Survival assays using Caenorhabditis elegans

Park, Hae‐Eun H.; Jung, Yoonji; Lee, Seung-Jae

doi:10.14348/molcells.2017.0017

Cited by 124 publications

(104 citation statements)

References 88 publications

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“…Number of surviving worms are scored every 24 or 48 hours till all worms are dead. To prevent confusion with progeny, the initial worms are transferred every two days or NGM plates are constituted with fluorodeoxyuridine (FUDR) to prevent eggs from hatching (Chen et al, 2015; Park et al, 2017). The impact of modification of RLS genes in C. elegans on lifespan can be evaluated in the absence or presence of cofounders such as Mn toxicity.…”

Section: Elegans Methods For Rls Studymentioning

confidence: 99%

Caenorhabditis elegans and its applicability to studies on restless legs syndrome

Chen

Ijomone

Lee

et al. 2019

Pharmacology of Restless Legs Syndrome (RLS)

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Restless legs syndrome (RLS) is a common neurological disorder in the US. This disorder is characterized by an irresistible urge to move the legs, although the symptoms vary in a wide range. The pathobiology of RLS has been linked to iron (Fe) deficiency and dopaminergic (DAergic) dysfunction. Several genetic factors have been reported to increase the risk of RLS. Caenorhabditis elegans (C. elegans) is a well-established animal model with a fully sequenced genome, which is highly conserved with mammals. Given the detailed knowledge of its genomic architecture, ease of genetic manipulation and conserved biosynthetic and metabolic pathways, as well as its small size, ease of maintenance, speedy generation time and large brood size, C. elegans provides numerous advantages in studying RLS-associated gene-environment interactions. Here we will review current knowledge about RLS symptoms, pathology and treatments, and discuss the application of C. elegans in RLS study, including the worm homologous genes and methods that could be performed to advance the pathophysiology RLS.

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Section: Elegans Methods For Rls Studymentioning

confidence: 99%

Caenorhabditis elegans and its applicability to studies on restless legs syndrome

Chen

Ijomone

Lee

et al. 2019

Pharmacology of Restless Legs Syndrome (RLS)

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“…Survival curves were performed as previously described [42]. Briefly, we prepared special NGM plates each containing 330 μl of 150 mM FUDR (Sigma Life Sciences, Darmstadt, Germany).…”

Section: Methodsmentioning

confidence: 99%

Consecutive signaling pathways are activated in progression of Duchenne muscular dystrophy inC. elegans

Geissel

Steber

Newbern³

et al. 2019

Preprint

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23Background: Duchenne muscular dystrophy (DMD) is a lethal, X-linked disease 24 characterized by progressive muscle degeneration. The condition is driven by nonsense 25 and missense mutations in the dystrophin gene, but the resulting changes in muscle-26 specific gene expression that take place in dystrophin's absence remain uncharacterized, 27 as they are potentially obscured by the chronic inflammation elicited by muscle damage in 28 humans. C. elegans possess a mild inflammatory response that allows for the 29 characterization of the transcriptome rearrangements affecting disease progression 30 independently of inflammation. 31Results: In effort to better understand these dynamics we have isolated and sequenced 32 body muscle-specific transcriptomes from C. elegans lacking functional dystrophin at 33 distinct stages of disease progression. We have identified two consecutively altered gene 34 networks, which are also disrupted in the dystrophin deficient mdx mouse model. We 35 found an upregulation of genes involved in mitochondrial function early in disease 36 progression, and an upregulation of genes related to muscle fibre repair in later stages. 37 This suggests that dystrophin may have a signaling role early in development, and its 38 absence may activate compensatory mechanisms that counteract muscle degradation 39 caused by loss of dystrophin. We have also developed a temperature-based screening 40 method for synthetic paralysis that can be used to rapidly identify genetic partners of 41 dystrophin. 42 Conclusions: Our results allow for the comprehensive identification of transcriptome 43 rearrangements that potentially serve as independent drivers of disease progression and 44 may in turn allow for the identification of new therapeutic targets for the treatment of DMD. 45 BACKGROUND 46 47Duchenne muscular dystrophy (DMD) is an X-linked, recessive disease caused by 48 out of frame mutations in the dystrophin gene [1]. The dystrophin gene codes for a 49 structural protein found beneath the sarcolemma, where it is anchored both to the 50 dystrophin glycoprotein complex (DGC) and cytoskeletal actin, thus stabilizing the protein 51 complex and the integrity of the cell membrane [2]. In humans, the absence of functional 52 dystrophin results in progressive degeneration of the skeletal and cardiac muscles. The 53 hallmark symptoms of DMD extend beyond muscle degeneration to include respiratory 54 failure, cardiomyopathy, and pseudohypertrophy. The condition remains the most 55 commonly diagnosed type of muscular dystrophy, affecting approximately 1 in 3,500 male 56 births globally. 57 While the role of dystrophin in forming a physical connection between the 58 extracellular matrix (ECM) and cytoskeleton has been well characterized [3], a 59 comprehensive molecular definition of dystrophin's function is not fully understood. 60 Vertebrate models of DMD include the mdx mouse [4] and the golden retriever muscular 61 dystrophy canine [5]. Both models have contributed significantly towar...

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“…The life span assay protocol described by [37] was slightly modified, where we age synchronized worms by timed egg laying on a plate for 2-3 hrs. Worms were then transferred to newly prepared NGM plates with heat-killed [38]…”

Section: Life Span Assaymentioning

confidence: 99%

Loss of intermediate filament IFB-1 reduces mobility, density and physiological function of mitochondria in C. elegans sensory neurons

Chang

Shanmugam

Bhan

et al. 2019

Preprint

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Mitochondria and intermediate filaments (IF) accumulations often occur duringimbalanced axonal transport leading to various types of neurodegenerative diseases. It is still poorly understood whether a link between neuronal IFs and mitochondrial mobility exist. In C. elegans, among the 11 cytoplasmic IF family proteins, IFB-1 is of particular interest as it is expressed in a subset of sensory neurons and forms an obligate heteropolymer with one of the essential IFA proteins critical for worm viability. Depletion of IFB-1 leads to dye-filling and chemotaxis defects as well as reduced life span. Axons grew shorter during development and mitochondria transport is slowed down leading to reduced densities of these organelles in neurons. Oxygen consumption and mitochondrial membrane potential is measurably reduced in worms carrying mutations in the ifb-1 gene. Membrane potential also seemed to play a role in transport such as after FCCP treatment increased directional switching of mitochondria are observed. Mitochondria colocalize with IFB-1 in worm neurons and appear in a complex with IFB-1 in pull-down assays. In summary, we propose a model in which neuronal intermediate filaments may serve as transient anchor points for mitochondria during their microtubule-based long-range transport in neurons.

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Survival assays using Caenorhabditis elegans

Cited by 124 publications

References 88 publications

Caenorhabditis elegans and its applicability to studies on restless legs syndrome

Caenorhabditis elegans and its applicability to studies on restless legs syndrome

Consecutive signaling pathways are activated in progression of Duchenne muscular dystrophy inC. elegans

Loss of intermediate filament IFB-1 reduces mobility, density and physiological function of mitochondria in C. elegans sensory neurons

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