Structure of the Marek's disease virus BamHI-H gene family: genes of putative importance for tumor induction

Bradley, Guy; Hayashi, Masanobu; Lancz, Gerald; Tanaka, Akiko; Nonoyama, Meihan

doi:10.1128/jvi.63.6.2534-2542.1989

Cited by 84 publications

(38 citation statements)

References 35 publications

(36 reference statements)

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“…Oncogenic MDV strains do not replicate well in cell culture and become attenuated rapidly during serial passage (10). Attenuation is accompanied by alterations in the sequence and expression of the MDV genome (3,4,13,21,41,44), loss of horizontal transmission (10), and a decreased ability to infect lymphocytes in vivo and in vitro (39).…”

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confidence: 99%

“…These approaches have led to the identification of a number of MDV genes and regions having possible significance for transformation. The repeats (terminal and inverted, respectively) flanking the unique long (UL) region of the MDV genome (TR L and IR L ) encode a family of RNAs that become disrupted during attenuation (3,4). This region also contains the meq gene, which encodes a leucine-zipper-containing protein expressed in LBCLs (18).…”

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Retention of oncogenicity by a Marek's disease virus mutant lacking six unique short region genes

Parcells

Anderson

Morgan

1995

J Virol

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We previously reported the construction of Marek's disease virus (MDV) strains having mutations in various genes that map to the unique short (US) region of the viral genome (These strains were constructed by using a high-passage-level serotype 1 MDV strain which grew well in chicken embryo fibroblasts. Despite the growth of the parent and mutant viruses in cell culture, in vivo studies were limited by poor growth of these strains in chickens. One of the mutants studied lacked 4.5 kbp of US region DNA and contained the lacZ gene of Escherichia coli inserted at the site of the deletion. The deletion removed MDV homologs to the US1, US2, and US10 genes of herpes simplex virus type 1 as well as three MDV-specific open reading frames. We now report the construction of a mutant MDV containing a similar deletion in the US region of the highly oncogenic RB1B strain. This mutant, RB1B⌬4.5lac, had a growth impairment in established chicken embryo fibroblasts similar to that described previously for MDVs lacking a functional US1 gene. In chickens, RB1B⌬4.5lac showed decreased early cytolytic infection, mortality, tumor incidence, and horizontal transmission. Several lymphoblastoid cell lines were established from RB1B⌬4.5lacinduced tumors, and virus reactivated from these cell lines was LacZ ؉ . These results indicate that the deleted genes are nonessential for the transformation of chicken T cells or for the establishment and maintenance of latency. On the basis of the growth impairment observed for RB1B⌬4.5lac in cell culture and in vivo, we conclude that deletion of these genes affects the lytic replication of MDV. This is the first MDV mutant constructed in the RB1B oncogenic strain, and the methodology described herein provides for the direct examination of MDV-encoded determinants of oncogenicity.

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Retention of oncogenicity by a Marek's disease virus mutant lacking six unique short region genes

Parcells

Anderson

Morgan

1995

J Virol

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“…Several laboratories demonstrated that the amplification of a 132-bp repeat in this region during prolonged passages of MDV correlates with the attenuation of viral oncogenicity (15,25,37). Bradley et al (3,4) further showed that expansion of this region results in the disruption of a 1.8-kb transcript(s) and suggested that this transcript is involved in MDV-induced transformation. Other transcripts that are initiated or terminated near the 132-bp repeat region have also been described (6).…”

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“…To further characterize this antigen, we proceeded to identify two Xgtll (gtll) clones (GA8 and RA2), derived from the MDV genome, that react with this monoclonal antibody (9). These two clones map within the BamHI H fragment at a region close to the 1.8-kb transcription unit (3,4,20). We also raised antisera against the recombinant B-galactosidase-MDV fusion proteins of these two clones.…”

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Structural analysis and transcriptional mapping of the Marek's disease virus gene encoding pp38, an antigen associated with transformed cells

Cui

Lee

Liu

et al. 1991

J Virol

100

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The gene encoding a Marek's disease virus (MDV) pp38 phosphoprotein has been identified, sequenced, and localized to the BamHI H fragment to the left of the putative MDV origin of replication. The open reading frame was defined by sequencing of a lacZ-pp38 fusion protein gene from a Agt 1 expression library. The entire open reading frame is 290 amino acids long and codes for a protein with a calculated molecular weight of 31,169, compared with the size of 38 kDa of the phosphorylated form estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Si nuclease protection analysis showed that the pp38 gene is transcribed leftward as an unspliced mRNA. On the basis of transcriptional mapping studies, the pp38 transcript is predicted to be about 1.8 kb in length without a poly(A) sequence. Its promoter-enhancer region overlaps that of the major rightward BamHI H 1.8-kb transcript implicated in tumor induction. This region

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“…Thus, it seemed that a particular sequence within BamHI-H and -K2 regions of MDV DNA was not preferentially cleaved by DNaseI. The transcriptional map of BamHI-H region was reported (4). Transcription of several mRNAs was found to initiate within BamHI-H region, with major transcripts initiating on either side of a putative MDV origin of lytic replication.…”

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Nucleosomal Structure of Marek's Disease Virus Genome in Transformed Lymphoblastoid Cell Lines, MDCC‐MSB1 and MDCC‐RP1

Hayashi

Nakamura

Isogai

et al. 1991

Microbiology and Immunology

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The latent MDV (Marek's disease virus) genomes are folded into nucleosomal structures in both virus-productive and -nonproductive lymphoblastoid cell lines, MDCC-MSB1 (MSB-1) and -RP1 (RP-1), respectively. There was no difference between transcriptionally active and inactive regions of MDV genome with regard to nucleosomal patterns. In order to investigate whether nucleosomal structure is correlated with the repression of the transcription of MDV genome in lymphoblastoid cells, we examined the DNaseI sensitivity of nucleosomal MDV DNA in lymphoblastoid cell lines, MSB-1 and RP-1. No difference in the DNaseI sensitivity between transcriptionally active and inactive MDV DNA regions in lymphoblastoid cells was observed.

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Structure of the Marek's disease virus BamHI-H gene family: genes of putative importance for tumor induction

Cited by 84 publications

References 35 publications

Retention of oncogenicity by a Marek's disease virus mutant lacking six unique short region genes

Retention of oncogenicity by a Marek's disease virus mutant lacking six unique short region genes

Structural analysis and transcriptional mapping of the Marek's disease virus gene encoding pp38, an antigen associated with transformed cells

Nucleosomal Structure of Marek's Disease Virus Genome in Transformed Lymphoblastoid Cell Lines, MDCC‐MSB1 and MDCC‐RP1

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