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Cells
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Caenorhabditis elegans: Model Organism, Endless Possibilities—Volume II
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Caenorhabditis elegans: Model Organism, Endless Possibilities—Volume II

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (15 May 2025) | Viewed by 2562

Special Issue Editor

Dr. Paola Fabrizio

E-Mail Website
Guest Editor
Laboratory of Biology and Modeling of the Cell, Ecole Normale Supérieure de Lyon, 69364 Lyon, France
Interests: genetics of aging; calorie restriction in model organisms C. elegans and S. cerevisiae; role of histone post-translational modifications in stress resistance and lifespan regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following the resounding success of our previous Special Issue titled "Caenorhabditis elegans: A Model Organism, Endless Possibilities," it is with great pleasure that we announce the launch of the second edition of this Special Issue.

Since its introduction as a model organism, Caenorhabditis elegans has continued to captivate researchers worldwide with its remarkable versatility and utility in addressing a myriad of biological questions. From elucidating fundamental cellular processes to modeling human diseases, C. elegans remains at the forefront of scientific inquiry.

Building upon the foundation laid by our inaugural edition, the second edition of this Special Issue aims to showcase the latest advances in cell biology, genetics and genomics research pertaining to C. elegans. We invite contributions that explore a wide range of topics, including, but not limited to the following:

  • Cell division and cell cycle regulation;
  • Organ development and programmed cell death (PCD);
  • Neurobiology and the nervous system;
  • Autophagy, apoptosis and other cellular processes;
  • Innate immunity and host–pathogen interactions;
  • Genetics and epigenetics of aging;
  • elegans as a model for human diseases;
  • Oxidative stress, mitochondrial function and longevity;
  • Genome-wide screens and high-throughput approaches;
  • Expression and function of small RNAs.

We encourage researchers from diverse backgrounds and disciplines to contribute their insights and discoveries to this Special Issue. By collectively exploring the endless possibilities offered by C. elegans, we aim to deepen our understanding of biological mechanisms and inspire future research directions.

We eagerly anticipate your contributions.

Dr. Paola Fabrizio
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

  • Caenorhabditis elegans
  • C. elegans
  • model organism

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Related Special Issue

Published Papers (2 papers)

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16 pages, 3293 KiB  
Article
Loss of γ-aminobutyric acid D-Type Motor Neurons in Young Adult Caenorhabditis elegans Following Exposition with Silica Nanoparticles
by Dang Tri Le, Stella Pauls, Gereon Poschmann, Kai Stühler and Anna von Mikecz
Cells 2025, 14(3), 190; https://doi.org/10.3390/cells14030190 - 27 Jan 2025
Viewed by 1121
Abstract
Although Caenorhabditis elegans is commonly used to assess the neurotoxicity of environmental pollutants, studies that explore the intricate biology of its nervous system, particularly those addressing long-term effects and aging in adult worms, are rare. These models offer significant advantages for understanding the [...] Read more.
Although Caenorhabditis elegans is commonly used to assess the neurotoxicity of environmental pollutants, studies that explore the intricate biology of its nervous system, particularly those addressing long-term effects and aging in adult worms, are rare. These models offer significant advantages for understanding the full spectrum of neurobiological impacts. Here, we investigated the effects of silica nanomaterials on the γ-aminobutyric acid (GABA) neural system in young to middle-aged nematodes and found a unique degeneration pattern characterized by loss of anterior- and posteriormost GABAergic D-type motor neurons. Four-day-old nematodes were identified as a vulnerable age group, where the pollutant-accelerated neurodegeneration that is typically seen in old C. elegans. Proteomics of 4-day-old C. elegans revealed significant alterations of protein abundance, including the downregulation of proteins such as glutamate dehydrogenase (gdh-1) and glutamate oxaloacetate transaminase (got-1.2), which are essentially involved in GABA metabolic pathways. Consistent with these findings, we demonstrated locomotion deficits in C. elegans exposed to nanoscale silica by establishing a semi-automated behavioral arena. Our setup not only visualizes but also automatically quantifies vulnerabilities at the individual worm level. This novel neurodegeneration model now enables the simulation of real-world pollutant mixtures and environmental conditions, capturing the complexity of the exposome. Full article
(This article belongs to the Special Issue Caenorhabditis elegans: Model Organism, Endless Possibilities—Volume II)
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Review

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18 pages, 1136 KiB  
Review
The Roles of Distinct Transcriptional Factors in the Innate Immunity of C. elegans
by Muhammad Irfan Afridi and Haijun Tu
Cells 2025, 14(5), 327; https://doi.org/10.3390/cells14050327 - 21 Feb 2025
Viewed by 878
Abstract
Deleterious molecules or factors produced by pathogens can hinder the normal physiological functioning of organisms. In response to these survival challenges, organisms rely on innate immune signaling as their first line of defense, which regulates immune-responsive genes and antimicrobial peptides to protect against [...] Read more.
Deleterious molecules or factors produced by pathogens can hinder the normal physiological functioning of organisms. In response to these survival challenges, organisms rely on innate immune signaling as their first line of defense, which regulates immune-responsive genes and antimicrobial peptides to protect against pathogenic infections. These genes are under the control of transcription factors, which are known to regulate the transcriptional activity of genes after binding to their regulatory sequences. Previous studies have employed Caenorhabditis elegans as a host–pathogen interaction model to demonstrate the essential role of different transcription factors in the innate immunity of worms. In this review, we summarize the advances made regarding the functioning of distinct transcription factors in the innate immune response upon pathogen infection. Finally, we discuss the open questions in the field, whose resolutions have the potential to expand our understanding of the mechanisms underlying the innate immunity of organisms. Full article
(This article belongs to the Special Issue Caenorhabditis elegans: Model Organism, Endless Possibilities—Volume II)
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