Construction of a double-jointed herpes simplex viral DNA molecule: Inverted repeats are required for segment inversion, and direct repeats promote deletions

Smiley, James R.; Fong, Bessie S.; Leung, Wai-Choi

doi:10.1016/0042-6822(81)90161-6

Cited by 82 publications

(85 citation statements)

References 21 publications

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“…The BamHI restriction fragment U of HSV-1 ANG DNA corresponds to BamHI V of the HSV-1 strains KOS and F (Knopf et al, 1983 ;K aerner et al, 1983 ;Smiley et al, 1981 ;Locker & Frenkel, 1979) and is contained within the repeat unit of a class II defective derived from HSV-1 ANG DNA. Post et al (1980) have shown that it is not possible to clone the corresponding fragment from HSV-1 F into E. coli.…”

Section: Localization Of a Deleted Sequence In A Jmgment Of A Class Imentioning

confidence: 99%

Sequence of the Putative Origin of Replication in the UL Region of Herpes Simplex Virus Type 1 ANG DNA

Gray

Kaerner

1984

Journal of General Virology

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SUMMARYInterest has been stimulated concerning the region mapping between 0-38 and 0.42 on the prototype configuration of the herpes simplex virus type 1 (HSV-1) genome due to the high probability of the presence there of a second origin of DNA replication. A 960 bp restriction fragment (HinfI E) of a class II defective HSV-I ANG DNA has been sequenced using the viral DNA rather than molecularly cloned DNA. This fragment includes the BamHI U/R cleavage site, mapping at approximately 0-4. Part of the sequence derived in this study displays homology with the origins of DNA replication contained in TRs/IRs of HSV-1 and HSV-2 DNA. The homologous region comprising 76 bp occurs as two copies, each of which contains two palindromically arranged copies of an 8 bp sequence identical to the 'consensus' sequence reported to be part of the origin of DNA replication at the terminus of the mammalian adenoviruses. It can be deduced from a comparison of this structure to the TRs/IRs origin of HSV-1 and HSV-2 that there are two origins of replication in the UL region of HSV-1 ANG DNA. Assuming that the orientation of the consensus sequence is relevant to the direction of DNA replication, one can conclude that the UL origin(s) of HSV-1 ANG is (are) bidirectional. It has not yet been possible to clone DNA fragments molecularly which include the region spanning the UL origin(s) of HSV-1 DNA.

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Section: Localization Of a Deleted Sequence In A Jmgment Of A Class Imentioning

confidence: 99%

Sequence of the Putative Origin of Replication in the UL Region of Herpes Simplex Virus Type 1 ANG DNA

Gray

Kaerner

1984

Journal of General Virology

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“…One of the earliest reports on HSV recombination dates to 1955; co-infection of chorioallantois with HSV strains of varying virulence led to recombinant progeny with altered virulence (1). Additional proof for recombination of the HSV genome comes from the observation that the subgenomic elements, U L and U S , undergo inversion with respect to each other, generating four possible isomeric forms (2)(3)(4). This genome isomerization appears to be a consequence of homologous recombination rather than of a site-specific event involving cleavage at the a sequences that reside in inverted orientations at the termini of U L and U S (5).…”

mentioning

confidence: 99%

In Vitro Strand Exchange Promoted by the Herpes Simplex Virus Type-1 Single Strand DNA-binding Protein (ICP8) and DNA Helicase-Primase

