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Mimicry of Short Linear Motifs by Bacterial Pathogens: A Drugging Opportunity

Hugo Sámano-Sánchez1, Toby J Gibson2

  • 1Structural and Computational Biology Unit, European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany; Collaboration for Joint PhD Degree between EMBL and Heidelberg University, Faculty of Biosciences, 69120 Heidelberg, Germany.

Trends in Biochemical Sciences
|May 16, 2020
PubMed

Insights

Pathogenic bacteria hijack host cells using short linear motif (SLiM) mimicry. Targeting these SLiM-regulated networks offers a novel strategy to combat bacterial infections and potentially replace antibiotics.

Area of Science:

  • Microbiology
  • Cell Biology
  • Drug Discovery

Background:

  • Bacterial pathogens employ sophisticated mechanisms to survive within hosts, often involving direct interaction with host cells.
  • Secreted bacterial proteins, including effectors and toxins, can disrupt host cell regulation via enzymatic activity or protein-protein interactions (PPIs).
  • Short linear motifs (SLiMs) are crucial peptide modules in eukaryotic cell signaling.

Purpose of the Study:

  • To review examples of pathogenic bacteria utilizing eukaryotic-like SLiM mimicry.
  • To discuss the potential of targeting SLiM-regulated host cell machinery for anti-infective therapies.
  • To highlight SLiM mimicry as a potential component of antibiotic replacement strategies.

Main Methods:

  • Literature review of bacterial SLiM mimicry in host-pathogen interactions.
  • Analysis of reported bacterial effector proteins and their targeted host pathways.
  • Survey of current drug development efforts targeting SLiM-regulated signaling.

Main Results:

  • Pathogenic bacteria extensively use SLiM mimicry to manipulate host cell processes.
  • Numerous examples demonstrate bacterial hijacking of host signaling pathways through SLiM interactions.
  • Drug discovery is exploring SLiM-targeted therapies for bacterial infections.

Conclusions:

  • Bacterial SLiM mimicry is a significant virulence factor and a targetable vulnerability.
  • Interfering with SLiM-regulated host networks presents a promising anti-infective approach.
  • Targeting SLiM mimicry could contribute to novel strategies for combating antibiotic resistance.
Keywords:
bacterial effector proteinsdrug repurposinghost-directed therapymotif mimicryshort linear motifstyrosine kinase inhibitor (TKI)

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