C. elegans Parkinson’s Model through Regulation of Xanthine Dehydrogenase (XDH-1) Expression by the RNA Editase, ADR-2
by Lindsey A. Starr, Luke E. McKay, Kylie N. Peter, Lena M. Seyfarth, Laura A. Berkowitz, Kim A. Caldwell and Guy A. Caldwell
J. Dev. Biol. 2023, 11(2), 20; https://doi.org/10.3390/jdb11020020 - 22 May 2023
Cited by 1 | Viewed by 2162
Abstract
Differential RNA editing by adenosine deaminases that act on RNA (ADARs) has been implicated in several neurological disorders, including Parkinson’s disease (PD). Here, we report results of a RNAi screen of genes differentially regulated in adr-2 mutants, normally encoding the only catalytically active [...] Read more.
Differential RNA editing by adenosine deaminases that act on RNA (ADARs) has been implicated in several neurological disorders, including Parkinson’s disease (PD). Here, we report results of a RNAi screen of genes differentially regulated in adr-2 mutants, normally encoding the only catalytically active ADAR in Caenorhabditis elegans, ADR-2. Subsequent analysis of candidate genes that alter the misfolding of human α-synuclein (α-syn) and dopaminergic neurodegeneration, two PD pathologies, reveal that reduced expression of xdh-1, the ortholog of human xanthine dehydrogenase (XDH), is protective against α-synuclein-induced dopaminergic neurodegeneration. Further, RNAi experiments show that WHT-2, the worm ortholog of the human ABCG2 transporter and a predicted interactor of XDH-1, is the rate-limiting factor in the ADR-2, XDH-1, WHT-2 system for dopaminergic neuroprotection. In silico structural modeling of WHT-2 indicates that the editing of one nucleotide in the wht-2 mRNA leads to the substitution of threonine with alanine at residue 124 in the WHT-2 protein, changing hydrogen bonds in this region. Thus, we propose a model where wht-2 is edited by ADR-2, which promotes optimal export of uric acid, a known substrate of WHT-2 and a product of XDH-1 activity. In the absence of editing, uric acid export is limited, provoking a reduction in xdh-1 transcription to limit uric acid production and maintain cellular homeostasis. As a result, elevation of uric acid is protective against dopaminergic neuronal cell death. In turn, increased levels of uric acid are associated with a decrease in ROS production. Further, downregulation of xdh-1 is protective against PD pathologies because decreased levels of XDH-1 correlate to a concomitant reduction in xanthine oxidase (XO), the form of the protein whose by-product is superoxide anion. These data indicate that modifying specific targets of RNA editing may represent a promising therapeutic strategy for PD. Full article
(This article belongs to the Special Issue Caenorhabditis elegans – a Model for Understanding Development and Disease)
►▼ Show Figures

Graphical abstract

16 pages, 8984 KiB  
Article
Reproductive-Toxicity-Related Endpoints in C. elegans Are Consistent with Reduced Concern for Dimethylarsinic Acid Exposure Relative to Inorganic Arsenic
by Jessica A. Camacho, Bonnie Welch, Robert L. Sprando and Piper R. Hunt
J. Dev. Biol. 2023, 11(2), 18; https://doi.org/10.3390/jdb11020018 - 26 Apr 2023
Cited by 1 | Viewed by 2091
Abstract
Exposures to arsenic and mercury are known to pose significant threats to human health; however, the effects specific to organic vs. inorganic forms are not fully understood. Caenorhabditis elegans’ (C. elegans) transparent cuticle, along with the conservation of key genetic pathways [...] Read more.
Exposures to arsenic and mercury are known to pose significant threats to human health; however, the effects specific to organic vs. inorganic forms are not fully understood. Caenorhabditis elegans’ (C. elegans) transparent cuticle, along with the conservation of key genetic pathways regulating developmental and reproductive toxicology (DART)-related processes such as germ stem cell renewal and differentiation, meiosis, and embryonic tissue differentiation and growth, support this model’s potential to address the need for quicker and more dependable testing methods for DART hazard identification. Organic and inorganic forms of mercury and arsenic had different effects on reproductive-related endpoints in C. elegans, with methylmercury (meHgCl) having effects at lower concentrations than mercury chloride (HgCl2), and sodium arsenite (NaAsO2) having effects at lower concentrations than dimethylarsinic acid (DMA). Progeny to adult ratio changes and germline apoptosis were seen at concentrations that also affected gravid adult gross morphology. For both forms of arsenic tested, germline histone regulation was altered at concentrations below those that affected progeny/adult ratios, while concentrations for these two endpoints were similar for the mercury compounds. These C. elegans findings are consistent with corresponding mammalian data, where available, suggesting that small animal model test systems may help to fill critical data gaps by contributing to weight of evidence assessments. Full article
(This article belongs to the Special Issue Caenorhabditis elegans – a Model for Understanding Development and Disease)
►▼ Show Figures

