Enterobacteria phage T4

Enterobacteria phage T4
Virus classification
Group: Group I (dsDNA)
Order: Caudovirales
Family: Myoviridae
Genus: T4likeviruses
Species: Enterobacteria phage T4

Enterobacteria phage T4 is a bacteriophage that infects Escherichia coli bacteria. The T4 phage is a member of the T-even phages, a group including enterobacteriophages T2 and T6. T4 is capable of undergoing only a lytic lifecycle and not the lysogenic lifecycle.

Genome and structure

The T4 phage's double-stranded DNA genome is about 169 kbp long[1] and encodes 289 proteins. The T4 genome is terminally redundant and is first replicated as a unit, then several genomic units are recombined end-to-end to form a concatemer. When packaged, the concatemer is cut at unspecific positions of the same length, leading to several genomes that represent circular permutations of the original.[2] The T4 genome bears eukaryote-like intron sequences.

Translation

The Shine-Dalgarno sequence GAGG dominates in bacteriophage T4 early genes, whereas the sequence GGAG is a target for the T4 endonuclease RegB that initiates the early mRNA degradation.[3]

Virus particle structure

T4 is a relatively large phage, at approximately 90 nm wide and 200 nm long (most phages range from 25 to 200 nm in length). The DNA genome is held in an icosahedral head, also known as a capsid. The T4’s tail is hollow so that it can pass its nucleic acid into the cell it is infecting after attachment. The tail attaches to a host cell with the help of tail fibres. The tail fibres are also important in recognizing host cell surface receptors, so they determine if a bacterium is within the phage's host range.

Infection process

The T4 phage initiates an E. coli infection by binding OmpC porin proteins and Lipopolysaccharide (LPS) on the surface of E. coli cells with its long tail fibers (LTF).[4][5] A recognition signal is sent through the LTFs to the baseplate. This unravels the short tail fibers (STF) that bind irreversibly to the E. coli cell surface. The baseplate changes conformation and the tail sheath contracts, causing GP5 at the end of the tail tube to puncture the outer membrane of the cell. The lysozyme domain of GP5 is activated and degrades the periplasmic peptidoglycan layer. The remaining part of the membrane is degraded and then DNA from the head of the phage can travel through the tail tube and enter the E. coli cell.

Life cycle

The lytic lifecycle (from entering a bacterium to its destruction) takes approximately 30 minutes (at 37 °C) and consists of:

After the life cycle is complete, the host cell bursts open and ejects the newly built viruses into the environment, destroying the host cell. T4 has a burst size of approximately 100-150 viral particles per infected host. Complementation, deletion, and recombination tests can be used to map out the rII gene locus by using T4. These bacteriophage infect a host cell with their information and then blow up the host cell, thereby propagating themselves.

Replication and packaging

The rate of DNA replication in a living cell was first measured as the rate of phage T4 DNA elongation in phage-infected E. coli.[6] During the period of exponential DNA increase at 37 °C, the rate was 749 nucleotides per second. The mutation rate per base pair per replication during phage T4 DNA synthesis is 1.7 per 108,[7] a highly accurate DNA copying mechanism, with only 1 error in 300 copies. The phage also codes for unique DNA repair mechanisms. The T4 DNA packaging motor has been found to load DNA into phage capsids at a rate up to 2000 base pairs per second. The power involved, if scaled up in size, would be equivalent to that of an average automobile engine.[8]

Multiplicity reactivation

Survival curves for phage T4 with DNA damaged by UV (top) or MMC (bottom) after single phage T4 infecting host cells (monocomplexes) or two or more phage T4 simultaneously infecting host cells (multicomplexes).

Multiplicity reactivation (MR) is the process by which two or more virus genomes, each containing inactivating genome damage, can interact within an infected cell to form a viable virus genome. Salvador Luria, while studying UV irradiated phage T4 in 1946, discovered MR and proposed that the observed reactivation of damaged phage occurs by a recombination mechanism.(see refs.[9][10][11]) This preceded the confirmation of DNA as the genetic material in 1952 in related phage T2 by the Hershey–Chase experiment.[12]

As remembered by Luria (1984,[13] pg. 97) the discovery of reactivation of irradiated phage (referred to as "multiplicity reactivation") immediately started a flurry of activity in the study of repair of radiation damage within the early phage group (reviewed by Bernstein[14] in 1981). It turned out later that the repair of damaged phage by mutual help that Luria had discovered was only one special case of DNA repair. Cells of all types, not just, bacteria and their viruses, but all organisms studied, including humans, are now known to have complex biochemical processes for repairing DNA damages (see DNA repair). DNA repair processes are also now recognized as playing critical roles in protecting against aging, cancer, and infertility.

