Mutation near the polyoma DNA replication origin permits productive infection of F9 embryonal carcinoma cells

Fujimura, Frank K.; Deininger, Prescott L.; Friedmann, Theodore; Linney, Elwood

doi:10.1016/0092-8674(81)90445-1

Cited by 197 publications

(172 citation statements)

References 34 publications

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“…The possibility remains that this observed specificity is not a consequence of an interaction between the Py A enhancer and the MoMuLV enhancer but rather to an interaction of the Mo-MuLV enhancer with some other component of the Py genome such as the origin for DNA replication or the early promoter. As all the previously characterized tissue-specific variants of Py and some MoMuLV have been observed, however, to undergo enhancer rearrangements with duplications and deletions of the A and B core sequences (13)(14)(15) and with no changes in the origin of DNA replication or early promoter, we feel that an interaction between the Py A enhancer and the Mo-MuLV enhancer is a likely cause of the pancreatic tissue specificity we observe. With either of these possibilities, however, it remains clear that combinational principles in which distinct genetic elements can act together to yield a different and unique tissue specificity must be invoked to explain this pancreas specificity.…”

Section: Discussionmentioning

confidence: 78%

“…It appears that alterations in the B enhancer can display a tissue specificity for expression in certain lines of embryonal carcinoma cells (13)(14)(15). In addition to transcriptional regulation, the Py enhancers and also the heterologous immunoglobulin heavy-chain core enhancer regulate permissivity or tissue specificity of Py viral DNA replication (11,16), indicating that some linkage exists between tissuespecific DNA replication and transcription.…”

mentioning

confidence: 99%

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A pancreas specificity results from the combination of polyomavirus and Moloney murine leukemia virus enhancer.

Rochford¹,

Campbell²,

Villarreal³

1987

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

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Section: Discussionmentioning

confidence: 78%

mentioning

confidence: 99%

A pancreas specificity results from the combination of polyomavirus and Moloney murine leukemia virus enhancer.

Rochford¹,

Campbell²,

Villarreal³

1987

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

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“…Polyomavirus mutants that productively infect EC cells have been isolated, and several of the mutations have been mapped to the enhancer region of the early promoter (16,42,53). Expression data provide evidence that the primary block for polyomavirus replication in EC cells is a defect in early viral expression, and the enhancer mutations relieve the defect by activating the early promoter (29).…”

mentioning

confidence: 99%

Proviral sequences that restrict retroviral expression in mouse embryonal carcinoma cells.

Loh¹,

Sievert²,

Scott³

1987

Mol. Cell. Biol.

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Embryonal carcinoma (EC) cells are nonpermissive for retrovirus replication. Restriction of retroviral expression in EC cells was studied by using DNA transfection techniques. To investigate the activity of the Moloney murine leukemia virus (M-MuLV) enhancer and promoter sequences, the M-MuLV long terminal repeat and the defined long terminal repeat deletions were linked to neo structural gene sequences that encode resistance to the neomycin analog G418. Transient expression data and drug resistance frequencies support the findings that the M-MuLV enhancer is not active in EC cells but that promoter sequences are functional. In addition, a proviral DNA fragment that encodes the leader RNA sequence of a M-MuLV recombinant retrovirus was found to restrict expression specifically in EC cells. Deletion analysis of the leader fragment localized the inhibitory sequences to a region that spans the M-MuLV tRNA primer binding site. It is not known whether restriction occurs at a transcriptional or posttranscriptional level, but steady-state RNA levels in transient expression assays were significantly reduced.

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“…The pluripotential mouse embryonal carcinoma (EC) cell is notable because infection of these cells by polyoma virus results in no virus replication (Swartzendruber & Lehman, 1975) and because no synthesis of polyoma early or late proteins occurs in infected cells (Dandolo et al, 1983 ;Fujimura et al, 1981 a, b). Mutant polyoma viruses (Fujimura et al, 1981a;Katinka et al, 1980Katinka et al, , 1981Sekikawa & Levine, 1981 ;Vasseur et al, 1980) able to grow in EC cells carry alterations in a non-coding region of the viral genome comprising the enhancer (deVilliers & Schaffner, 1981;Tyndall et aL, 1981) of early gene transcription, This suggests that EC cells differ from fibroblast cells in that EC cells do not efficiently transcribe viral genes whose regulation is controlled by enhancers. Direct evidence METHODS Cells and media.…”

Section: Introductionmentioning

confidence: 99%

Restricted Replication of Herpes Simplex Virus Type 1 in Murine Embryonal Carcinoma Cells

Bell

Campione-Piccardo

Craig

et al. 1987

Journal of General Virology

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SUMMARYHerpes simplex virus type i (HSV-1) has a broad host range but the KOS strain of HSV-1 did not replicate efficiently in murine embryonal carcinoma (EC) cells. The yield of infectious HSV-1 from EC cells was 100-to 1000-fold lower than that from fibroblast cell lines of mouse, monkey or human origin. The thymidine kinase (TK) gene of HSV-1 is expressed early during the infectious cycle. The levels of TK mRNA and of TK activity in infected EC ceils were only two-to threefold lower than levels from infected fibroblast cells. Infected EC cells supported replication of about half as much HSV-1 DNA as did fibroblast cells. The reduced yield of infectious virus was consistent with a paucity of virions in infected EC cells examined by electron microscopy, suggesting a major block late during the HSV-I infectious cycle. We isolated a variant strain of HSV-1, called KOSEC, which replicated as efficiently in EC cells as in mouse fibroblasts. KOSEC infected EC and fibroblast cells, synthesized more TK mRNA, more TK enzyme, and more HSV-1 DNA than did the same cells infected with the KOS stain. Both HSV-1 strains induced similar levels of synthesis of gD, an early viral glycoprotein. By co-infection of EC cells with the KOS and KOSEC virus, both the elevated virus yield and the elevated TK synthesis seen in KOSECinfected cells appeared to be recessive. Apparently a viral mutation that affects expression of some early viral functions can also overcome the EC cell restriction to HSV-1 replication.

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Mutation near the polyoma DNA replication origin permits productive infection of F9 embryonal carcinoma cells

Cited by 197 publications

References 34 publications

A pancreas specificity results from the combination of polyomavirus and Moloney murine leukemia virus enhancer.

A pancreas specificity results from the combination of polyomavirus and Moloney murine leukemia virus enhancer.

Proviral sequences that restrict retroviral expression in mouse embryonal carcinoma cells.

Restricted Replication of Herpes Simplex Virus Type 1 in Murine Embryonal Carcinoma Cells

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