R1 plasmid

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The R1 plasmid is a plasmid that was first isolated from Salmonella paratyphi bacteria in 1963. [1] It is a short plasmid, composed of 97,566 nucleotides and 120 genes, that belongs to the IncFII plasmid group. [2] There are about 1-2 copies of the R1 plasmid per chromosome. [3]

Contents

Figure 1. Map of the R1 Plasmid isolated by Katherine E. L. Cox and Joel F. Schildbach. Figure 1. Map of the R1 Plasmid isolated by Katherine E L Cox and Joel F Schildbach.jpg
Figure 1. Map of the R1 Plasmid isolated by Katherine E. L. Cox and Joel F. Schildbach.

The R1 plasmid imparts multi-drug antibiotic resistance to its host bacteria. [4] The "R" in "R1" stands for "resistance", and the R1 plasmid contains resistance factors, or R factors, giving it the power to resist certain antibiotics. [1]

It's known as a "low copy" plasmid, meaning that it exists in relatively few copies in any given bacteria. This characteristic allows the R1 plasmid to have an efficient plasmid stabilization system, that aids in stabilizing medium copy number plasmids. [5] R1 must rely on a "Type II" segregation system. This plasmid system ensures that at least one copy is contained in each daughter cell after cell division. [4]

Structure

The R1 plasmid belongs to the IncFII plasmid group. [2] The Inc plasmid group stands for incompatibility, and plasmids are classified into this group when 2 plasmids can't steadily propagate in the same host. [6] The major incompatibility group involved in resistance and virulence gene transfer is the IncF group. Since R1 is an IncFII plasmid, that means it carries the FII replicon. This plasmid subtype often carries blaCTX-M genes. [7]

Key Genes/Operons

There are 120 genes on the R1 plasmid, and these genes can be sorted into 3 different groups. The largest group, as seen in green in Figure 1, is the conjugative plasmid backbone. The region pictured in purple is primarily a Tn21-like transposon, and the smallest region pictured in yellow contains sequences resembling Klabsiella oxytoca.

Replication

Partitioning

conjugation: enables horizontal gene transfer via conjugation, spreading the plasmid between bacteria.

Antibiotic resistance genes: provides multidrug resistance to commonly used antibiotics

Figure 2: Hok sok system R1 plasmid absent Hok sok system R1 plasmid absent.gif
Figure 2: Hok sok system R1 plasmid absent

Addiction systems: stabilizes plasmid inheritance by killing plasmid-free segregants.

Maintenance and stability: ensures plasmid molecules remain monomeric, aiding stable inheritance.

ParM is a prokaryotic actin homologue which provides the force to drive copies of the R1 plasmid to opposite ends of rod shaped bacteria before division.

CopA-like RNA, an antisense RNA involved in replication control of the plasmid.

Replication

Replication of the R1 plasmid begins at the oriRI site on the plasmid. RepA is the plasma-encoded initiator protein that binds to oriRI in order to initiate replication. [13] RepA needs a 188-bp region of DNA at minimum in order to bind. Initiation of the leading strand, primed by DnaG, occurs at a G-type priming signal. This signal is located 400 bp downstream of the RepA-binding sequences. [13]

A newly synthesized RepA protein is used by an oriR on the same template that it was synthesized on, a cis-specific action. [3]

Partitioning System

Ensures active segregation of plasmids during cell division, preventing plasmid loss. [8]

The R1 plasmid partitioning is a mechanism needed for the inheritance of the R1 plasmid. The par system is composed of the ParR and the ParC regions, that interact together. The par system determines the position of the replicon, ensuring that at the end of DNA Replication, the plasmid copies are well-positioned to start cell division. The par system also allows for the initiation of  ParM formation. ParM produces two important cytoskeletal proteins, MreB, and actin. ParM is directed to move the plasmid copies to opposite cell poles. Cell division takes place, resulting in the partitioned plasmids in two daughter cells. [13]

