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Cells
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Caenorhabditis elegans: Cell Biology and Physiology
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Caenorhabditis elegans: Cell Biology and Physiology

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

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 8695

Special Issue Editors

Prof. Dr. Shangbang Gao

E-Mail Website
Guest Editor
College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China
Interests: neuronal circuit; motor neuron disease; electrophysiology; molecular biology; Caenorhabditis elegans
Dr. Zhitao Hu

E-Mail Website
Guest Editor
Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4072, Australia
Interests: synapses; neurotransmitter release; behavioral plasticity; Caenorhabditis elegans

Special Issue Information

Dear Colleagues,

Even though a nematode worm is significantly anatomically simpler than a human, Caenorhabditis elegans does share essential similarities at the molecular level with human and mammals, making it a good candidate for a model organism. Compared to the other model animals, Caenorhabditis elegans is easy to feed, manipulate, and maintain. In particular, research into Caenorhabditis elegans is cost effective and has obvious advantages in many aspects. Caenorhabditis elegans is used to study neural development and the function of the neuronal circuit. It is well suited for this application due to the availability of a comprehensive connectivity map and only 302 neurons and ~7000 synapses. Its transparent body makes it possible to observe the fate and probed fluorescence of individual cells using simple microscopy, or more advanced techniques such as super-resolution microscopy and EM. Worms have a very short life cycle and grow in large numbers, allowing for a large genetic screen for mutants that are critical for the life process. Caenorhabditis elegans has also been broadly used in drug screening for human neuropsychiatric disorders. Moreover, Caenorhabditis elegans is a highly important model to study ageing processes because the organism passes through several distinct phases of life, which can be observed physiologically and genetically throughout their 2-week lifespan. Hence, this Special Issue is expected to provide a collection of cutting-edge research and systemic reviews in a diverse array of topics, including physiology, neurobiology, cell development, behavior, aging, ecology, gene regulation, and the disease model by using the model animal Caenorhabditis elegans.

Topics of interests include, but are not limited to, the following:

  • The molecular mechanism for synapse and neuronal development.
  • The neural circuit mechanism for behavior.
  • Transcriptional and post-transcriptional gene regulation.
  • Intracellular signaling, organelles, and cell polarity.
  • Regeneration and degeneration.
  • Epigenetics and genome organization.
  • The metabolism, stress, lifespan, and aging.
  • The advanced interdisciplinary technique and its methods.

Prof. Dr. Shangbang Gao
Dr. Zhitao Hu
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. 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.