MR is usually represented by "survival curves" where survival of plaque forming ability of multiply infected cells (multicomplexes) is plotted against dose of genome damaging agent. For comparison, the survival of phage plaque forming ability of singly infected cells (monocomplexes) is also plotted against dose of genome damaging agent. The top figure shows the survival curves for phage T4 multicomplexes and monocomplexes with increasing dose of UV light. Since survival is plotted on a log scale it is clear that survival of multicomplexes exceeds that of monocomplexes by very large factors (depending on dose). The UV inactivation curve for multicomplexes has an initial shoulder. Other phage T4 DNA damaging agents with shoulders in their multicomplex survival curves are X-rays[15][16] and ethyl methane sulfonate (EMS).[14] The presence of a shoulder has been interpreted to mean that two recombinational processes are used.[17] The first one repairs DNA with high efficiency (in the "shoulder"), but is saturated in its ability as damage increases; the second pathway functions at all levels of damage. Surviving T4 phage released from multicomplexes show no increase in mutation, indicating that MR of UV irradiated phage is an accurate process.[17]

The bottom figure shows the survival curves for inactivation of phage T4 by the DNA damaging agent mitomycin C (MMC). In this case the survival curve for multicomplexes has no initial shoulder, suggesting that only the second recombinational repair process described above is active. The efficiency of repair by this process is indicated by the observation that a dose of MMC that allows survival of only 1 in 1,000 monocomplexes allows survival of about 70% of multicomplexes. Similar multicomplex survival curves (without shoulders) were also obtained for the DNA damaging agents P32 decay, psoralen plus near-UV irradiation (PUVA), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), methyl methane sulfonate (MMS) and nitrous acid.[14]

Several of the genes found to be necessary for MR in phage T4 proved to be orthologs for genes essential for recombination in prokaryotes, eukaryotes and archaea. This includes, for instance, T4 gene uvsX[18] which specifies a protein that has three-dimensional structural homology to RecA from Escherichia coli and the homologous protein RAD51 in eukaryotes and RadA in archaea. It has been suggested that the efficient and accurate recombinational repair of DNA damages during MR may be analogous to the recombinational repair process that occurs during meiosis in eukaryotes.[19]

History

The specific time and place of T4 phage isolation remains unclear, though they were likely found in sewage or fecal material. T4 and similar phages were described in a paper by Thomas F. Anderson, Max Delbrück, and Milislav Demerec in November 1944.[20]

A number of Nobel Prize winners worked with phage T4 or T4-like phages including Max Delbrück, Salvador Luria, Alfred Hershey, James D. Watson, and Francis Crick. Other important scientists who worked with phage T4 include Michael Rossmann, Seymour Benzer, Bruce Alberts, Gisela Mosig,[21] Richard Lenski, and James Bull.

