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Bacterial and host determinants of MAL activation upon EPEC infection: the roles of Tir, ABRA, and FLRT3

Robert J W Heath1, John M Leong, Balázs Visegrády

  • 1Center for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.

Plos Pathogens
|April 15, 2011
PubMed

Insights

Enteropathogenic E. coli (EPEC) infection activates host cell signaling pathways. This study identifies novel proteins, including ABRA and FLRT3, crucial for EPEC-induced MAL nuclear accumulation and cytoskeletal regulation.

Area of Science:

  • Microbiology
  • Cell Biology
  • Molecular Biology

Background:

  • Pathogenic microbes trigger host cell responses, including actin cytoskeleton rearrangements and transcriptional changes.
  • Enteropathogenic E. coli (EPEC) and Enterohemorrhagic E. coli (EHEC) use type III secretion systems to inject effectors, subverting the host cytoskeleton to form attaching and effacing lesions.

Purpose of the Study:

  • To investigate the impact of bacterial pathogens on host cell signaling, specifically transcription factor activation.
  • To identify novel components involved in pathogen-induced cytoskeletal signaling pathways.

Main Methods:

  • Utilized a MAL translocation assay to monitor signaling to transcription factor activation.
  • Employed an expression screen to identify novel activators of Serum Response Factor (SRF).
  • Investigated the role of specific tyrosine phosphorylation sites on the translocated intimin receptor.

Main Results:

  • Demonstrated that EPEC infection induces nuclear accumulation of MAL-GFP, a cofactor of SRF.
  • Identified FLRT3, C22orf28, and TESK1 as novel SRF activators.
  • Showed that ABRA (actin-binding Rho-activating protein) is essential for EPEC-induced MAL nuclear accumulation and FLRT3 pathway involvement.
  • Confirmed ABRA's importance in maintaining the structure of EPEC pedestals.

Conclusions:

  • Uncovered novel components in pathogen-activated cytoskeleton signaling pathways leading to MAL activation.
  • Highlighted the critical role of ABRA and FLRT3 in the host cell response to EPEC infection.
  • Provided new insights into the molecular mechanisms underlying EPEC-induced cytoskeletal subversion.

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