Expression profile of Caenorhabditis elegans mutant for the Werner syndrome gene ortholog reveals the impact of vitamin C on development to increase life span

Dallaire, Alexandra; Proulx, Sophie; Simard, Martin J.; Lebel, Michel

doi:10.1186/1471-2164-15-940

Cited by 18 publications

(17 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The established antioxidant role of vitamin C1849, has not been really proven when it comes to C. elegans 50. This is partially due to conflicting reports about its impact on C. elegans lifespan375152. Our results contribute to this discussion, showing for the first time that when offered concurrently with the oxidative factor, it can lead to abolishing OS implications.…”

Section: Discussionmentioning

confidence: 74%

Chemically induced oxidative stress affects ASH neuronal function and behavior in C. elegans

Gourgou

Chronis

2016

Sci Rep

View full text Add to dashboard Cite

Oxidative stress (OS) impact on a single neuron’s function in vivo remains obscure. Using C. elegans as a model organism, we report the effect of paraquat (PQ)-induced OS on wild type worms on the function of the ASH polymodal neuron. By calcium (Ca2+) imaging, we quantified ASH activation upon stimulus delivery. PQ-treated worms displayed higher maximum depolarization (peak of the Ca2+ transients) compared to untreated animals. PQ had a similar effect on the ASH neuron response time (rising slope of the Ca2+ transients), except in very young worms. OS effect on ASH was partially abolished in vitamin C-treated worms. We performed octanol and osmotic avoidance tests, to investigate the OS effect on ASH-dependent behaviors. PQ-treated worms have enhanced avoidance behavior compared to untreated ones, suggesting that elevated ASH Ca2+ transients result in enhanced ASH-mediated behavior. The above findings suggest a possible hormetic effect of PQ, as a factor inducing mild oxidative stress. We also quantified locomotion parameters (velocity, bending amplitude), which are not mediated by ASH activation. Bending amplitude did not differ significantly between treated and untreated worms; velocity in older adults decreased. The differential effect of OS on behavioral patterns may mirror a selective impact on the organism’s neurons.

show abstract

Section: Discussionmentioning

confidence: 74%

Chemically induced oxidative stress affects ASH neuronal function and behavior in C. elegans

Gourgou

Chronis

2016

Sci Rep

View full text Add to dashboard Cite

show abstract

“…AA modified the expression of genes involved in locomotion and development of the anatomical structure. Conversely, in the wild-type worms, AA only influenced the biological process of proteolysis [ 32 ].…”

Section: Ascorbic Acid and The Aging Process: In Vitro Modelsmentioning

confidence: 99%

Vitamin C, Aging and Alzheimer’s Disease

et al. 2017

View full text Add to dashboard Cite

Accumulating evidence in mice models of accelerated senescence indicates a rescuing role of ascorbic acid in premature aging. Supplementation of ascorbic acid appeared to halt cell growth, oxidative stress, telomere attrition, disorganization of chromatin, and excessive secretion of inflammatory factors, and extend lifespan. Interestingly, ascorbic acid (AA) was also found to positively modulate inflamm-aging and immunosenescence, two hallmarks of biological aging. Moreover, ascorbic acid has been shown to epigenetically regulate genome integrity and stability, indicating a key role of targeted nutrition in healthy aging. Growing in vivo evidence supports the role of ascorbic acid in ameliorating factors linked to Alzheimer’s disease (AD) pathogenesis, although evidence in humans yielded equivocal results. The neuroprotective role of ascorbic acid not only relies on the general free radical trapping, but also on the suppression of pro-inflammatory genes, mitigating neuroinflammation, on the chelation of iron, copper, and zinc, and on the suppression of amyloid-beta peptide (Aβ) fibrillogenesis. Epidemiological evidence linking diet, one of the most important modifiable lifestyle factors, and risk of Alzheimer's disease is rapidly increasing. Thus, dietary interventions, as a way to epigenetically modulate the human genome, may play a role in the prevention of AD. The present review is aimed at providing an up to date overview of the main biological mechanisms that are associated with ascorbic acid supplementation/bioavailability in the process of aging and Alzheimer’s disease. In addition, we will address new fields of research and future directions.

show abstract

“…RNA sequences used to identify editing sites were generated for this study and obtained from Hillier et al (2009), Mangone et al (2010), Wu et al (2011), Kim et al (2013), Schmeisser et al (2013a,b), Dallaire et al (2014), Grün et al (2014), Stoeckius et al (2014), and Weimer et al (2014). All reads were trimmed to 50 nt, and identical reads were merged.…”

Section: Rna Editing Sites Identificationmentioning

confidence: 99%

A-to-I RNA editing promotes developmental stage–specific gene and lncRNA expression

et al. 2016

View full text Add to dashboard Cite

A-to-I RNA editing is a conserved widespread phenomenon in which adenosine (A) is converted to inosine (I) by adenosine deaminases (ADARs) in double-stranded RNA regions, mainly noncoding. Mutations in ADAR enzymes in cause defects in normal development but are not lethal as in human and mouse. Previous studies in indicated competition between RNA interference (RNAi) and RNA editing mechanisms, based on the observation that worms that lack both mechanisms do not exhibit defects, in contrast to the developmental defects observed when only RNA editing is absent. To study the effects of RNA editing on gene expression and function, we established a novel screen that enabled us to identify thousands of RNA editing sites in nonrepetitive regions in the genome. These include dozens of genes that are edited at their 3' UTR region. We found that these genes are mainly germline and neuronal genes, and that they are down-regulated in the absence of ADAR enzymes. Moreover, we discovered that almost half of these genes are edited in a developmental-specific manner, indicating that RNA editing is a highly regulated process. We found that many pseudogenes and other lncRNAs are also extensively down-regulated in the absence of ADARs in the embryo but not in the fourth larval (L4) stage. This down-regulation is not observed upon additional knockout of RNAi. Furthermore, levels of siRNAs aligned to pseudogenes in ADAR mutants are enhanced. Taken together, our results suggest a role for RNA editing in normal growth and development by regulating silencing via RNAi.

show abstract

Expression profile of Caenorhabditis elegans mutant for the Werner syndrome gene ortholog reveals the impact of vitamin C on development to increase life span

Cited by 18 publications

References 43 publications

Chemically induced oxidative stress affects ASH neuronal function and behavior in C. elegans

Chemically induced oxidative stress affects ASH neuronal function and behavior in C. elegans

Vitamin C, Aging and Alzheimer’s Disease

A-to-I RNA editing promotes developmental stage–specific gene and lncRNA expression

Contact Info

Product

Resources

About