See also

References

  1. ↑ Miller, ES; Kutter, E; Mosig, G; Arisaka, F; Kunisawa, T; Rüger, W (March 2003). "Bacteriophage T4 genome.". Microbiology and molecular biology reviews : MMBR 67 (1): 86–156, table of contents. doi:10.1128/MMBR.67.1.86-156.2003. PMC 150520. PMID 12626685.
  2. ↑ Madigan M, Martinko J (editors) (2006). Brock Biology of Microorganisms (11th ed.). Prentice Hall. ISBN 0-13-144329-1.
  3. ↑ Malys N (2012). "Shine-Dalgarno sequence of bacteriophage T4: GAGG prevails in early genes". Molecular Biology Reports 39 (1): 33–9. doi:10.1007/s11033-011-0707-4. PMID 21533668.
  4. ↑ Yu, F.; Mizushima, S. (1982). "Roles of lipopolysaccharide and outer membrane protein OmpC of Escherichia coli K-12 in the receptor function for bacteriophage T4". Journal of Bacteriology 151 (2): 718–722. PMC 220313. PMID 7047495.
  5. ↑ Furukawa, H.; Mizushima, S. (1982). "Roles of cell surface components of Escherichia coli K-12 in bacteriophage T4 infection: Interaction of tail core with phospholipids". Journal of Bacteriology 150 (2): 916–924. PMC 216445. PMID 7040345.
  6. ↑ McCarthy D, Minner C, Bernstein H, Bernstein C (1976). "DNA elongation rates and growing point distributions of wild-type phage T4 and a DNA-delay amber mutant". J Mol Biol 106 (4): 963–81. doi:10.1016/0022-2836(76)90346-6. PMID 789903.
  7. ↑ Drake JW (1970) The Molecular Basis of Mutation. Holden-Day, San Francisco ISBN 0816224501 ISBN 978-0816224500
  8. ↑ Rao, Venigalla B; Black, Lindsay W (1 January 2010). "Structure and assembly of bacteriophage T4 head". Virology Journal 7 (1): 356. doi:10.1186/1743-422X-7-356.
  9. ↑ Luria SE (1947). "Reactivation of Irradiated Bacteriophage by Transfer of Self-Reproducing Units". Proc. Natl. Acad. Sci. U.S.A. 33 (9): 253–64. doi:10.1073/pnas.33.9.253. PMC 1079044. PMID 16588748.
  10. ↑ LURIA SE, DULBECCO R (1948). "Lethal mutations, and inactivation of individual genetic determinants in bacteriophage". Genetics 33 (6): 618. PMID 18100306.
  11. ↑ Luria SE, Dulbecco R (1949). "Genetic Recombinations Leading to Production of Active Bacteriophage from Ultraviolet Inactivated Bacteriophage Particles". Genetics 34 (2): 93–125. PMC 1209443. PMID 17247312.
  12. ↑ HERSHEY AD, CHASE M (1952). "Independent functions of viral protein and nucleic acid in growth of bacteriophage". J. Gen. Physiol. 36 (1): 39–56. doi:10.1085/jgp.36.1.39. PMC 2147348. PMID 12981234.
  13. ↑ Salvador E. Luria. A Slot Machine, A Broken Test Tube: An Autobiography. Harper & Row, New York: 1984. Pp. 228. ISBN 0-06-015260-5 (USA and Canada)
  14. 1 2 3 Bernstein C (1981). "Deoxyribonucleic acid repair in bacteriophage". Microbiol. Rev. 45 (1): 72–98. PMC 281499. PMID 6261109.
  15. ↑ WATSON JD (1952). "The properties of x-ray inactivated bacteriophage". J. Bacteriol. 63 (4): 473–85. PMC 169298. PMID 14938320.
  16. ↑ HARM W (1958). "Multiplicity reactivation, marker rescue, and genetic recombination in phage T4 following x-ray inactivation". Virology 5 (2): 337–61. doi:10.1016/0042-6822(58)90027-8. PMID 13544109.
  17. 1 2 Yarosh DB (1978). "UV-induced mutation in bacteriophage T4". J. Virol. 26 (2): 265–71. PMC 354064. PMID 660716.
  18. ↑ Story RM, Bishop DK, Kleckner N, Steitz TA (1993). "Structural relationship of bacterial RecA proteins to recombination proteins from bacteriophage T4 and yeast". Science 259 (5103): 1892–6. doi:10.1126/science.8456313. PMID 8456313.
  19. ↑ Bernstein C (1979). "Why are babies young? Meiosis may prevent aging of the germ line". Perspect. Biol. Med. 22 (4): 539–44. doi:10.1353/pbm.1979.0041. PMID 573881.
  20. ↑ Abedon, ST (June 2000). "The murky origin of Snow White and her T-even dwarfs.". Genetics 155 (2): 481–6. PMC 1461100. PMID 10835374.
  21. ↑ Nossal, NG; Franklin, JL; Kutter, E; Drake, JW (November 2004). "Anecdotal, historical and critical commentaries on genetics. Gisela Mosig.". Genetics 168 (3): 1097–104. PMID 15579671.

Further reading

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