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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15 pages, 16114 KiB  
Article
C. elegans Hemidesmosomes Sense Collagen Damage to Trigger Innate Immune Response in the Epidermis
by Yi Zhu, Wenna Li, Yifang Dong, Chujie Xia and Rong Fu
Cells 2023, 12(18), 2223; https://doi.org/10.3390/cells12182223 - 6 Sep 2023
Cited by 3 | Viewed by 2355
Abstract
The collagens are an enormous family of extracellular matrix proteins that play dominant roles in cell adhesion, migration and tissue remodeling under many physiological and pathological conditions. However, their function mechanisms in regulating innate immunity remain largely undiscovered. Here we use C. elegans [...] Read more.
The collagens are an enormous family of extracellular matrix proteins that play dominant roles in cell adhesion, migration and tissue remodeling under many physiological and pathological conditions. However, their function mechanisms in regulating innate immunity remain largely undiscovered. Here we use C. elegans epidermis as the model to address this question. The C. elegans epidermis is covered with a collagen-rich cuticle exoskeleton and can produce antimicrobial peptides (AMPs) against invading pathogens or physical injury. Through an RNAi screen against collagen-encoding genes, we found that except the previously reported six DPY collagens and the BLI-1 collagen, the majority of collagens tested appear unable to trigger epidermal immune defense when damaged. Further investigation suggests that the six DPY collagens form a specific substructure, which regulates the interaction between BLI-1 and the hemidesmosome receptor MUP-4. The separation of BLI-1 with MUP-4 caused by collagen damage leads to the detachment of the STAT transcription factor-like protein STA-2 from hemidesmosomes and the induction of AMPs. Our findings uncover the mechanism how collagens are organized into a damage sensor and how the epidermis senses collagen damage to mount an immune defense. Full article
(This article belongs to the Special Issue Caenorhabditis elegans: Cell Biology and Physiology)
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23 pages, 3938 KiB  
Article
Calcineurin-Dependent Homeostatic Response of C. elegans Muscle Cells upon Prolonged Activation of Acetylcholine Receptors
by Franklin Florin, Benjamin Bonneau, Luis Briseño-Roa, Jean-Louis Bessereau and Maëlle Jospin
Cells 2023, 12(17), 2201; https://doi.org/10.3390/cells12172201 - 3 Sep 2023
Cited by 2 | Viewed by 2106
Abstract
Pharmacological adaptation is a common phenomenon observed during prolonged drug exposure and often leads to drug resistance. Understanding the cellular events involved in adaptation could provide new strategies to circumvent this resistance issue. We used the nematode Caenorhabditis elegans to analyze the adaptation [...] Read more.
Pharmacological adaptation is a common phenomenon observed during prolonged drug exposure and often leads to drug resistance. Understanding the cellular events involved in adaptation could provide new strategies to circumvent this resistance issue. We used the nematode Caenorhabditis elegans to analyze the adaptation to levamisole, an ionotropic acetylcholine receptor agonist, used for decades to treat nematode parasitic infections. Genetic screens in C. elegans identified “adapting mutants” that initially paralyze upon exposure to levamisole as the wild type (WT), but recover locomotion after a few hours whereas WT remain paralyzed. Here, we show that levamisole induces a sustained increase in cytosolic calcium concentration in the muscle cells of adapting mutants, lasting several hours and preceding a decrease in levamisole-sensitive acetylcholine receptors (L-AChR) at the muscle plasma membrane. This decrease correlated with a drop in calcium concentration, a relaxation of the animal’s body and a resumption of locomotion. The decrease in calcium and L-AChR content depends on calcineurin activation in muscle cells. We also showed that levamisole adaptation triggers homeostatic mechanisms in muscle cells including mitochondria remodeling, lysosomal tubulation and an increase in autophagic activity. Levamisole adaptation thus provides a new experimental paradigm for studying how cells cope with calcium stress. Full article
(This article belongs to the Special Issue Caenorhabditis elegans: Cell Biology and Physiology)
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Review

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18 pages, 804 KiB  
Review
Amyotrophic Lateral Sclerosis Mechanism: Insights from the Caenorhabditis elegans Models
by Lili Chen, Shumei Zhang, Sai Liu and Shangbang Gao
Cells 2024, 13(1), 99; https://doi.org/10.3390/cells13010099 - 3 Jan 2024
Cited by 1 | Viewed by 3475
Abstract
Amyotrophic Lateral Sclerosis (ALS) is a debilitating neurodegenerative condition characterized by the progressive degeneration of motor neurons. Despite extensive research in various model animals, the cellular signal mechanisms of ALS remain elusive, impeding the development of efficacious treatments. Among these models, a well-characterized [...] Read more.
Amyotrophic Lateral Sclerosis (ALS) is a debilitating neurodegenerative condition characterized by the progressive degeneration of motor neurons. Despite extensive research in various model animals, the cellular signal mechanisms of ALS remain elusive, impeding the development of efficacious treatments. Among these models, a well-characterized and diminutive organism, Caenorhabditis elegans (C. elegans), has emerged as a potent tool for investigating the molecular and cellular dimensions of ALS pathogenesis. This review summarizes the contributions of C. elegans models to our comprehension of ALS, emphasizing pivotal findings pertaining to genetics, protein aggregation, cellular pathways, and potential therapeutic strategies. We analyze both the merits and constraints of the C. elegans system in the realm of ALS research and point towards future investigations that could bridge the chasm between C. elegans foundational discoveries and clinical applications. Full article
(This article belongs to the Special Issue Caenorhabditis elegans: Cell Biology and Physiology)
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