On the terminally redundant sequences of bacteriophage T3 DNA

Fujisawa, Hisao; Sugimoto, Kazunori

doi:10.1016/0042-6822(83)90342-2

Cited by 23 publications

(13 citation statements)

References 20 publications

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“…Analogous duplicative events have been proposed for the HSV-1 a sequence (21,67) as well as for bacteriophage T3 and T7 (22,23). In phage T7, detection of abundant short hairpin fragments derived from a potential stem-loop adjacent to the terminal repeat inspired a model in which a nick at the base of the stem-loop primes DNA synthesis back through the repeat.…”

Section: Discussionmentioning

confidence: 99%

“…Analysis of a recombinant GPCMV that produced only type II genomes provided strong evidence that duplication of the terminal repeat must occur with each cleavage event (53), a phenomenon characteristic of bacteriophages T3 and T7 (22,23). But in addition to duplicative cleavage, GPCMV must also be capable of simple, nonduplicative cleavage to produce type I genomes which lack the right-terminal repeat.…”

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confidence: 99%

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Dramatic Effects of 2-Bromo-5,6-Dichloro-1-β- d -Ribofuranosyl Benzimidazole Riboside on the Genome Structure, Packaging, and Egress of Guinea Pig Cytomegalovirus

Nixon¹,

McVoy

2004

J Virol

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The halogenated benzimidazoles BDCRB (2-bromo-5,6-dichloro-1-␤-D-riborfuranosyl benzimidazole riboside) and TCRB (2,5,6-trichloro-1-␤-D-riborfuranosyl benzimidazole riboside) were the first compounds shown to inhibit cleavage and packaging of herpesvirus genomes. Both inhibit the formation of unit length human cytomegalovirus (HCMV) genomes by a poorly understood mechanism (M. R. Underwood et al., J. Virol. 72:717-715, 1998; P. M. Krosky et al., J. Virol. 72:4721-4728, 1998). Because the simple genome structure of guinea pig cytomegalovirus (GPCMV) provides a useful model for the study of herpesvirus DNA packaging, we investigated the effects of BDCRB on GPCMV. GPCMV proved to be sensitive to BDCRB (50% inhibitory concentration ‫؍‬ 4.7 M), although somewhat less so than HCMV. In striking contrast to HCMV, however, a dose of BDCRB sufficient to reduce GPCMV titers by 3 logs (50 M) had no effect on the quantity of GPCMV genomic DNA that was formed in infected cells. Electron microscopy revealed that this DNA was in fact packaged within intranuclear capsids, but these capsids failed to egress from the nucleus and failed to protect the DNA from nuclease digestion. The terminal structure of genomes formed in the presence of BDCRB was also altered. Genomes with ends lacking a terminal repeat at the right end, which normally exist in an equimolar ratio with those having one copy of the repeat at the right end, were selectively eliminated by BDCRB treatment. At the left end, BDCRB treatment appeared to induce heterogeneous truncations such that 2.7 to 4.9 kb of left-end-terminal sequences were missing. These findings suggest that BDCRB induces premature cleavage events that result in truncated genomes packaged within capsids that are permeable to nuclease. Based on these and other observations, we propose a model for duplication of herpesvirus terminal repeats during the cleavage and packaging process that is similar to one proposed for bacteriophage T7 (Y. B. Chung, C. Nardone, and D. C. Hinkle, J. Mol. Biol. 216:939-948, 1990).The Herpesviridae family of viruses includes several significant human pathogens, including herpes simplex virus type 1 (HSV-1) and HSV-2, varicella-zoster virus, Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus, and human cytomegalovirus (HCMV). Herpesviruses have large (130 to 235 kb) double-stranded linear DNA genomes that circularize shortly after infection (24,46,47,57). Viral DNA is replicated to form large concatemers of head-to-tail linked genomes that are packaged and cleaved to produce encapsidated unit length genomes (4,6,33,43,46,57,60,71).Mechanistically, herpesvirus DNA packaging is highly reminiscent of the large double-stranded DNA bacteriophage, in that packaging proceeds in one direction and cleavage occurs one genome length in from concatemer ends (43,46,49,60,71). As in many bacteriophage, cleavage of herpesvirus DNA cannot take place until two requirements have been met: (i) a near-genome length of DNA has entered the capsid and (ii) specific cis-acting DNA ...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Dramatic Effects of 2-Bromo-5,6-Dichloro-1-β- d -Ribofuranosyl Benzimidazole Riboside on the Genome Structure, Packaging, and Egress of Guinea Pig Cytomegalovirus

Nixon¹,

McVoy

2004

J Virol

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“…We undertook the present study with the aim of clarifying, at the nucleotide level, the putative phylogenetic relationship of phage K 11 with phages T3 and T7 by sequencing the termini of K I 1 DNA. Our results show that this phage has a characteristic terminal redundancy (TR) which we have compared to the known sequences of the TR of T7 (Moffat et al, 1984) and of T3 (Fujisawa & Sugimoto, 1983). [The function of the TRs of T7-related phages is not clearly established but current views favour the hypothesis of Watson (1972) according to which a TR is necessary for the formation of intracellular concatemers of phage genomes; these concatemers would be essential for the complete replication of linear phage genomes.…”

