Copper-induced germline apoptosis in Caenorhabditis elegans: The independent roles of DNA damage response signaling and the dependent roles of MAPK cascades

2009 ◽  
Vol 180 (2) ◽  
pp. 151-157 ◽  
Author(s):  
Shunchang Wang ◽  
Lijun Wu ◽  
Yun Wang ◽  
Xun Luo ◽  
Yun Lu
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Dna Damage Response ◽  
Mapk Cascades ◽  
Damage Response

scholarly journals Bisphenol A exposure triggers apoptosis via three signaling pathways in Caenorhabditis elegans

RSC Advances ◽  
2017 ◽  
Vol 7 (52) ◽  
pp. 32624-32631 ◽  
Author(s):  
Yun Wang ◽  
Lianfeng Zhang ◽  
Xun Luo ◽  
Shunchang Wang ◽  
Yuanyuan Wang
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Growth Factor ◽  
Bisphenol A ◽  
Signaling Pathways ◽  
Dna Damage Response ◽  
Mitogen Activated Protein Kinase ◽  
Mapk Cascades ◽  
Damage Response ◽  
Mitogen Activated Protein

Bisphenol A can trigger germline apoptosis via three signaling pathways including DNA damage response (DDR) pathway, mitogen-activated protein kinase (MAPK) cascades and insulin-like growth factor-1 (IGF-1) network in Caenorhabditis elegans.

scholarly journals A simple answer to complex questions: Caenorhabditis elegans as an experimental model for examining the DNA damage response and disease genes

2017 ◽  
Vol 233 (4) ◽  
pp. 2781-2790 ◽  
Author(s):  
Matthias Rieckher ◽  
Arturo Bujarrabal ◽  
Markus A. Doll ◽  
Najmeh Soltanmohammadi ◽  
Björn Schumacher
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Experimental Model ◽  
Dna Damage Response ◽  
Disease Genes ◽  
Damage Response

Altered DNA damage response in Caenorhabditis elegans with impaired poly(ADP-ribose) glycohydrolases genes expression

DNA Repair ◽  
2007 ◽  
Vol 6 (3) ◽  
pp. 329-343 ◽  
Author(s):  
Jean-François St-Laurent ◽  
Steve N. Gagnon ◽  
Florence Dequen ◽  
Isabelle Hardy ◽  
Serge Desnoyers
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Dna Damage Response ◽  
Genes Expression ◽  
Damage Response

scholarly journals Checkpoint silencing during the DNA damage response in Caenorhabditis elegans embryos

2007 ◽  
Vol 178 (5) ◽  
pp. 887-887
Author(s):  
Antonia H. Holway ◽  
Seung-Hwan Kim ◽  
Adriana La Volpe ◽  
W. Matthew Michael
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Dna Damage Response ◽  
Damage Response

scholarly journals Small RNA-mediated genomic silencing promotes telomere stability in the absence of telomerase

2018 ◽  
Author(s):  
Charlie Longtine ◽  
Stephen Frenk ◽  
Shawn Ahmed
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Dna Damage Response ◽  
Small Rna ◽  
Small Rnas ◽  
Argonaute Protein ◽  
Heterochromatin Formation ◽  
Damage Response ◽  
The Stability ◽  
Telomere Erosion

AbstractTelomerase deficiency in human somatic cells results in telomere erosion and senescence. Small RNAs that target telomeres have been observed in diverse organisms but their functions are not well characterized. We define an endogenous small RNA pathway in Caenorhabditis elegans that promotes heterochromatin formation at telomeres via Dicer, the perinuclear Argonaute protein WAGO-1 and the nuclear Argonaute protein HRDE-1. Loss of telomerase induces biogenesis of siRNAs that target the telomeric lncRNA TERRA, whereas loss of both telomerase and small RNA-mediated telomeric silencing induces TERRA expression, DNA damage, and an accelerated sterility phenotype. These phenotypes can be rescued by exogenous telomeric siRNAs or by loss of the DNA damage response protein EXO-1. Thus, endogenous siRNAs interact with TERRA to promote heterochromatin formation in a manner that is critical for the stability of naturally eroding telomeres. We propose that small RNA-mediated genome silencing could be broadly relevant to regulation of proliferative aging.

scholarly journals Effects of Manganese on Genomic Integrity in the Multicellular Model Organism Caenorhabditis elegans

2021 ◽  
Vol 22 (20) ◽  
pp. 10905
Author(s):  
Merle M. Nicolai ◽  
Ann-Kathrin Weishaupt ◽  
Jessica Baesler ◽  
Vanessa Brinkmann ◽  
Anna Wellenberg ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Dna Damage Response ◽  
Excision Repair ◽  
Model Organism ◽  
Neurological Dysfunction ◽  
Genomic Integrity ◽  
Mn Toxicity ◽  
Damage Response

Although manganese (Mn) is an essential trace element, overexposure is associated with Mn-induced toxicity and neurological dysfunction. Even though Mn-induced oxidative stress is discussed extensively, neither the underlying mechanisms of the potential consequences of Mn-induced oxidative stress on DNA damage and DNA repair, nor the possibly resulting toxicity are characterized yet. In this study, we use the model organism Caenorhabditis elegans to investigate the mode of action of Mn toxicity, focusing on genomic integrity by means of DNA damage and DNA damage response. Experiments were conducted to analyze Mn bioavailability, lethality, and induction of DNA damage. Different deletion mutant strains were then used to investigate the role of base excision repair (BER) and dePARylation (DNA damage response) proteins in Mn-induced toxicity. The results indicate a dose- and time-dependent uptake of Mn, resulting in increased lethality. Excessive exposure to Mn decreases genomic integrity and activates BER. Altogether, this study characterizes the consequences of Mn exposure on genomic integrity and therefore broadens the molecular understanding of pathways underlying Mn-induced toxicity. Additionally, studying the basal poly(ADP-ribosylation) (PARylation) of worms lacking poly(ADP-ribose) glycohydrolase (PARG) parg-1 or parg-2 (two orthologue of PARG), indicates that parg-1 accounts for most of the glycohydrolase activity in worms.

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