Bacteriophage T12

Bacteriophage T12
Virus classification
Group:	Group I (dsDNA)
Order:	Unclassified

Bacteriophage T12 is a bacteriophage that infects the bacterial species , and converts a harmless strain of bacteria into a virulent strain. It carries the speA gene which codes for erythrogenic toxin A. speA is also known as streptococcal pyogenic exotoxin A, scarlet fever toxin A, or even scarlatinal toxin. Note that when the term 'spe'A is italicized, the reference is to the gene. In contrast, when the term 'spe'A is not italicized, the toxin itself is being referred to. Erythrogenic toxin A converts a harmless, nonvirulent strain of Streptococcus pyogenes to a virulent strain through lysogeny, a life cycle which is characterized by the ability of the genome to become a part of and be stably maintained in the host cell for generations. Phages with a lysogenic life cycle are also called temperate phages. A virulent strain of bacteria is one that is "extremely infective" and causes medical, clinical symptoms. Bacteriophage T12, a member of a family of related speA-carrying bacteriophages, is also a prototypic phage for all the speA-containing phages of Streptococcus pyogenes, meaning that its genome is the prototype for the genomes of all such phages of S.pyogenes. It is the main suspect as the cause of Scarlet Fever, an infectious disease that affects small children.

The possibility of bacteriophage involvement in speA production was first introduced in 1926 when Cantacuzene and Boncieu reported that nonvirulent strains of S.pyogenes were transformed to virulent strains through some transferable element. Frobisher and Brown reported similar results in 1927, and in 1949, the reports were confirmed by Bingel Later, in 1964, Zabriskie reported that phage T12 could cause speA production by lysogeny in strains that it became a part of. In 1980, Johnson, Schlievert and Watson were able to confirm this and show that the gene for speA production was transferred from toxigenic strains of bacteria to non-toxigenic strains through lysogeny. In their experiment, every transformed, toxin-producing bacterial colony was lysogenic, i.e. contained the T12 gene. In addition, none of the colonies containing the T12 genome was negative for speA, and therefore, the conclusion was drawn that all lysogens produced the toxin. However, McKane and Ferretti reported, in 1981, that a mutant of phage T12 induced speA production virulently. This mutant, the bacteriophage T253, entered the lytic cycle, a life cycle in which the host cell is destroyed. In 1983, Johnson and Schlievert published a map of the T12 genome, revealing also that three rounds of packaging occur in the genome. The very next year, Johnson and Schlievert and Weeks and Ferreti also found, independently, that the bacteriophage T12 carries the structural gene for speA. In 1986, Johson, Tomai and Schlievert mapped the attachment site (attP) for T12 adjacent to the speA gene, and established that all bacterial strains producing the toxin carry either phage T12 itself, or a closely related bacteriophage. And finally, in 1997, McShan and Ferretti published that they had found the second attachment site (attR) for T12, while also revealing in another publication, which was also credited to Tang, that bacteriophage T12 inserts into a gene that encodes a serine tRNA in the host.

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