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Updated: May 22, 2026

A Facile Protocol to Generate Site-Specifically Acetylated Proteins in Escherichia Coli
11:08

A Facile Protocol to Generate Site-Specifically Acetylated Proteins in Escherichia Coli

Published on: December 9, 2017

Acetylated mitochondrial MDH2 regulates CTR2 transcription to induce cuproptosis during Escherichia coli infection

Hao Wang1, Peng Xiao2, Liping Chen3

  • 1College of Food Science and Technology, Yunnan Agricultural University, Kunming, China.

Nature Communications
|May 20, 2026
PubMed

Insights

Pathogenic Escherichia coli triggers a specific cell death pathway called cuproptosis by disrupting copper balance. Inhibiting this process reduces infection-related liver damage, revealing a new therapeutic target.

Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogenesis

Background:

  • Pathogenic bacteria often manipulate host cell death pathways for survival, but mechanisms are unclear.
  • Understanding bacterial manipulation of host cell death is crucial for developing new treatments.

Purpose of the Study:

  • To elucidate the mechanism by which pathogenic Escherichia coli (E. coli) manipulates host cell death.
  • To investigate the role of copper homeostasis and cuproptosis in E. coli infection.

Main Methods:

  • Investigated E. coli's effect on copper homeostasis and cell death pathways.
  • Analyzed the role of copper transporter CTR2 and mitochondrial malate dehydrogenase 2 (MDH2).
  • Examined the gut-LPS-liver axis in infection models.

Main Results:

  • E. coli upregulates CTR2, disrupting copper homeostasis and inducing cuproptosis.
  • Lipopolysaccharide (LPS) activates cuproptosis hallmarks via the gut-LPS-liver axis during infection.
  • MDH2 acts as a transcriptional regulator for CTR2 expression and metabolic reprogramming.
  • Inhibiting cuproptosis significantly reduced infection-induced liver damage.

Conclusions:

  • E. coli utilizes cuproptosis as a mechanism to promote pathogenesis.
  • Targeting cuproptosis offers a potential therapeutic strategy against E. coli infections.
  • Modulating metal-dependent cell death pathways is a promising approach for treating bacterial infections.

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