Prophage
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A prophage is a bacteriophage (often shortened to "phage") genome that is integrated into the circular bacterial chromosome or exists as an extrachromosomal plasmid within the bacterial cell.[1] Integration of prophages into the bacterial host is the characteristic step of the lysogenic cycle of temperate phages. Prophages remain latent in the genome through multiple cell divisions until activation by an external factor, such as UV light, leading to production of new phage particles that will lyse the cell and spread. As ubiquitous mobile genetic elements, prophages play important roles in bacterial genetics and evolution, such as in the acquisition of virulence factors.
Prophage induction
[edit]Upon detection of host cell damage by UV light or certain chemicals, the prophage is excised from the bacterial chromosome in a process called prophage induction. After induction, viral replication begins via the lytic cycle. In the lytic cycle, the virus commandeers the cell's reproductive machinery. The cell may fill with new viruses until it lyses or bursts, or it may release the new viruses one at a time in an exocytotic process. The period from infection to lysis is termed the latent period. A virus following a lytic cycle is called a virulent virus. Prophages are important agents of horizontal gene transfer, and are considered part of the mobilome. Genes are transferred via transduction as the prophage genome is imperfectly excised from the host chromosome and integrated into a new host (specialized transduction) or as fragments of host DNA are packaged into the phage particles and introduced into a new host (generalized transduction).[2] All families of bacterial viruses that have circular (single-stranded or double-stranded) DNA genomes or replicate their genomes through rolling circle replication (e.g., Caudovirales) have temperate members.[3]
During infections by the bacterial pathogen Clostridioides difficile, spontaneous prophage release from the bacterial chromosome is common.[4] The presence of deoxycholic acid in the intestinal environment can promote induction of C. difficle biofilm formation as well as the induction of prophage release.[4]
Zygotic induction
[edit]Zygotic induction occurs when a bacterial cell carrying the DNA of a bacterial virus transfers its own DNA along with the viral DNA (prophage) into the new host cell. This has the effect of causing the host cell to break apart.[5] The DNA of the bacterial cell is silenced before entry into the cell by a repressor protein which is encoded for by the prophage. Upon the transfer of the bacterial cell's DNA into the host cell, the repressor protein is no longer encoded for, and the bacterial cell's original DNA is then turned on in the host cell. This mechanism eventually will lead to the release of the virus as the host cell splits open and the viral DNA is able to spread.[5] This new discovery provided key insights into bacterial conjugation and contributed to the early repression model of gene regulation, which provided an explanation as to how the lac operon and λ bacteriophage genes are negatively regulated.[6]
Prophage reactivation
[edit]Bacteriophage λ is able to undergo a type of recombinational repair called prophage reactivation.[6][7] Prophage reactivation can occur by recombination between a UV-damaged infecting phage λ chromosome and a homologous phage genome integrated into the bacterial DNA and existing in a prophage state. Prophage reactivation in the case of phage λ appears to be an accurate recombinational repair process that is mediated by the recA+ and red+ gene products.[citation needed]
Cost/benefit to the host
[edit]Lysis of host cells during prophage induction can cause the collapse of a microbial population.[8][9] On the other hand, induction, transduction and superinfection exclusion mechanisms confer many beneficial functions to the host. Induction of prophages allows hosts to compete in the microbial ecology by infecting and lysing susceptible bacteria.[10] Phages also enable the host to pick up and integrate antibiotic resistance genes from nearby cells.[9][10][8][11] Additionally, phages can enable the host to acquire virulence and pathogenicity genes.[9][11] Modulation of biofilm formation is also affected by infection by lysogenic phages.[11] Superinfection exclusion, or protection against infection by multiple phages, can be conferred by prophage integration.[12] Additionally, phage-mediated recombination mechanisms may remodel the host chromosome and provide new ways for cells to regulate metabolism and gene expression, such as those involved in sporulation and competence.[11][13]
Applications
[edit]Prophages can tell researchers a lot about the relationship between a bacterium and a host.[14] With data from more nonpathogenic bacteria, researchers will be able to gather evidence as to whether or not prophages contribute to the survival value of the host. Prophage genomics has the potential to lead to ecological adaptations of the relationships between bacteria.[14] Another important area of interest is the control of prophage gene expression with many of the lysogenic conversion genes (gene conversion) being tightly regulated.[15] This process is capable of converting non-pathogenic bacteria into pathogenic bacteria that can now produce harmful toxins[15] such as in staph infections. Since the specific mechanisms of prophage are not yet detailed, this research could provide the community with this tool for future research.[14]
Economic impact
[edit]Exotoxins encoded by prophages cause pathogenic outcomes in agriculture and aquaculture.[16]
References
[edit]- ^ Saussereau E, Debarbieux L (2012). "Bacteriophages in the Experimental Treatment of Pseudomonas aeruginosa Infections in Mice". Advances in Virus Research. Vol. 83. pp. 127–128. doi:10.1016/B978-0-12-394438-2.00004-9. ISBN 978-0-12-394438-2. PMID 22748810.
