Identification of the redox-stress signaling threshold (RST): Increased RST helps to delay aging in C. elegans

2021 ◽  
Author(s):  
Jiao Meng ◽  
Zhenyu Lv ◽  
Yuanyuan Wang ◽  
Chang Chen
Keyword(s):  
Stress Signaling ◽  
Redox Stress ◽  
C Elegans

scholarly journals Glycosylation of KEAP 1 links nutrient sensing to redox stress signaling

2017 ◽  
Vol 36 (15) ◽  
pp. 2233-2250 ◽  
Author(s):  
Po‐Han Chen ◽  
Timothy J Smith ◽  
Jianli Wu ◽  
Priscila F Siesser ◽  
Brittany J Bisnett ◽  
...  
Keyword(s):  
Nutrient Sensing ◽  
Stress Signaling ◽  
Redox Stress

scholarly journals Elevated mitochondria-coupled NAD(P)H in endoplasmic reticulum of dopamine neurons

2016 ◽  
Vol 27 (21) ◽  
pp. 3214-3220 ◽  
Author(s):  
Kristal R. Tucker ◽  
Samantha L. Cavolo ◽  
Edwin S. Levitan
Keyword(s):  
Endoplasmic Reticulum ◽  
Brain Slice ◽  
Multiphoton Microscopy ◽  
Dopamine Neurons ◽  
Stress Signaling ◽  
Pyridine Nucleotides ◽  
Redox Stress ◽  
Mitochondrial Mass ◽  
Transport Chain ◽  
Redox Coenzymes

Pyridine nucleotides are redox coenzymes that are critical in bioenergetics, metabolism, and neurodegeneration. Here we use brain slice multiphoton microscopy to show that substantia nigra dopamine neurons, which are sensitive to stress in mitochondria and the endoplasmic reticulum (ER), display elevated combined NADH and NADPH (i.e., NAD(P)H) autofluorescence. Despite limited mitochondrial mass, organellar NAD(P)H is extensive because much of the signal is derived from the ER. Remarkably, even though pyridine nucleotides cannot cross mitochondrial and ER membranes, inhibiting mitochondrial function with an uncoupler or interrupting the electron transport chain with cyanide (CN−) alters ER NAD(P)H. The ER CN− response can occur without a change in nuclear NAD(P)H, raising the possibility of redox shuttling via the cytoplasm locally between neuronal mitochondria and the ER. We propose that coregulation of NAD(P)H in dopamine neuron mitochondria and ER coordinates cell redox stress signaling by the two organelles.

Fitness Trade-Offs and Environmentally Induced Mutation Buffering in Isogenic C. elegans

Science ◽  
2011 ◽  
Vol 335 (6064) ◽  
pp. 82-85 ◽  
Author(s):  
M. Olivia Casanueva ◽  
Alejandro Burga ◽  
Ben Lehner
Keyword(s):  
Stress Resistance ◽  
Reproductive Fitness ◽  
Stress Signaling ◽  
Bet Hedging ◽  
Hedging Strategy ◽  
Induced Mutation ◽  
C Elegans ◽  
Trade Offs ◽  
Environmental Responses ◽  
Unpredictable Environment

Mutations often have consequences that vary across individuals. Here, we show that the stimulation of a stress response can reduce mutation penetrance in Caenorhabditis elegans. Moreover, this induced mutation buffering varies across isogenic individuals because of interindividual differences in stress signaling. This variation has important consequences in wild-type animals, producing some individuals with higher stress resistance but lower reproductive fitness and other individuals with lower stress resistance and higher reproductive fitness. This may be beneficial in an unpredictable environment, acting as a “bet-hedging” strategy to diversify risk. These results illustrate how transient environmental stimuli can induce protection against mutations, how environmental responses can underlie variable mutation buffering, and how a fitness trade-off may make variation in stress signaling advantageous.

scholarly journals N6-adenosine methylation of ribosomal RNA affects lipid oxidation and stress resistance

2020 ◽  
Vol 6 (17) ◽  
pp. eaaz4370 ◽  
Author(s):  
Noa Liberman ◽  
Zach K. O’Brown ◽  
Andrew Scott Earl ◽  
Konstantinos Boulias ◽  
Maxim V. Gerashchenko ◽  
...  
Keyword(s):  
Ribosomal Rna ◽  
Stress Resistance ◽  
Dietary Supplementation ◽  
Stress Sensitivity ◽  
Stress Signaling ◽  
Omega 3 ◽  
C Elegans ◽  
Selective Translation ◽  
Specific Mrnas ◽  
Global Translation