Section: On the Evolution Of The Terminal Redundancies Ofmentioning

confidence: 98%

“…Although we have no rigorous proof for this, our interpretation is favoured by (i) analogy to what is known for the related phages T7 (Dunn & Studier, 1983) and T3 (Fujisawa & Sugimoto, 1983), (ii) identification, on agarose gels, of the small restriction fragments produced upon endonuclease KpnI digestion of TR sequences and (iii) full resistance of K11 DNA to S1 nuclease digestion. Fujisawa & Sugimoto (1983) were able to show regions of strong homology at both extremes of the TR of T7 and T3, but the direct linear homology between the middle portions of these sequences (comprising about 80 and 150 nucleotides in T7 and T3, respectively) was rather poor or non-existent. We made similar observations with regard to the TR of K 11 as compared with that of T7 and T3 (Fig.…”

Section: On the Evolution Of The Terminal Redundancies Ofmentioning

confidence: 99%

“…1), revealed fragments HpaI L and HpaI 0 as suitable for direct sequencing of the termini by the method of Maxam & Gilbert (1977). The terminal 5' nucleotides were determined by P 1 digestion of the labelled fragments followed by identification of the resulting labelled nucleoside 5'-monophosphates by thin-layer chromatography (Fujisawa & Sugimoto, 1983). The TR sequence, as determined from both ends of K11 DNA, is depicted in Fig.…”

Section: On the Evolution Of The Terminal Redundancies Ofmentioning

confidence: 99%

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On the Evolution of the Terminal Redundancies of Klebsiella Phage No. 11 and of Coliphages T3 and T7

Dietz¹,

Kössel²,

Hausmann³

1985

Journal of General Virology

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SUMMARYThe phylogenetic relationship between Klebsiella phage No. 11 and the classical coilphages T7 and T3, postulated in a previous study, was investigated at the nucleotide level by sequencing the termini of phage No. 11 DNA. This DNA was found to have a terminal redundancy of 181 base pairs. Comparison of the terminal sequences of T7, T3 and No. 11 DNA suggests that the terminal redundancies of the three phages contain different expansions and variations of the short "founder sequence' 5' TTAACCTTGGG 3' of a common ancestor.In a previous study (Korsten et al., 1979) we reported evidence that the capsule-specific Klebsiella phage No. 11 (henceforth called K 11) is distantly related to the classical coliphages T3 and T7. This evidence was based mainly on the fact that phage K11, like T3 and T7, codes for an early protein of molecular weight about 100000 which shows an RNA polymerase activity specific for promoters located on the phage genome and not found on the DNA of the host. However, the template specificity of the phage K11 polymerase was totally different from that of T3 or T7: the RNA polymerases of these phages did not transcribe phage K11 DNA to any extent, and vice versa. (This is in contrast to the 20 to 50% heterologous transcriptional activity found upon comparing the RNA polymerases ofT3 and T7.) No compelling evidence for a phylogenetic common origin of phages K11 on the one hand, and T3 and T7 on the other, was provided by other criteria, since the first showed no serological crossreactions with the latter and K11 DNA did not efficiently form heteroduplexes with DNA ofT3 or T7. Also, a comparison of the electrophoretic patterns of Kll-coded intracellular proteins with those of T7 revealed marked differences in the molecular weights of most proteins; thus, only a few of these could be considered obviously homologous (Korsten et al., 1979). We undertook the present study with the aim of clarifying, at the nucleotide level, the putative phylogenetic relationship of phage K 11 with phages T3 and T7 by sequencing the termini of K I 1 DNA. Our results show that this phage has a characteristic terminal redundancy (TR) which we have compared to the known sequences of the TR of T7 (Moffat et al

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A simple method of distinguishing the bacterial viruses T3 and T7, and a critical reevaluation of their heterologous and homologous exclusion

Krüger

Mann

Hansen

et al. 1988

J. Basic Microbiol.

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A method is presented allowing a clear distinction between bacterial viruses T3 and T7 by plating on selectively permissive host cells. The indicator strains are Escherichia coli cells containing either cloned pif genes (exclusively permissive for T3) or the EcoRV DNA restriction system (permissive only for T7): The efficiencies of plating of the two phages on these hosts differ by more than 8 orders of magnitude. This method was applied to reinvestigate the controversial question of mutual exclusion between T3 and T7. Under single-burst conditions, about 50% of coinfected cells (permissive for both viruses) produced T3 and T7 progeny while about 25% reproduced only T3 and about 25% only T7. The burst size of co-infected cells was slightly reduced, compared to controls infected with only one virus type. Homologous exclusion among T3 phages was also not seen; rather, there was a gene dosage effect: T3-encoded RNA polymerase activity as well as T3-specific RNA synthesis increased proportionally to the multiplicity of infection (2.5-20 plaque-forming units/cell).

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On the terminally redundant sequences of bacteriophage T3 DNA

Cited by 23 publications

References 20 publications

Dramatic Effects of 2-Bromo-5,6-Dichloro-1-β- d -Ribofuranosyl Benzimidazole Riboside on the Genome Structure, Packaging, and Egress of Guinea Pig Cytomegalovirus

Dramatic Effects of 2-Bromo-5,6-Dichloro-1-β- d -Ribofuranosyl Benzimidazole Riboside on the Genome Structure, Packaging, and Egress of Guinea Pig Cytomegalovirus

On the Evolution of the Terminal Redundancies of Klebsiella Phage No. 11 and of Coliphages T3 and T7

A simple method of distinguishing the bacterial viruses T3 and T7, and a critical reevaluation of their heterologous and homologous exclusion

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