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Legionella effector protein SidG disrupts host cytoskeleton via targeting Arp2/3 complex

Jiayang Liu1, Siyao Liu2, Rundong Shu1

  • 1State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun, China.

Plos Pathogens
|February 9, 2026
PubMed

Insights

Legionella pneumophila uses the effector SidG to disrupt host cell cytoskeletal architecture. This bacterial protein hijacks the host GTPase Rac1 to target the Arp2/3 complex, promoting efficient bacterial invasion.

Area of Science:

  • Microbiology
  • Cell Biology
  • Biochemistry

Background:

  • Legionella pneumophila is an intracellular bacterial pathogen.
  • It utilizes the Dot/Icm type IV secretion system (T4SS) to inject numerous effector proteins into host cells.
  • Understanding effector functions is key to L. pneumophila pathogenesis.

Purpose of the Study:

  • To identify and characterize the function of the L. pneumophila effector protein SidG.
  • To elucidate the mechanism by which SidG manipulates host cell processes.
  • To determine SidG's role in bacterial invasion.

Main Methods:

  • Identification of SidG as a Dot/Icm effector.
  • Biochemical assays to study SidG's interaction with Rac1 and the Arp2/3 complex.
  • Analysis of SidG's impact on cytoskeletal architecture.
  • Assessment of SidG's role in bacterial invasion assays.

Main Results:

  • SidG possesses a Cys-His-Asp triad and its function is regulated by Rac1.
  • Activated SidG targets the Arp2/3 complex via its acidic domain.
  • SidG disrupts the actin cytoskeleton through Rac1- and Arp2/3-dependent pathways.
  • SidG is essential for efficient L. pneumophila invasion in a Cys-His-Asp motif-dependent manner.

Conclusions:

  • SidG employs a sophisticated mechanism, co-opting host Rac1 to allosterically regulate its activity towards the Arp2/3 complex.
  • This interaction disrupts host cytoskeletal dynamics, facilitating bacterial entry.
  • The study reveals a novel pathogenic strategy employed by L. pneumophila.

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