scholarly journals Precoce and opposite response of proteasome activity after acute or chronic exposure of C. elegans to γ-radiation

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Cécile Dubois ◽  
Catherine Lecomte ◽  
Sébastien Pyr dit Ruys ◽  
Mira Kuzmic ◽  
Claire Della-Vedova ◽  
...  
Keyword(s):  
Chronic Exposure ◽  
Proteasome Activity ◽  
Γ Radiation ◽  
C Elegans ◽  
Opposite Response

MUTAGENESIS IN CAENORHABDITIS ELEGANS. II. A SPECTRUM OF MUTATIONAL EVENTS INDUCED WITH 1500 R OF γ-RADIATION

Genetics ◽  
1985 ◽  
Vol 109 (3) ◽  
pp. 493-511
Author(s):  
Raja E Rosenbluth ◽  
Cheryl Cuddeford ◽  
David L Baillie
Keyword(s):  
Dose Response ◽  
Response Curve ◽  
Chromosomal Rearrangements ◽  
Γ Radiation ◽  
Recessive Lethal ◽  
C Elegans ◽  
Chromosome Breaks ◽  
Additional Chromosome ◽  
Γ Ray ◽  
Do So

ABSTRACT We previously established a γ-ray dose-response curve for recessive lethal events (lethals) captured over the eT1 balancer. In this paper we analyze the nature of lethal events produced, with a frequency of 0.04 per eT1 region, at a dose of 1500 r. To do so, we developed a protocol that, in the absence of cytogenetics, allows balanced lethals to be analyzed for associated chromosomal rearrangements. A set of 35 lethal strains was chosen for the analysis. Although the dosage was relatively low, a large number of multiple-break events were observed. The fraction of lethals associated with rearrangements was found to be 0.76. Currently most X- and γ-ray dosages used for mutagenesis in C. elegans are 6000-8000 r. From our data we conservatively estimated that 43% of rearrangements induced with 8000 r would be accompanied by additional chromosome breaks in the genome. With 1500 r the value was 5%.—The 35 lethals studied were derived from 875 screened F1's. Among these lethals there were (1) at least two unc-36 duplications, (2) at least four translocations, (3) at least six deficiencies of chromosome V (these delete about 90% of the unc-60 to unc-42 region) and (4) several unanalyzed rearrangements. Thus, it is possible to recover desired rearrangements at reasonable rates with a dose of only 1500 r.—We suggest that the levels of ionizing radiation employed in most published C. elegans studies are excessive and efforts should be made to use reduced levels in the future.

Induction of minisatellite mutations in the mouse germline by low-dose chronic exposure to γ-radiation and fission neutrons

2000 ◽  
Vol 453 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Yuri E. Dubrova ◽  
Mark Plumb ◽  
Julia Brown ◽  
Emma Boulton ◽  
Dudley Goodhead ◽  
...  
Keyword(s):  
Chronic Exposure ◽  
Low Dose ◽  
Γ Radiation ◽  
Fission Neutrons

scholarly journals Royalactin induces copious longevity via increased translation and proteasome activity in C. elegans

2018 ◽  
Author(s):  
Giel Detienne ◽  
Pieter Van de Walle ◽  
Wouter De Haes ◽  
Bram Cockx ◽  
Bart P. Braeckman ◽  
...  
Keyword(s):  
Protein Turnover ◽  
Life History Traits ◽  
Protein Translation ◽  
Proteasome Activity ◽  
C Elegans ◽  
Defensive Responses ◽  
Trade Offs ◽  
Growth Factor Signalling ◽  
Epidermal Growth ◽  
Growth Pathway

AbstractAs demonstrated in various animal models, organismal longevity can be achieved via interventions that at the mechanistic level could be considered to entail ‘defensive’ responses: most long-lived mutants focus on somatic maintenance, while reducing growth pathway signalling and protein translation and turnover. We here provide evidence that the opposite mechanism can also lead to longevity and improved health.We report on the mode of action of royalactin, a glycoprotein activator of epidermal growth factor signalling, capable of extending lifespan in several animals. We show that in Caenorhabditis elegans, royalactin-induced longevity depends on increased protein translation and entails increased proteasome activity. We propose the term ‘copious longevity’ to describe this newly-elucidated mechanism. In contrast to what is true for many other lifespan-extending interventions, we observed no obvious trade-offs between royalactin-induced longevity and several life history traits. Our data point towards increased protein turnover to support healthy ageing, and provide a means for future comparative studies of defensive vs. copious mechanisms.

scholarly journals Protein homeostasis is maintained by proteasomes containing PSMB9 induced by EEF1A2 upon mitochondrial stress

