ArticleNature cell biology2009
Listeria monocytogenes ActA-mediated escape from autophagic recognition.
Article in Nature cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 248 papers, 2 of them syntheses that pooled it.
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Who cites it
248 citing papers in PubMed, 2 syntheses or guidelines pooled it, 430 citations in OpenAlex.
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- Kinetic control of macrophage death by PTM-turnover crosstalk in infection and inflammation.Cell chemical biology · 2026Review
- Mechanisms and strategies of host xenophagy manipulation by intracellular bacteria.Cellular and molecular life sciences : CMLS · 2026Review
- Listeriosis: a re-emerging threat to public health-a comprehensive review of its epidemiology, pathogenesis, and control measures.Infection · 2026Review
- Ubiquitination and autophagy in host-pathogen interactions: from immune surveillance to therapeutic targeting.Nature reviews. Immunology · 2026Review
- Restricting intracellularAutophagy · 2026Article
- Proximity labeling of thebioRxiv : the preprint server for biology · 2026Article
- Development and application of ActA-based competitive ELISA for the specific diagnosis of ovine listeriosis.BMC veterinary research · 2025Article
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- Listeriosis.Nature reviews. Disease primers · 2025Review
- A Microfluidic Platform for Actin-Based Membrane Remodeling Reveals the Stabilizing Role of Branched Actin Networks on Lipid Microdomains.Small science · 2025Article
- Unc-51-like kinase 1 (ULK1) regulates bacterial ubiquitylation and p62 recruitment during xenophagic clearance ofmSphere · 2025Article
- The intracellular bacterium Orientia tsutsugamushi uses the autotransporter ScaC to activate BICD adaptors for dynein-based motility.Nature communications · 2025Article
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- Staphylococcal SplA and SplB serine proteases target ubiquitin(-like) specific proteases.AMB Express · 2025Article
188 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy degrades unnecessary organelles and misfolded protein aggregates, as well as cytoplasm-invading bacteria. Nevertheless, the bacteria Listeria monocytogenes efficiently escapes autophagy. We show here that recruitment of the Arp2/3 complex and Ena/VASP, via the bacterial ActA protein, to the bacterial surface disguises the bacteria from autophagic recognition, an activity that is independent of the ability to mediate bacterial motility. L. monocytogenes expressing ActA mutants that lack the ability to recruit the host proteins initially underwent ubiquitylation, followed by recruitment of p62 (also known as SQSTM1) and LC3, before finally undergoing autophagy. The ability of ActA to mediate protection from ubiquitylation was further demonstrated by generating aggregate-prone GFP-ActA-Q79C and GFP-ActA-170(*) chimaeras, consisting of GFP (green fluorescent protein), the ActA protein and segments of polyQ or Golgi membrane protein GCP170 (ref. 6). GFP-ActA-Q79C and GFP-ActA-170(*) formed aggregates in the host cell cytoplasm, however, these ActA-containing aggregates were not targeted for association with ubiquitin and p62. Our findings indicate that ActA-mediated host protein recruitment is a unique bacterial disguise tactic to escape from autophagy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.