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Related Concept Videos

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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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Related Experiment Video

Updated: Jan 17, 2026

Simultaneous Mapping and Quantitation of Ribonucleotides in Human Mitochondrial DNA
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Simultaneous Mapping and Quantitation of Ribonucleotides in Human Mitochondrial DNA

Published on: November 14, 2017

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Ribonucleotide incorporation into mitochondrial DNA drives inflammation.

Amir Bahat1, Dusanka Milenkovic1, Eileen Cors1

  • 1Max Planck Institute for Biology of Ageing, Cologne, Germany.

Nature
|September 24, 2025
PubMed
Summary
This summary is machine-generated.

Metabolic imbalance causes ribonucleotides to enter mitochondrial DNA (mtDNA), triggering inflammation. Supplying deoxyribonucleosides can reduce this age-related inflammatory response and senescence-associated secretory phenotype (SASP).

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Studying Ribonucleotide Incorporation: Strand-specific Detection of Ribonucleotides in the Yeast Genome and Measuring Ribonucleotide-induced Mutagenesis
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Studying Ribonucleotide Incorporation: Strand-specific Detection of Ribonucleotides in the Yeast Genome and Measuring Ribonucleotide-induced Mutagenesis

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Immunology

Background:

  • Metabolic dysregulation is linked to inflammatory responses.
  • Imbalanced nucleotide synthesis can lead to mitochondrial DNA (mtDNA) release and innate immune activation via cGAS-STING signaling.
  • The precise mechanisms by which nucleotide deficiency drives mtDNA-dependent inflammation remain unclear.

Purpose of the Study:

  • To elucidate how nucleotide deficiency contributes to mtDNA-dependent inflammation.
  • To investigate the role of ribonucleotide misincorporation into mtDNA.
  • To explore the link between nucleotide imbalance, senescence, and the senescence-associated secretory phenotype (SASP).

Main Methods:

  • Analysis of mtDNA in aged mice lacking MGME1 and in aged wild-type mice.
  • Investigation of cells lacking YME1L.
  • Study of cell-cycle-arrested senescent cells.
  • Assessment of mtDNA release, cGAS-STING activation, and SASP.
  • Evaluation of the effects of exogenous deoxyribonucleosides.

Main Results:

  • Nucleotide imbalance increases ribonucleotide incorporation into mtDNA, particularly in age-dependent renal inflammation and in aged tissues.
  • Reduced deoxyribonucleotide synthesis elevates mtDNA ribonucleotide content in senescent cells.
  • This aberrant mtDNA leads to cytosolic release, cGAS-STING activation, and SASP.
  • Exogenous deoxyribonucleosides can suppress the observed SASP.

Conclusions:

  • Mitochondrial DNA is highly sensitive to aberrant ribonucleotide incorporation.
  • Imbalanced nucleotide metabolism drives age- and mtDNA-dependent inflammatory responses.
  • Nucleotide imbalance contributes to the senescence-associated secretory phenotype (SASP).