2021 ◽  
Author(s):  
Minji Kim ◽  
Lukasz Samluk ◽  
Tomasz Maciej Stępkowski ◽  
Ida Suppanz ◽  
Remigiusz Adam Serwa ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Elongation Factor ◽  
Small Heat Shock Protein ◽  
Therapeutic Strategies ◽  
Proteasome Activity ◽  
Protein Homeostasis ◽  
Translation Elongation Factor ◽  
Translation Elongation ◽  
C Elegans ◽  
Age Related

Perturbed proteostasis and mitochondrial dysfunction are often associated with age-related diseases such as Alzheimer′s and Parkinson′s diseases. However, the link between them remains incompletely understood. Mitochondrial dysfunction causes proteostasis imbalance, and cells respond to restore proteostasis by increasing proteasome activity and molecular chaperons in yeast and C. elegans. Here, we demonstrate the presence of similar responses in humans. Mitochondrial dysfunction upregulates a small heat shock protein HSPB1 and an immunoproteasome subunit PSMB9 leading to an increase in proteasome activity. HSPB1 and PSMB9 are required to prevent protein aggregation upon mitochondrial dysfunction. Moreover, PSMB9 expression is dependent on a translation elongation factor EEF1A2, and PSMB9-containing proteasomes are located near mitochondria, enabling fast local degradation of aberrant proteins. Our findings put a step forward in understanding the stress response triggered by mitochondrial dysfunction, and may be useful for therapeutic strategies to prevent or delay the onset of age-related diseases and attenuate their progression.

Development of apical pits in chloride cells of the gills of Pimephales promelas after chronic exposure to acid water

1983 ◽  
Vol 41 ◽  
pp. 462-463
Author(s):  
Richard L. Leino ◽  
Jon G. Anderson ◽  
J. Howard McCormick
Keyword(s):  
Confidence Interval ◽  
Chronic Exposure ◽  
Lake Superior ◽  
Pimephales Promelas ◽  
Chloride Cells ◽  
Fathead Minnows ◽  
Secondary Lamellae ◽  
Untreated Water ◽  
Water Ph ◽  
Flow Through

Groups of 12 fathead minnows were exposed for 129 days to Lake Superior water acidified (pH 5.0, 5.5, 6.0 or 6.5) with reagent grade H2SO4 by means of a multichannel toxicant system for flow-through bioassays. Untreated water (pH 7.5) had the following properties: hardness 45.3 ± 0.3 (95% confidence interval) mg/1 as CaCO3; alkalinity 42.6 ± 0.2 mg/1; Cl- 0.03 meq/1; Na+ 0.05 meq/1; K+ 0.01 meq/1; Ca2+ 0.68 meq/1; Mg2+ 0.26 meq/1; dissolved O2 5.8 ± 0.3 mg/1; free CO2 3.2 ± 0.4 mg/1; T= 24.3 ± 0.1°C. The 1st, 2nd and 3rd gills were subsequently processed for LM (methacrylate), TEM and SEM respectively.Three changes involving chloride cells were correlated with increasing acidity: 1) the appearance of apical pits (figs. 2,5 as compared to figs. 1, 3,4) in chloride cells (about 22% of the chloride cells had pits at pH 5.0); 2) increases in their numbers and 3) increases in the % of these cells in the epithelium of the secondary lamellae.

The Effect of Vitamin A on the Intermittent Nitrogen Dioxide Gas Exposure in Hamsters

1976 ◽  
Vol 34 ◽  
pp. 176-177
Author(s):  
J.C.S. Kim ◽  
M.G. Jourden ◽  
E.S. Carlisle
Keyword(s):  
Electron Microscopy ◽  
Vitamin A ◽  
Nitrogen Dioxide ◽  
Chronic Exposure ◽  
Light And Electron Microscopy ◽  
Specific Effect ◽  
Deficient Diet ◽  
Intermittent Exposure ◽  
Hypovitaminosis A ◽  
Gas Exposure

Chronic exposure to nitrogen dioxide in rodents has shown that injury reaches a maximum after 24 hours, and a reparative adaptive phase follows (1). Damage occurring in the terminal bronchioles and proximal portions of the alveolar ducts in rats has been extensively studied by both light and electron microscopy (1).The present study was undertaken to compare the response of lung tissue to intermittent exposure to 10 ppm of nitrogen dioxide gas for 4 hours per week, while the hamsters were on a vitamin A deficient diet. Ultrastructural observations made from lung tissues obtained from non-gas exposed, hypovitaminosis A animals and gas exposed animals fed a regular commercially prepared diet have been compared to elucidate the specific effect of vitamin A on nitrogen dioxide gas exposure. The interaction occurring between vitamin A and nitrogen dioxide gas has not previously been investigated.

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.

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