Related Experiment Video

Updated: Jun 26, 2026

Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
08:38

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

Published on: February 22, 2019

Obligatory intracellular bacterium Anaplasma phagocytophilum AnkA regulates actin dynamics and spatiotemporal

Mingqun Lin1, Nan Duan1, Yasuko Rikihisa1

  • 1Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio, United States of America.

Plos Pathogens
|June 24, 2026
PubMed

Insights

Anaplasma phagocytophilum uses the AnkA effector to disrupt host cell actin, controlling its release and infection cycle. This study reveals AnkA

Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Anaplasma phagocytophilum causes human granulocytic anaplasmosis, an emerging infectious disease.
  • The bacterium exhibits a biphasic developmental cycle within human neutrophils, involving proliferation and release.
  • The mechanism coordinating A. phagocytophilum growth and release remains largely unknown.

Purpose of the Study:

  • To elucidate the mechanism by which Anaplasma phagocytophilum regulates its release from host cells.
  • To investigate the role of the type IV secretion system (T4SS) effector AnkA in bacterial release.
  • To identify host cell factors interacting with AnkA and influencing bacterial release.

Main Methods:

  • Investigated F-actin disruption at the host cell plasma membrane during bacterial release.
  • Utilized pharmacological inhibitors (cytochalasin D, latrunculin B) to assess F-actin's role.
  • Employed immunoprecipitation followed by mass spectrometry to identify AnkA interacting proteins.
  • Performed shRNA-knockdown experiments for Actn4 and gelsolin.
  • Conducted in vitro pyrene-actin polymerization assays.
  • Observed localization and effects of ectopically expressed GFP-tagged AnkA fragments.

Main Results:

  • Localized cortical F-actin disruption precedes A. phagocytophilum release.
  • Disruption of F-actin led to premature, less infectious bacterial release.
  • AnkA localizes with cortical F-actin and interacts with actin, α-actinin 4 (Actn4), and gelsolin.
  • Knockdown of Actn4 or gelsolin enhanced premature bacterial release.
  • AnkA's C-terminus promotes actin polymerization, while the N-terminus interacts with Actn4.
  • AnkA modulates host cell actin dynamics, affecting membrane ruffling and stress fibers.

Conclusions:

  • AnkA is the first identified bacterial molecule to interact with gelsolin and Actn4.
  • AnkA regulates the spatiotemporal release of A. phagocytophilum by controlling F-actin dynamics.
  • This study reveals a novel mechanism of intracellular pathogen release orchestrated by a T4SS effector.

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