ArticlePloS one2018
A streamlined method for transposon mutagenesis of Rickettsia parkeri yields numerous mutations that impact infection.
Article in PloS one, 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, 43 citations in OpenAlex.
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- High-Throughput Pipeline for Protein Expression and Solubility Profiling Using Synthetically Generated Plasmids.Current protocols · 2025Article
- Phosphatidylserine-binding receptor, CD300f, on macrophages mediates host invasion of pathogenic and non-pathogenic rickettsiae.Infection and immunity · 2025Article
- A platform supporting generation and isolation of random transposon mutants inJournal of bacteriology · 2025Article
- Rickettsia parkeri forms extensive, stable contacts with the rough endoplasmic reticulum.The Journal of cell biology · 2025Article
- ThemBio · 2025Article
- Development of a Recombinase-Mediated Cassette Exchange System for Gene Knockout and Expression of Non-Native Gene Sequences inVaccines · 2025Article
- Pathogenic rickettsiae encode a secreted lipase that facilitates intracytosolic colonization in host cells.PloS one · 2025Article
- An expanded genetic toolkit for inducible expression and targeted gene silencing inJournal of bacteriology · 2024Article
- Cell-selective proteomics reveal novel effectors secreted by an obligate intracellular bacterial pathogen.Nature communications · 2024Article
- An expanded genetic toolkit for inducible expression and targeted gene silencing inbioRxiv : the preprint server for biology · 2024Article
- PathogenicJournal of bacteriology · 2024Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The rickettsiae are obligate intracellular alphaproteobacteria that exhibit a complex infectious life cycle in both arthropod and mammalian hosts. As obligate intracellular bacteria, rickettsiae are highly adapted to living inside a variety of host cells, including vascular endothelial cells during mammalian infection. Although it is assumed that the rickettsiae produce numerous virulence factors that usurp or disrupt various host cell pathways, they have been challenging to genetically manipulate to identify the key bacterial factors that contribute to infection. Motivated to overcome this challenge, we sought to expand the repertoire of available rickettsial loss-of-function mutants, using an improved mariner-based transposon mutagenesis scheme. Here, we present the isolation of over 100 transposon mutants in the spotted fever group species Rickettsia parkeri. Transposon insertions disrupted genes whose products are implicated in a variety of pathways, including bacterial replication and metabolism, the type IV secretion system, factors with previously established roles in host cell interactions and pathogenesis, or are of unknown function. Given the need to identify critical virulence factors, forward genetic screens such as this will provide an excellent platform to more directly investigate rickettsial biology and pathogenesis.
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Registered trials
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