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Related Concept Videos

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Related Experiment Video

Updated: Jan 27, 2026

Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
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Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses

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Targeted interplay between bacterial pathogens and host autophagy.

Padhmanand Sudhakar1,2,3, Anne-Claire Jacomin4, Isabelle Hautefort1

  • 1a Earlham Institute, Norwich Research Park , Norwich , UK.

Autophagy
|March 27, 2019
PubMed
Summary
This summary is machine-generated.

Pathogens subvert autophagy, a key defense mechanism. This study reveals how bacteria target host autophagy receptors and modulate its processes, uncovering genus-specific interactions and potential host defense strategies against infection.

Keywords:
AutophagyCALCOCO2/NDP52MAP1LC3/LC3MAP1LC3/LC3-interacting region motifSQSTM1/p62bacterial regulation of hostinterplaymicrobiotapathogen recognition

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Area of Science:

  • Cellular Biology
  • Microbiology
  • Immunology

Background:

  • Autophagy plays a critical role in clearing pathogens, but many bacteria have evolved mechanisms to evade or manipulate this cellular process.
  • A systems-level understanding of how host autophagy receptors selectively target bacterial proteins and how pathogens modulate autophagy remains incomplete.

Purpose of the Study:

  • To predict and analyze interactions between human autophagy proteins and effector proteins from 56 pathogenic bacterial species.
  • To identify bacterial proteins that can modulate core autophagy components and understand pathogen-specific autophagy modulation patterns.

Main Methods:

  • Predicted potential interactions using recognition motifs for selective autophagy receptors (SQSTM1/p62, CALCOCO2/NDP52, MAP1LC3/LC3).
  • Employed structure-based interaction prediction to identify bacterial proteins affecting core autophagy.
  • Experimentally confirmed the interplay between *Salmonella* protease YhjJ and autophagy.

Main Results:

  • Autophagy receptors generally target genus-specific bacterial proteins, with observed complementarity between SQSTM1/p62 and CALCOCO2/NDP52 targets across multiple pathogens.
  • Outer membrane vesicles from *Bacillus* species indicated selective targeting of pathogenic over non-pathogenic proteins.
  • Identified pathogen-specific patterns of autophagy modulation and bacterial proteins that are both modulators and targets of autophagy.

Conclusions:

  • Bacterial pathogens employ diverse strategies to subvert host autophagy, involving genus-specific targeting and modulation of autophagy pathways.
  • Complementarity in autophagy receptor targeting may influence host susceptibility to chronic infections.
  • Understanding these host-pathogen interactions at a systems level provides insights into host defense mechanisms and potential therapeutic targets.