R-factor

Resistance transfer factor (shortened as R-factor or RTF) is an old name for a plasmid that codes for antibiotic resistance. R-factor was first demonstrated in Shigella in 1959 by Japanese scientists.[1] Often, R-factors code for more than one antibiotic resistance factor: genes that encode resistance to unrelated antibiotics may be carried on a single R-factor, sometimes up to 8 different resistances. Many R-factors can pass from one bacterium to another through bacterial conjugation and are a common means by which antibiotic resistance spreads between bacterial species, genera and even families.[2] For example, RP1, a plasmid that encodes resistance to ampicillin, tetracycline and kanamycin originated in a species of Pseudomonas, from the family Pseudomonadaceae, but can also be maintained in bacteria belonging to the family Enterobacteriaceae, such as Escherichia coli.[3]

This article is about the plasmid. For information about the residual factor in crystallography, see R-factor (crystallography). For the racing video game, see rFactor.

Transmission

Bacteria containing F-factors (said to be "F+") have the capability for horizontal gene transfer; they can construct a sex pilus, which emerges from the donor bacterium and ensnares the recipient bacterium, draws it in, and eventually triggers the formation of a mating bridge, merging the cytoplasms of two bacteria via a controlled pore. This pore allows the transfer of genetic material, such as a plasmid. Conjugation allows two bacteria, not necessarily from the same species, to transfer genetic material one way.[4] Since many R-factors contain F-plasmids, antibiotic resistance can be easily spread among a population of bacteria. Also, R-factors can be taken up by "DNA pumps" in their membranes via transformation, or less commonly through viral mediated transduction, or via bacteriophage, although conjugation is the most common means of antibiotic resistance spread. They contain the gene called RTF (Resistance transfer factor).

References
  1. Macuch P, Seckarova A, Parrakova E, Krcmery V, Vymola F (1967). "Transfer of tetracycline resistance from Escherichia coli to other Enterobacteriaceae in vitro". Zeitschrift für Allgemeine Mikrobiologie. 7 (2): 159–62. doi:10.1002/jobm.19670070212. PMID 4876865.
  2. Institute of Medicine (US) Forum on Microbial Threats (2010). "Workshop Overview: AMR Genes". Antibiotic Resistance: Implications for Global Health and Novel Intervention Strategies: Workshop Summary. National Academies Press. doi:10.17226/12925. ISBN 978-0-309-18534-9. PMID 21595116. NBK54257/. The vast majority of antimicrobial resistance genes reside on mobile genetic elements such as insertion sequences, integrons, transposons, and plasmids, ... Bacteria readily acquire these genetic elements from the environment, exchange them through conjugation, and receive them via infection by bacterial viruses (bacteriophages, or phages).
  3. Saunders, J. R.; Grinsted, J. (November 1972). "Properties of RP4, an R Factor Which Originated in Pseudomonas aeruginosa S8". Journal of Bacteriology. 112 (2): 690–6. PMC 251476. PMID 4628745.
  4. "Prokaryotic Cell Structure: Pili". Archived from the original on 2016-12-07. Retrieved 2017-01-19.


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