Figure 1

Review

Jump to: Research, Other

12 pages, 1346 KiB  
Review
Identifying Molecular Roadblocks for Transcription Factor-Induced Cellular Reprogramming In Vivo by Using C. elegans as a Model Organism
by Ismail Özcan and Baris Tursun
J. Dev. Biol. 2023, 11(3), 37; https://doi.org/10.3390/jdb11030037 - 31 Aug 2023
Viewed by 1494
Abstract
Generating specialized cell types via cellular transcription factor (TF)-mediated reprogramming has gained high interest in regenerative medicine due to its therapeutic potential to repair tissues and organs damaged by diseases or trauma. Organ dysfunction or improper tissue functioning might be restored by producing [...] Read more.
Generating specialized cell types via cellular transcription factor (TF)-mediated reprogramming has gained high interest in regenerative medicine due to its therapeutic potential to repair tissues and organs damaged by diseases or trauma. Organ dysfunction or improper tissue functioning might be restored by producing functional cells via direct reprogramming, also known as transdifferentiation. Regeneration by converting the identity of available cells in vivo to the desired cell fate could be a strategy for future cell replacement therapies. However, the generation of specific cell types via reprogramming is often restricted due to cell fate-safeguarding mechanisms that limit or even block the reprogramming of the starting cell type. Nevertheless, efficient reprogramming to generate homogeneous cell populations with the required cell type’s proper molecular and functional identity is critical. Incomplete reprogramming will lack therapeutic potential and can be detrimental as partially reprogrammed cells may acquire undesired properties and develop into tumors. Identifying and evaluating molecular barriers will improve reprogramming efficiency to reliably establish the target cell identity. In this review, we summarize how using the nematode C. elegans as an in vivo model organism identified molecular barriers of TF-mediated reprogramming. Notably, many identified molecular factors have a high degree of conservation and were subsequently shown to block TF-induced reprogramming of mammalian cells. Full article
(This article belongs to the Special Issue Caenorhabditis elegans – a Model for Understanding Development and Disease)
►▼ Show Figures

Figure 1

22 pages, 3415 KiB  
Review
An Emerging Animal Model for Querying the Role of Whole Genome Duplication in Development, Evolution, and Disease
by Mara Schvarzstein, Fatema Alam, Muhammad Toure and Judith L. Yanowitz
J. Dev. Biol. 2023, 11(2), 26; https://doi.org/10.3390/jdb11020026 - 06 Jun 2023
Viewed by 2722
Abstract
Whole genome duplication (WGD) or polyploidization can occur at the cellular, tissue, and organismal levels. At the cellular level, tetraploidization has been proposed as a driver of aneuploidy and genome instability and correlates strongly with cancer progression, metastasis, and the development of drug [...] Read more.
Whole genome duplication (WGD) or polyploidization can occur at the cellular, tissue, and organismal levels. At the cellular level, tetraploidization has been proposed as a driver of aneuploidy and genome instability and correlates strongly with cancer progression, metastasis, and the development of drug resistance. WGD is also a key developmental strategy for regulating cell size, metabolism, and cellular function. In specific tissues, WGD is involved in normal development (e.g., organogenesis), tissue homeostasis, wound healing, and regeneration. At the organismal level, WGD propels evolutionary processes such as adaptation, speciation, and crop domestication. An essential strategy to further our understanding of the mechanisms promoting WGD and its effects is to compare isogenic strains that differ only in their ploidy. Caenorhabditis elegans (C. elegans) is emerging as an animal model for these comparisons, in part because relatively stable and fertile tetraploid strains can be produced rapidly from nearly any diploid strain. Here, we review the use of Caenorhabditis polyploids as tools to understand important developmental processes (e.g., sex determination, dosage compensation, and allometric relationships) and cellular processes (e.g., cell cycle regulation and chromosome dynamics during meiosis). We also discuss how the unique characteristics of the C. elegans WGD model will enable significant advances in our understanding of the mechanisms of polyploidization and its role in development and disease. Full article
(This article belongs to the Special Issue Caenorhabditis elegans – a Model for Understanding Development and Disease)
►▼ Show Figures

Figure 1

Other

Jump to: Research, Review

10 pages, 1543 KiB  
Obituary
Andy Golden: Mentorship through the Years
by Anna K. Allen, Xiaofei Bai, Edward S. Davis, Amy Fabritius, Aimee Jaramillo-Lambert, Peter A. Kropp, Christopher T. Richie, Jill M. Schumacher, Sanjay Shrestha, Kathryn Stein and Ann K. Corsi
J. Dev. Biol. 2023, 11(4), 41; https://doi.org/10.3390/jdb11040041 - 03 Nov 2023
Viewed by 1585
Abstract
The C [...] Full article
(This article belongs to the Special Issue Caenorhabditis elegans – a Model for Understanding Development and Disease)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-6
Back to TopTop