ArticleThe Journal of cell biology1997
The isolated comet tail pseudopodium of Listeria monocytogenes: a tail of two actin filament populations, long and axial and short and random.
Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 113 citations in OpenAlex.
- A pore-forming toxin initiates ABI1 complex switching to promote bacterial cell-to-cell spread.Nature communications · 2026Article
- Role of Flotillin-1 In Listeria monocytogenes Cell-to-Cell Spreading.The Journal of infectious diseases · 2025Article
- Characterization of c-Src During Listeria monocytogenes Cell-to-Cell Spreading.The Journal of infectious diseases · 2025Article
- ThemBio · 2025Article
- Structural and functional mechanisms of actin isoforms.The FEBS journal · 2025Review
- Pushing boundaries: mechanisms enabling bacterial pathogens to spread between cells.Infection and immunity · 2024Review
- Phosphorylation of the small heat shock protein HspB1 regulates cytoskeletal recruitment and cell motility.Molecular biology of the cell · 2022Article
- Mechanical Forces Govern Interactions of Host Cells with Intracellular Bacterial Pathogens.Microbiology and molecular biology reviews : MMBR · 2022Review
- Article
- Cytoskeleton Force Exertion in Bulk Cytoplasm.Frontiers in cell and developmental biology · 2020Review
- Article
- Actin-based motility and cell-to-cell spread of bacterial pathogens.Current opinion in microbiology · 2017Review
- Bacterial spread from cell to cell: beyond actin-based motility.Trends in microbiology · 2015Review
- Control of polarized assembly of actin filaments in cell motility.Cellular and molecular life sciences : CMLS · 2015Review
- The diaphanous-related formins promote protrusion formation and cell-to-cell spread of Listeria monocytogenes.The Journal of infectious diseases · 2015Article
- Actin network disassembly powers dissemination of Listeria monocytogenes.Journal of cell science · 2014Article
- Electron tomography and simulation of baculovirus actin comet tails support a tethered filament model of pathogen propulsion.PLoS biology · 2014Article
- Three-dimensional architecture of actin filaments in Listeria monocytogenes comet tails.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Ultrastructure of protrusive actin filament arrays.Current opinion in cell biology · 2013Review
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Listeria monocytogenes is driven through infected host cytoplasm by a comet tail of actin filaments that serves to project the bacterium out of the cell surface, in pseudopodia, to invade neighboring cells. The characteristics of pseudopodia differ according to the infected cell type. In PtK2 cells, they reach a maximum length of approximately 15 microm and can gyrate actively for several minutes before reentering the same or an adjacent cell. In contrast, the pseudopodia of the macrophage cell line DMBM5 can extend to >100 microm in length, with the bacteria at their tips moving at the same speed as when at the head of comet tails in bulk cytoplasm. We have now isolated the pseudopodia from PtK2 cells and macrophages and determined the organization of actin filaments within them. It is shown that they possess a major component of long actin filaments that are more or less splayed out in the region proximal to the bacterium and form a bundle along the remainder of the tail. This axial component of filaments is traversed by variable numbers of short, randomly arranged filaments whose number decays along the length of the pseudopodium. The tapering of the tail is attributed to a grading in length of the long, axial filaments. The exit of a comet tail from bulk cytoplasm into a pseudopodium is associated with a reduction in total F-actin, as judged by phalloidin staining, the shedding of alpha-actinin, and the accumulation of ezrin. We propose that this transition reflects the loss of a major complement of short, random filaments from the comet, and that these filaments are mainly required to maintain the bundled form of the tail when its borders are not restrained by an enveloping pseudopodium membrane. A simple model is put forward to explain the origin of the axial and randomly oriented filaments in the comet tail.
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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.