During stress, global translation is reduced, but specific transcripts are actively translated. How stress-responsive mRNAs are selectively translated is unknown. We show that METL-5 methylates adenosine 1717 on 18S ribosomal RNA in C. elegans, enhancing selective ribosomal binding and translation of specific mRNAs. One of these mRNAs, CYP-29A3, oxidizes the omega-3 polyunsaturated fatty acid eicosapentaenoic acid to eicosanoids, key stress signaling molecules. While metl-5–deficient animals grow normally under homeostatic conditions, they are resistant to a variety of stresses. metl-5 mutant worms also show reduced bioactive lipid eicosanoids and dietary supplementation of eicosanoid products of CYP-29A3 restores stress sensitivity of metl-5 mutant worms. Thus, methylation of a specific residue of 18S rRNA by METL-5 selectively enhances translation of cyp-29A3 to increase production of eicosanoids, and blocking this pathway increases stress resistance. This study suggests that ribosome methylation can facilitate selective translation, providing another layer of regulation of the stress response.

scholarly journals A role for TSPO in mitochondrial Ca2+ homeostasis and redox stress signaling

2017 ◽  
Vol 8 (6) ◽  
pp. e2896-e2896 ◽  
Author(s):  
Jemma Gatliff ◽  
Daniel A East ◽  
Aarti Singh ◽  
Maria Soledad Alvarez ◽  
Michele Frison ◽  
...  
Keyword(s):  
Stress Signaling ◽  
Redox Stress

scholarly journals Ye Tian: Surveilling stress to live longer

2021 ◽  
Vol 220 (10) ◽  
Author(s):  
Lucia Morgado-Palacin
Keyword(s):  
Signaling Pathways ◽  
Model System ◽  
Stress Signaling ◽  
Mitochondrial Stress ◽  
C Elegans

Ye Tian investigates how mitochondrial stress signaling pathways regulate longevity using C. elegans as a model system.

The glycomes of Caenorhabditis elegans and other model organisms

2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell
Keyword(s):  
Caenorhabditis Elegans ◽  
Current Knowledge ◽  
Structural Data ◽  
Model Organisms ◽  
Entire Genome ◽  
C Elegans ◽  
The Face ◽  
Area Of Concern ◽  
Nematode Worm

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.

How do histone modifications contribute to transgenerational epigenetic inheritance in C. elegans?

2020 ◽  
Vol 48 (3) ◽  
pp. 1019-1034 ◽  
Author(s):  
Rachel M. Woodhouse ◽  
Alyson Ashe
Keyword(s):  
Histone Modifications ◽  
Molecular Mechanisms ◽  
Epigenetic Inheritance ◽  
Nematode Caenorhabditis Elegans ◽  
Histone Methyltransferases ◽  
Transgenerational Epigenetic Inheritance ◽  
C Elegans ◽  
Recent Developments ◽  
Gene Regulatory

Gene regulatory information can be inherited between generations in a phenomenon termed transgenerational epigenetic inheritance (TEI). While examples of TEI in many animals accumulate, the nematode Caenorhabditis elegans has proven particularly useful in investigating the underlying molecular mechanisms of this phenomenon. In C. elegans and other animals, the modification of histone proteins has emerged as a potential carrier and effector of transgenerational epigenetic information. In this review, we explore the contribution of histone modifications to TEI in C. elegans. We describe the role of repressive histone marks, histone methyltransferases, and associated chromatin factors in heritable gene silencing, and discuss recent developments and unanswered questions in how these factors integrate with other known TEI mechanisms. We also review the transgenerational effects of the manipulation of histone modifications on germline health and longevity.

Centrosome Aurora A gradient ensures single polarity axis in C. elegans embryos

2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak
Keyword(s):  
Symmetry Breaking ◽  
Cell Fate ◽  
Cell Cortex ◽  
Axis Formation ◽  
Aurora A Kinase ◽  
Aurora A ◽  
C Elegans ◽  
Cell Embryo ◽  
Polarity Establishment

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.

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