Bacteriophage T12
| Bacteriophage T12 | |
|---|---|
| Virus classification | |
| Group: | Group I (dsDNA)
|
| Order: | Unclassified
|
Bacteriophage T12 is a bacteriophage that infects the bacteria Streptococcus pyogenes, and is member of a family of related speA-carrying bacteriophages. It carries the speA gene which codes for erythrogenic toxin A and converts a harmless strain of bacteria into a virulent strain.[1] The phage is implicated in the contraction of Scarlet Fever, an infectious disease that affects small children.[2]
General Characteristics
Bacteriophage T12 is a temperate phage of Streptococcus pyogenes. Temperate phages are characterized by their ability to become a part of and be stably maintained in the host cell for generations.[1] Thus, the life cycle of T12 can be categorized as a lysogenic cycle.[2] T12 is also a prototypic phage for all the speA-containing phages of Streptococcus pyogenes.[3]
Integration of bacteriophage T12 occurs upstream of the speA gene, and within a gene that encodes a serine tRNA. More specifically, the phage integrates within the anticodon loop of the tRNA. As in other phages that integrate into a tRNA gene, the junction of phage and host chromosomes is at the 5' end of the T12 sequence. T12 duplicates the 3' end of the gene precisely, allowing the tRNA coding sequence to remain intact. Phage T12 is the first example of a phage from a gram-positive, low G-C content host that uses this kind of integration site.[1]
Genome
The physical map of Bacteriophage T12 has been constructed and is found to be terminally redundant and circularly permuted with a total length of 36.0kb.[4] The phage genome is also reported to carry the speA (streptococcal pyrogenic exotoxin A) gene,[5] which is a 1.7kb segment of the phage T12 genome flanked by SalI and HindIII sites.[6]
Bacteriophage T12 control
Bacteriophages are very robust organisms, are very hard to kill[7] and very easily spread.[8] UV light can enhance phage T12 production along with the production of streptococcal pyrogenic exotoxin A, also knows as the scarlatinal toxin.[9] However, this is only to a point. The UV light stresses lysogenic bateria causing them to propagate and burst the host bacterial cells.[10] In the case of T12 exposure to UV light increases the propagation of bacteriophage T12 at 20 seconds of exposure. After 20 seconds of exposure the UV light starts to kill the bacteriophage.[11]
Detection Assays
The presence of lysogenic Bacteriophage T12 can be tested through plaque assays if the strain being used as the indicator strain is susceptible to the phage being tested for. Plaque assays consist of pouring a soft agar solution with an indicator strain onto an agar plate. The indicator strain used should be a strain of bacteria that is susceptible to the phage that is being tested for. After the soft agar is set the samples that are being tested for phage are then spread plated onto the soft agar plates. The plates are then incubated overnight and checked for clearings (plaques) the next day. During the time the plates are incubating, if phage are present they with go through the lysogenic phage cycle and start infecting the indicator strains causing lysis. The lysis of the indicator strains is what causes the plaque. Titers of plaques can be found by diluting the samples and counting plaque forming units (PFUs).[12]
In the case of bacteriophage T12 biochemical tests such as southern blots can be used to detect the Streptococcal Pyrogenic Exotoxin A that the phage produces from the speA gene. This was done in research by Johnson, Tomai and Schlievert in 1985 was by isolating the DNA of the Streptococcal strains and running a restriction digest using BglII. After the digest was complete the DNA samples were run a DNA gel to separate the DNA. The DNA from this gel was then transferred to nitrocellulose paper and incubated with probes specific for speA. An image of this southern blot can be seen in Figure 1 of this article. [13]
References
- ^ a b c McShan, WM; Tang, YF; Ferretti, JJ (1997). "Bacteriophage T12 of Streptococcus pyogenes integrates into the gene encoding a serine tRNA". Molecular Microbiology. 23 (4): 719–28. doi:10.1046/j.1365-2958.1997.2591616.x. PMID 9157243.
{{cite journal}}: Cite has empty unknown parameter:|author-name-separator=(help); Unknown parameter|author-separator=ignored (help) - ^ a b Johnson, LP; Tomai, MA; Schlievert, PM (1986). "Bacteriophage involvement in group a streptococcal pyrogenic exotoxin a production". Journal of Bacteriology. 166 (2): 623–7. PMC 214650. PMID 3009415.
