ArticleCellular microbiology2018
Actin-based motility allows Listeria monocytogenes to avoid autophagy in the macrophage cytosol.
Article in Cellular microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
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- Listeria promotes systemic infection by targeting the host deubiquitinase CYLD.Nature communications · 2026Article
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- Innate immune responses to Rickettsia: emerging themes and contrasts between species.Current opinion in microbiology · 2026Review
- Clindamycin susceptibility and virulence characterization ofFrontiers in microbiology · 2026Article
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- 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
- Stress-dependent activation of themBio · 2025Article
- The battle between bacterial infection and autophagy in aquatic animals.Frontiers in immunology · 2025Review
- Tax1bp1 enhances bacterial virulence and promotes inflammatory responses duringbioRxiv : the preprint server for biology · 2024Article
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- Human Listeriosis.Clinical microbiology reviews · 2023Review
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- RibU is an essential determinant ofProceedings of the National Academy of Sciences of the United States of America · 2022Article
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- A dynamically evolving war between autophagy and pathogenic microorganisms.Journal of Zhejiang University. Science. B · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Listeria monocytogenes grows in the host cytosol and uses the surface protein ActA to promote actin polymerisation and mediate actin-based motility. ActA, along with two secreted bacterial phospholipases C, also mediates avoidance from autophagy, a degradative process that targets intracellular microbes. Although it is known that ActA prevents autophagic recognition of L. monocytogenes in epithelial cells by masking the bacterial surface with host factors, the relative roles of actin polymerisation and actin-based motility in autophagy avoidance are unclear in macrophages. Using pharmacological inhibition of actin polymerisation and a collection of actA mutants, we found that actin polymerisation prevented the colocalisation of L. monocytogenes with polyubiquitin, the autophagy receptor p62, and the autophagy protein LC3 during macrophage infection. In addition, the ability of L. monocytogenes to stimulate actin polymerisation promoted autophagy avoidance and growth in macrophages in the absence of phospholipases C. Time-lapse microscopy using green fluorescent protein-LC3 macrophages and a probe for filamentous actin showed that bacteria undergoing actin-based motility moved away from LC3-positive membranes. Collectively, these results suggested that although actin polymerisation protects the bacterial surface from autophagic recognition, actin-based motility allows escape of L. monocytogenes from autophagic membranes in the macrophage cytosol.
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Registered trials
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