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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
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Related Experiment Video

Updated: Jul 10, 2026

Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans
09:18

Quantifying Tissue-Specific Proteostatic Decline in Caenorhabditis elegans

Published on: September 7, 2021

Proteostasis Rebalancing by LET-607 Deficiency Promotes Longevity.

Haixiang Tong1, Wei Li1, Pangui Yuan1

  • 1School of Life Sciences, Chongqing University, Chongqing, China.

Aging Cell
|July 9, 2026
PubMed
Summary
This summary is machine-generated.

Aging disrupts proteostasis, requiring coordinated subsystem balance. A trade-off between endoplasmic reticulum unfolded protein response (UPRER) and cytosolic UPR (UPRcyto) in C. elegans influences lifespan, with reduced UPRER and increased UPRcyto promoting longevity.

Keywords:
HSF‐1longevityproteostasisunfolded protein response

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Lipid Supplementation for Longevity and Gene Transcriptional Analysis in Caenorhabditis elegans
07:25

Lipid Supplementation for Longevity and Gene Transcriptional Analysis in Caenorhabditis elegans

Published on: December 9, 2022

Area of Science:

  • Cellular Biology
  • Aging Research
  • Genetics

Background:

  • Proteostasis, the maintenance of protein homeostasis, is crucial for cellular function and declines with age.
  • Cellular resources are finite, necessitating trade-offs between different proteostatic pathways.
  • The principles governing the coordination of proteostatic subsystems and potential trade-offs remain incompletely understood.

Purpose of the Study:

  • To investigate the interplay between the endoplasmic reticulum unfolded protein response (UPRER) and the cytosolic unfolded protein response (UPRcyto) in C. elegans.
  • To determine the role of the transcription factor LET-607 in regulating this proteostatic balance.
  • To explore the impact of this balance on lifespan and aging.

Main Methods:

  • Utilized C. elegans as a model organism.
  • Measured UPRER and UPRcyto activity in wild-type and LET-607 deficient animals.
  • Investigated the molecular mechanisms linking LET-607, the one-carbon cycle, histone modifications, and UPR activation.
  • Assessed lifespan in genetically modified strains.

Main Results:

  • Wild-type C. elegans maintain a balance of high UPRER and low UPRcyto activity, enforced by LET-607.
  • LET-607 deficiency disrupts this balance, leading to decreased UPRER and increased UPRcyto activity.
  • LET-607 deficient animals exhibit extended lifespan, dependent on UPRcyto activation.
  • LET-607 deficiency downregulates the one-carbon cycle, reducing S-adenosylmethionine levels and alleviating H3K9me-mediated repression of UPRcyto genes.

Conclusions:

  • A novel transcriptional mechanism enforces a proteostatic trade-off between UPRER and UPRcyto.
  • The evolutionarily conserved UPR balance in wild-type animals is suboptimal for maximizing lifespan.
  • This finding supports the antagonistic pleiotropy theory of aging, suggesting that traits beneficial for reproduction may be detrimental to longevity.