References

  1. 1 2 Datta N, Kontomichalou P (Oct 1965). "Penicillinase Synthesis Controlled By Infectious R Factors In Enterobacteriaceae". Nature. 208 (5007): 239–241. Bibcode:1965Natur.208..239D. doi:10.1038/208239a0. PMID   5326330. S2CID   42688587.
  2. 1 2 3 4 Nordstrom K (Jan 2006). "Plasmid R1--replication and its control". Plasmid. 55 (1): 1–26. doi:10.1016/j.plasmid.2005.07.002. PMID   16199086.
  3. 1 2 Masai H, Kaziro Y, Arai K (1983-11-10). "Definition of oriR, the minimum DNA segment essential for initiation of R1 plasmid replication in vitro". Proceedings of the National Academy of Sciences of the United States of America. 80 (22): 6814–6818. doi:10.1073/pnas.80.22.6814. ISSN   0027-8424. PMC   390076 . PMID   6316326.
  4. 1 2 Campbell CS, Mullins RD (Dec 2007). "In vivo visualization of type II plasmid segregation: bacterial actin filaments pushing plasmids". The Journal of Cell Biology. 179 (5): 1059–1066. doi: 10.1083/jcb.200708206 . PMC   2099209 . PMID   18039937.
  5. ↑ Subramanian G, ed. (2012). Biopharmaceutical production technology. Weinheim: Wiley-VCH. ISBN   978-3-527-65312-6. OCLC   794328715.
  6. ↑ Anandan S, Devanga Ragupathi NK, Gajendiran R, Kuroda M, Shibayama K, Veeraraghavan B, et al. (2019-03-01). "IncFII plasmid carrying antimicrobial resistance genes in Shigella flexneri: Vehicle for dissemination" . Journal of Global Antimicrobial Resistance. 16: 215–219. doi:10.1016/j.jgar.2018.10.014. ISSN   2213-7165. PMID   30342929.
  7. ↑ Beceiro A, Tomas M, Bou G (2013-04-22). "Antimicrobial Resistance and Virulence: a Successful or Deleterious Association in the Bacterial World?". Clinical Microbiology Reviews. 26 (2): 185–230. doi:10.1128/cmr.00059-12. PMC   3623377 . PMID   23554414.
  8. 1 2 Møller-Jensen J, Jensen RB, Gerdes K (2000-08-20). "Plasmid and chromosome partitioning: surprises from phylogeny". Molecular Microbiology. 37 (3): 455–466. doi:10.1046/j.1365-2958.2000.01975.x. ISSN   0950-382X. PMID   10931339.
  9. ↑ Leplae R, Summers AO, Toussaint A, Frost LS (2005-09-12). "Mobile genetic elements: the agents of open source evolution" . Nature Reviews Microbiology. 3 (9): 722–732. doi:10.1038/nrmicro1235. ISSN   1740-1534. PMID   16138100.
  10. ↑ Independovirus (2007-07-29), Mechanizm działania systemu hok/sok w obecności plazmidu R1 , retrieved 2025-04-11
  11. ↑ Gerdes K, Thisted T (1992-01-05). "Mechanism of post-segregational killing by the hok/sok system of plasmid R1" . Journal of Molecular Biology. 223 (1): 41–54. doi:10.1016/0022-2836(92)90714-U. ISSN   0022-2836. PMID   1370544.
  12. ↑ Henares B, Kommineni S, Chumsakul O, Ogasawara N, Ishikawa S, Nakano MM (2014-01-15). "The ResD Response Regulator, through Functional Interaction with NsrR and Fur, Plays Three Distinct Roles in Bacillus subtilis Transcriptional Control". Journal of Bacteriology. 196 (2): 493–503. doi:10.1128/JB.01166-13. ISSN   0021-9193. PMC   3911253 . PMID   24214949.
  13. 1 2 3 Moller-Jensen J, Borch J, Dam M, Jensen RB, Roepstorff P, Gerdes K (2003-12-01). "Bacterial Mitosis: ParM of Plasmid R1 Moves Plasmid DNA by an Actin-like Insertional Polymerization Mechanism". Molecular Cell. 12 (6): 1477–1487. doi: 10.1016/S1097-2765(03)00451-9 . ISSN   1097-2765. PMID   14690601.
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