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The trp operon in Escherichia coli exemplifies a repressible operon. It regulates the synthesis of tryptophan through repressor-mediated transcriptional control and attenuation. This dual regulatory mechanism ensures tryptophan biosynthesis occurs only when needed, conserving cellular resources.Structure of the trp OperonThe trp operon consists of five structural genes (trpE, trpD, trpC, trpB, and trpA) that encode enzymes for tryptophan biosynthesis. These genes are transcribed as a single...
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Related Experiment Video

Updated: Jan 27, 2026

Chemical Dimerization-Induced Protein Condensates on Telomeres
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Telomere Dysfunction Induces Sirtuin Repression that Drives Telomere-Dependent Disease.

Hisayuki Amano1, Arindam Chaudhury2, Cristian Rodriguez-Aguayo3

  • 1Department of Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030, USA; Huffington Center on Aging, Baylor College of Medicine, Houston, TX 77030, USA.

Cell Metabolism
|April 2, 2019
PubMed
Summary

Telomere shortening triggers sirtuin repression via p53, impacting stem cells and aging. NAD+ precursors and Sirt1 activation may mitigate these effects and fibrotic disorders.

Keywords:
liver diseasemetabolismp53sirtuinstelomeres

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Area of Science:

  • Cellular Biology
  • Aging Research
  • Molecular Medicine

Background:

  • Telomere shortening is linked to stem cell dysfunction, fibrosis, and premature aging.
  • The precise molecular mechanisms underlying these telomere-related disorders remain unclear.

Purpose of the Study:

  • To investigate the molecular link between telomere shortening and sirtuin regulation.
  • To explore potential therapeutic strategies for telomere-dependent disorders.

Main Methods:

  • Utilized telomerase knockout mice to study liver telomere shortening.
  • Analyzed p53-dependent regulation of sirtuins via microRNAs and transcriptional pathways.
  • Assessed the effects of nicotinamide mononucleotide (NMN) administration on telomere length, DNA damage response, and liver fibrosis.

Main Results:

  • Telomere shortening in mice livers induced p53-dependent repression of all seven sirtuins.
  • Non-mitochondrial sirtuins were regulated post-transcriptionally by p53 and microRNAs.
  • Mitochondrial sirtuins were regulated transcriptionally via PGC-1α/β.
  • NMN administration maintained telomere length, reduced p53 activity, improved mitochondrial function, and rescued liver fibrosis.

Conclusions:

  • Sirtuins are downstream targets of dysfunctional telomeres.
  • Increasing Sirt1 activity, potentially with other sirtuins, can stabilize telomeres.
  • Targeting sirtuin pathways offers a promising therapeutic approach for telomere-dependent diseases like fibrosis.