scholarly journals A Measurable Increase in Oxidative Damage Due to Reduction in Superoxide Detoxification Fails to Shorten the Life Span of Long-Lived Mitochondrial Mutants of Caenorhabditis elegans

Genetics ◽  
2007 ◽  
Vol 177 (4) ◽  
pp. 2063-2074 ◽  
Author(s):  
Wen Yang ◽  
Jingjing Li ◽  
Siegfried Hekimi
Keyword(s):  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Life Span

scholarly journals Increased life span from overexpression of superoxide dismutase in Caenorhabditis elegans is not caused by decreased oxidative damage

2011 ◽  
Vol 51 (8) ◽  
pp. 1575-1582 ◽  
Author(s):  
Filipe Cabreiro ◽  
Daniel Ackerman ◽  
Ryan Doonan ◽  
Caroline Araiz ◽  
Patricia Back ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Life Span

scholarly journals Proteostasis collapse is a driver of cell aging and death

2019 ◽  
Vol 116 (44) ◽  
pp. 22173-22178 ◽  
Author(s):  
Mantu Santra ◽  
Ken A. Dill ◽  
Adam M. R. de Graff
Keyword(s):  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Life Span ◽  
Protein Function ◽  
Tipping Point ◽  
Cell Aging ◽  
Molecular Processes ◽  
Increased Temperature ◽  
Oxidant Concentration

What molecular processes drive cell aging and death? Here, we model how proteostasis—i.e., the folding, chaperoning, and maintenance of protein function—collapses with age from slowed translation and cumulative oxidative damage. Irreparably damaged proteins accumulate with age, increasingly distracting the chaperones from folding the healthy proteins the cell needs. The tipping point to death occurs when replenishing good proteins no longer keeps up with depletion from misfolding, aggregation, and damage. The model agrees with experiments in the worm Caenorhabditis elegans that show the following: Life span shortens nonlinearly with increased temperature or added oxidant concentration, and life span increases in mutants having more chaperones or proteasomes. It predicts observed increases in cellular oxidative damage with age and provides a mechanism for the Gompertz-like rise in mortality observed in humans and other organisms. Overall, the model shows how the instability of proteins sets the rate at which damage accumulates with age and upends a cell’s normal proteostasis balance.

scholarly journals Caenorhabditis elegans Genes Affecting Interindividual Variation in Life-span Biomarker Gene Expression

2017 ◽  
Vol 72 (10) ◽  
pp. 1305-1310 ◽  
Author(s):  
Alexander Mendenhall ◽  
Matthew M Crane ◽  
Patricia M Tedesco ◽  
Thomas E Johnson ◽  
Roger Brent
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Life Span ◽  
Interindividual Variation

scholarly journals Genetic, Behavioral and Environmental Determinants of Male Longevity in Caenorhabditis elegans

Genetics ◽  
2000 ◽  
Vol 154 (4) ◽  
pp. 1597-1610 ◽  
Author(s):  
David Gems ◽  
Donald L Riddle
Keyword(s):  
Caenorhabditis Elegans ◽  
Life Span ◽  
Wild Type ◽  
Neuronal Function ◽  
Nematode Caenorhabditis Elegans ◽  
Wild Isolate ◽  
Young Males ◽  
C Elegans ◽  
Single Sex ◽  
Solitary Males

Abstract Males of the nematode Caenorhabditis elegans are shorter lived than hermaphrodites when maintained in single-sex groups. We observed that groups of young males form clumps and that solitary males live longer, indicating that male-male interactions reduce life span. By contrast, grouped or isolated hermaphrodites exhibited the same longevity. In one wild isolate of C. elegans, AB2, there was evidence of copulation between males. Nine uncoordinated (unc) mutations were used to block clumping behavior. These mutations had little effect on hermaphrodite life span in most cases, yet many increased male longevity even beyond that of solitary wild-type males. In one case, the neuronal function mutant unc-64(e246), hermaphrodite life span was also increased by up to 60%. The longevity of unc-4(e120), unc-13(e51), and unc-32(e189) males exceeded that of hermaphrodites by 70–120%. This difference appears to reflect a difference in sex-specific life span potential revealed in the absence of male behavior that is detrimental to survival. The greater longevity of males appears not to be affected by daf-2, but is influenced by daf-16. In the absence of male-male interactions, median (but not maximum) male life span was variable. This variability was reduced when dead bacteria were used as food. Maintenance on dead bacteria extended both male and hermaphrodite longevity.

Knock-down of transcription factor skinhead-1 exacerbates arsenite-induced oxidative damage in Caenorhabditis elegans

BioMetals ◽  
2021 ◽  
Author(s):  
Yijie Mao ◽  
Ling Yao ◽  
Xuejun Jiang ◽  
Golamaully Sumayyah ◽  
Zhen Zou ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Knock Down
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