{{cite journal}}: Cite has empty unknown parameter:|author-name-separator=(help); Unknown parameter|author-separator=ignored (help) - ^ McShan, WM (1997 Oct). "Genetic diversity in temperate bacteriophages of Streptococcus pyogenes: identification of a second attachment site for phages carrying the erythrogenic toxin A gene". Journal of bacteriology. 179 (20): 6509–11. PMID 9335304.
{{cite journal}}: Check date values in:|date=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Johnson, LP (1983). "A physical map of the group A streptococcal pyrogenic exotoxin bacteriophage T12 genome". Molecular & general genetics : MGG. 189 (2): 251–5. doi:10.1007/BF00337813. PMID 6304466,.
{{cite journal}}: Check|pmid=value (help); Unknown parameter|coauthors=ignored (|author=suggested) (help)CS1 maint: extra punctuation (link) - ^ Johnson, LP; Schlievert, PM (1984). "Group a streptococcal phage T12 carries the structural gene for pyrogenic exotoxin type A". Molecular & General Genetics. 194 (1–2): 52–6. doi:10.1007/BF00383496. PMID 6374381.
{{cite journal}}: Cite has empty unknown parameter:|author-name-separator=(help); Unknown parameter|author-separator=ignored (help) - ^ Weeks, CR; Ferretti, JJ (1984). "The gene for type a streptococcal exotoxin (erythrogenic toxin) is located in bacteriophage T12". Infection and Immunity. 46 (2): 531–6. PMC 261567. PMID 6389348.
{{cite journal}}: Cite has empty unknown parameter:|author-name-separator=(help); Unknown parameter|author-separator=ignored (help) - ^ Broxmeyer, L (2004). "Bacteriophages: Antibacterials with a future?". Medical Hypotheses. 62 (6): 889–93. doi:10.1016/j.mehy.2004.02.002. PMID 15142642.
{{cite journal}}: Cite has empty unknown parameter:|author-name-separator=(help); Unknown parameter|author-separator=ignored (help) - ^ Ramirez, E; Carbonell, X; Villaverde, A (2001). "Phage spread dynamics in clonal bacterial populations is depending on features of the founder cell". Microbiological Research. 156 (1): 35–40. doi:10.1078/0944-5013-00087. PMID 11372651.
{{cite journal}}: Cite has empty unknown parameter:|author-name-separator=(help); Unknown parameter|author-separator=ignored (help) - ^ Wagner, PL; Waldor, MK (2002). "Bacteriophage control of bacterial virulence". Infection and Immunity. 70 (8): 3985–93. doi:10.1128/IAI.70.8.3985-3993.2002. PMC 128183. PMID 12117903.
{{cite journal}}: Cite has empty unknown parameter:|author-name-separator=(help); Unknown parameter|author-separator=ignored (help) - ^ Atsumi, S; Little, JW (2006). "Role of the lytic repressor in prophage induction of phage lambda as analyzed by a module-replacement approach". Proceedings of the National Academy of Sciences of the United States of America. 103 (12): 4558–63. doi:10.1073/pnas.0511117103. PMC 1450210. PMID 16537413.
{{cite journal}}: Cite has empty unknown parameter:|author-name-separator=(help); Unknown parameter|author-separator=ignored (help) - ^ Zabriskie, JB (1964). "The Role of Temperate Bacteriophage in the Production of Erythrogenic Toxin by Group a Streptococci". The Journal of Experimental Medicine. 119 (5): 761–80. doi:10.1084/jem.119.5.761. PMC 2137738. PMID 14157029.
{{cite journal}}: Cite has empty unknown parameter:|author-name-separator=(help); Unknown parameter|author-separator=ignored (help) - ^ Panec, Marie. "Plaque Assay Protocols". Microbe Library. American Society for Microbiology. Retrieved 28 November 2012.
- ^ Johnson, L P (16). "Bacteriophage involvement in group A streptococcal pyrogenic exotoxin A production". Journal of Bacteriology. 166 (2): 623–627.
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