Nimonkar

Boehmer

2002

Journal of Biological Chemistry

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The genome of herpes simplex virus type-1 undergoes a high frequency of homologous recombination in the absence of a virus-encoded RecA-type protein. We hypothesized that viral homologous recombination is mediated by the combined action of the viral single strand DNA-binding protein (ICP8) and helicase-primase. Our results show that ICP8 catalyzes the formation of recombination intermediates (joint molecules) between circular single-stranded acceptor and linear duplex donor DNA. Joint molecules formed by invasion of a 3-terminal strand displaces the non-complementary 5-terminal strand, thereby creating a loading site for the helicaseprimase. Helicase-primase acts on these joint molecules to promote ATP-dependent branch migration. Finally, we have reconstituted strand exchange by the synchronous action of ICP8 and helicase-primase. Based on these data, we present a recombination mechanism for a eukaryotic DNA virus in which a single strand DNAbinding protein and helicase cooperate to promote homologous pairing and branch migration.Homologous recombination is a fundamental biological process. It serves, among other purposes, to repair DNA damage such as double strand DNA breaks or to reinitiate DNA replication at stalled replication forks. Herpes simplex virus (HSV) 1 undergoes a high frequency of homologous recombination during its replicative cycle. One of the earliest reports on HSV recombination dates to 1955; co-infection of chorioallantois with HSV strains of varying virulence led to recombinant progeny with altered virulence (1). Additional proof for recombination of the HSV genome comes from the observation that the subgenomic elements, U L and U S , undergo inversion with respect to each other, generating four possible isomeric forms (2-4). This genome isomerization appears to be a consequence of homologous recombination rather than of a site-specific event involving cleavage at the a sequences that reside in inverted orientations at the termini of U L and U S (5). Nevertheless, the a sequences may act as recombination hotspots. In this context, the a sequences are the sites of double-stranded (ds) DNA breaks created either by a structure-specific endonuclease 2 or during cleavage and packaging of the viral genome (6, 7). The terminal a sequences have also been shown to be involved in the circularization of the viral genome by homologous recombination (8). This process occurs immediately after infection by the virus and appears to be mediated by host factors (9, 10). The frequency of recombination has been estimated to be on the order of 0.5-0.7%/kilobase of the viral genome (11). Furthermore, a screen for replication-competent HSV-1 origins from a library in which particular origin elements were substituted with random sequences resulted in the isolation of wild-type origins at a frequency of 25% as a consequence of homologous recombination (12).Insight into the mechanism by which homologous recombination proceeds during HSV-1 replication is provided by several lines of evidence; it was shown that plasmi...

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“…Because certain viral gene products are not essential for replication of the virus in cell culture (2, 3) and because requirements for packaging of the DNA into virions permit some variation in size ofthe genome (4), it has proved possible by use of recombinant DNA technology to generate viable mutants containing sizable deletions or insertions of specific genetic information (5)(6)(7)(8)(9)(10). For example, mutants containing duplications of HSV-1 DNA sequences inserted into the viral thymidine kinase (TK) gene (tk) (resulting in a selectable TK-phenotype) have yielded information about regulatory signals in the HSV-1 genome (8) and about HSV-1 DNA sequences that mediate the inversion of genome segments (6,7,10).…”

mentioning

confidence: 99%

Expression of herpes simplex virus glycoprotein C from a DNA fragment inserted into the thymidine kinase gene of this virus.

Lee¹,

Pogue‐Geile²,

Pereira³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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Previous reports have described mutants of herpes simplex virus type 1 that fail to produce or accumulate one of the major glycoproteins, glycoprotein C (gC). This defect is not lethal in cell culture, has been associated with the syncytial plaque morphology of some mutants, and may result from mutations that map to a region on the genome noncontiguous with the structural gene for gC. To investigate the conditions required for, and consequences of, gC expression in a specific genetic background, we have inserted a wild-type allele of the gC gene into the thymidine kinase gene (tk) of a gC-fusion-inducing viral mutant, strain MP. This was accomplished by identifying cloned viral DNA fragments homologous to gC mRNA, inserting the appropriate fragments into the viral tk cloned in pBR322, and then cotransfecting cells with the recombinant plasmids and DNA from strain MP, for selection of insertional TK-mutants. All TK-mutants containing insertions of appropriate sequences (in either orientation) into tk were found to express gC while maintaining the syncytial plaque morphology of strain MP. Elimination of the insertion from one of the TK-mutants was accompanied by loss of ability to produce gC. Our results permit more precise mapping of the DNA sequence encoding gC, to a subfragment of Sal I fragment R (map coordinates 0.620-0.640) and indicate also that promoter sequences for the gC gene may be located in this fragment. Moreover, we can conclude that the previously described regulatory mutation of strain MP does not prevent expression of gC from the DNA inserted into its gene tk and that the syncytial phenotype of MP cannot be due solely to absence of gC.

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Construction of a double-jointed herpes simplex viral DNA molecule: Inverted repeats are required for segment inversion, and direct repeats promote deletions

Cited by 82 publications

References 21 publications

Sequence of the Putative Origin of Replication in the UL Region of Herpes Simplex Virus Type 1 ANG DNA

Sequence of the Putative Origin of Replication in the UL Region of Herpes Simplex Virus Type 1 ANG DNA

In Vitro Strand Exchange Promoted by the Herpes Simplex Virus Type-1 Single Strand DNA-binding Protein (ICP8) and DNA Helicase-Primase

Expression of herpes simplex virus glycoprotein C from a DNA fragment inserted into the thymidine kinase gene of this virus.

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