- ^ Borodovich T, Shkoporov AN, Ross RP, Hill C (2022-04-13). "Phage-mediated horizontal gene transfer and its implications for the human gut microbiome". Gastroenterology Report. 10: goac012. doi:10.1093/gastro/goac012. PMC 9006064. PMID 35425613.
- ^ Krupovic M, Prangishvili D, Hendrix RW, Bamford DH (December 2011). "Genomics of bacterial and archaeal viruses: dynamics within the prokaryotic virosphere". Microbiology and Molecular Biology Reviews. 75 (4): 610–635. doi:10.1128/MMBR.00011-11. PMC 3232739. PMID 22126996.
- ^ a b Schüler MA, Daniel R, Poehlein A (2024). "Novel insights into phage biology of the pathogen Clostridioides difficile based on the active virome". Front Microbiol. 15: 1374708. doi:10.3389/fmicb.2024.1374708. PMC 10993401. PMID 38577680.
- ^ a b Griffiths A, Miller J, Suzuki D, Lewontin R, Gelbart W (2002). An Introduction to Genetic Analysiss (7th ed.). New York, NY: Freeman. ISBN 978-0-7167-3520-5.
- ^ a b Blanco M, Devoret R (March 1973). "Repair mechanisms involved in prophage reactivation and UV reactivation of UV-irradiated phage lambda". Mutation Research. 17 (3): 293–305. Bibcode:1973MRFMM..17..293B. doi:10.1016/0027-5107(73)90001-8. PMID 4688367.
- ^ Bernstein C (March 1981). "Deoxyribonucleic acid repair in bacteriophage". Microbiological Reviews. 45 (1): 72–98. doi:10.1128/mr.45.1.72-98.1981. PMC 281499. PMID 6261109.
- ^ a b Haaber J, Leisner JJ, Cohn MT, Catalan-Moreno A, Nielsen JB, Westh H, et al. (November 2016). "Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells". Nature Communications. 7 (1): 13333. Bibcode:2016NatCo...713333H. doi:10.1038/ncomms13333. PMC 5103068. PMID 27819286.
- ^ a b c Hu J, Ye H, Wang S, Wang J, Han D (2021-12-13). "Prophage Activation in the Intestine: Insights Into Functions and Possible Applications". Frontiers in Microbiology. 12: 785634. doi:10.3389/fmicb.2021.785634. PMC 8710666. PMID 34966370.
- ^ a b Wendling CC, Refardt D, Hall AR (February 2021). "Fitness benefits to bacteria of carrying prophages and prophage-encoded antibiotic-resistance genes peak in different environments". Evolution; International Journal of Organic Evolution. 75 (2): 515–528. doi:10.1111/evo.14153. PMC 7986917. PMID 33347602.
- ^ a b c d Fortier LC, Sekulovic O (July 2013). "Importance of prophages to evolution and virulence of bacterial pathogens". Virulence. 4 (5): 354–365. doi:10.4161/viru.24498. PMC 3714127. PMID 23611873.
- ^ Bondy-Denomy J, Qian J, Westra ER, Buckling A, Guttman DS, Davidson AR, Maxwell KL (December 2016). "Prophages mediate defense against phage infection through diverse mechanisms". The ISME Journal. 10 (12): 2854–2866. Bibcode:2016ISMEJ..10.2854B. doi:10.1038/ismej.2016.79. PMC 5148200. PMID 27258950.
- ^ Menouni R, Hutinet G, Petit MA, Ansaldi M (January 2015). "Bacterial genome remodeling through bacteriophage recombination". FEMS Microbiology Letters. 362 (1): 1–10. doi:10.1093/femsle/fnu022. PMID 25790500.
- ^ a b c Canchaya C, Proux C, Fournous G, Bruttin A, Brüssow H (June 2003). "Prophage genomics". Microbiology and Molecular Biology Reviews. 67 (2): 238–76, table of contents. doi:10.1128/MMBR.67.2.238-276.2003. PMC 156470. PMID 12794192.
- ^ a b Feiner R, Argov T, Rabinovich L, Sigal N, Borovok I, Herskovits AA (October 2015). "A new perspective on lysogeny: prophages as active regulatory switches of bacteria". Nature Reviews. Microbiology. 13 (10): 641–650. doi:10.1038/nrmicro3527. PMID 26373372. S2CID 11546907.
- ^ Cobián Güemes AG, Youle M, Cantú VA, Felts B, Nulton J, Rohwer F (September 2016). "Viruses as Winners in the Game of Life". Annual Review of Virology. 3 (1). Annual Reviews: 197–214. doi:10.1146/annurev-virology-100114-054952. PMID 27741409. S2CID 36517589.
See also
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