Control of Adenovirus Gene Expression: Cellular Gene Products Restrict Expression of Adenovirus Host Range Mutants in Nonpermissive Cells

Katze, Michael G.; Persson, Håkan; Johansson, Börje; Philipson, Lennart

doi:10.1128/jvi.46.1.50-59.1983

Cited by 24 publications

(5 citation statements)

References 31 publications

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Section: Introductionmentioning

confidence: 99%

“…An alternative type of transcriptional activation is that induced by the adenovirus ElA gene product (and the herpes virus immediate early gene product, ICP4) (22)(23)(24)(25)(26)(27)(28)(29)(30)(31). The ElA gene product stimulates expression of its own gene and the other adenovirus RNA polymerase II-transcribed genes, as well as a number of heterologous genes, in a trans-acting manner (22)(23)(24)(25)(26)(27)(28)(29)(30)(31). The mechanism of activation of transcription by ElA is unknown: In several different genes, sites required for transcriptional activity have been localized to sequences upstream of the mRNA initiation sites (26,(28)(29)(30); however, it is unclear if the ElA gene product acts directly or indirectly at these sites (24,26,(28)(29)(30)(31).…”

Section: Introductionmentioning

confidence: 99%

“…The ElA gene product stimulates expression of its own gene and the other adenovirus RNA polymerase II-transcribed genes, as well as a number of heterologous genes, in a trans-acting manner (22)(23)(24)(25)(26)(27)(28)(29)(30)(31). The mechanism of activation of transcription by ElA is unknown: In several different genes, sites required for transcriptional activity have been localized to sequences upstream of the mRNA initiation sites (26,(28)(29)(30); however, it is unclear if the ElA gene product acts directly or indirectly at these sites (24,26,(28)(29)(30)(31). Also, it is unknown whether ElA has any effect on transcription by RNA polymerases I or III.…”

Section: Introductionmentioning

confidence: 99%

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Differential activation of RNA polymerase III-transcribed genes by the polyomavirus enhancer and the adenovirus E1A gene products

Berger

Folk

1985

Nucl Acids Res

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We have compared the effect of the polyomavirus cis-acting transcriptional enhancer and the adenovirus trans-acting E1A gene on expression of RNA polymerase III-transcribed genes (the adenovirus VAI gene and a bacterial tRNA gene) using DNA transfection and transient expression assays. The polyomavirus enhancer has little effect upon transcription of the VAI gene by RNA polymerase III in any cell type tested (murine, hamster, or human). In contrast, expression of the E1A gene within adenovirus infected cells stimulates transcription of RNA polymerase III-transcribed genes from co-transfected DNAs. Human 293 cells, which constitutively produce adenovirus E1A gene products, also express high levels of RNA polymerase III transcripts from transfected DNAs.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Differential activation of RNA polymerase III-transcribed genes by the polyomavirus enhancer and the adenovirus E1A gene products

Berger

Folk

1985

Nucl Acids Res

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“…However, the enhancement of EiB gene expression by E4 gene products is only a rough tendency and exceptions are detected as shown in Table 3. This delicate situation suggests that a cellular factor(s) is involved in the enhancement, in a way similar to how the pre-early function of the AdS ElA gene is mediated through a cellular factor, which suppresses transcription of the other early gene (7,15,22,24,26). Direct evidence for the enhancement of ElB gene expression by E4 gene expression is necessary to substantiate this supposition.…”

Section: Discussionmentioning

confidence: 98%

Expression of the E4 gene is required for establishment of soft-agar colony-forming rat cell lines transformed by the adenovirus 12 E1 gene

Shiroki¹,

Hashimoto²,

Saito³

et al. 1984

J Virol

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Rat 3Y1 cells were transfected with recombinant gARC (pSV2gpt carrying the adenovirus 12 early region 1 [El] gene), and focus formation was observed in monolayer cultures after culture of cells in gpt-selective medium (Eagle medium containing 10% fetal calf serum, xanthine, thymidine, aminopterin, and mycophenolic acid) for 10 days, followed by focus formation. Transformed ElY cell lines were then established from these foci. The ElY cells were transformed morphologically similarly to cells transformed with intact adenovirus 12 DNA but formed no colonies in soft-agar culture and induced tumors in transplanted rats only after a long incubation period. For the establishment of completely transformed cells, 3Y1 cells were transformed with combinations of gARC, pE3 (pBR322 carrying the adenovirus 12 E3 gene), and gE4 (pSV2gpt carrying the adenovirus 12 E4 gene) DNA. E1-3Y cells (3Y1 cells transformed with gARC and pE3 DNA), E1-4Y cells (3Y1 cells transformed with gARC and gE4 DNA), and E1-3-4Y cells (3Y1 cells transformed with gARC, pE3, and gE4 DNA) were established. These transformed cell lines were compared for growth in Eagle medium with 2 or 10% fetal calf serum, colony formation in soft-agar culture, and tumor growth in rats transplanted with the transformed cells. Several transformed cell lines of E1-4Y and E1-3-4Y cells showed colony formation in soft-agar culture and abundant expression of the E1B gene. T antigen f was seen by immunofluorescence as flecks in these cells, in which the E4 gene was transcribed, but was not seen in ElY cells, suggesting that T antigen f was encoded by the E4 gene. The suggestion was confirmed by the observation that T antigen f was detected in COS-1 cells transfected singly with gE4 DNA by immunofluorescence with polyclonal and monoclonal antibodies. Transcription of the E4 gene was confirmed in gE4-transfected COS-1 cells. T antigen f, one of the E4 gene products, was identified as a polypeptide of molecular weight 11,000 (E4-11K) by immunoprecipitation with monoclonal antibodies. The above results also suggest that expression of the E4 gene gives cells the advantage of forming colonies in soft-agar culture. A tendency was noticed for ElB gene expression to be enhanced by E4 gene expression. The relationship between enhancement of colony formation in soft-agar culture and enhancement of E1B gene expression is discussed. Recently, evidence has accumulated showing that the transforming genes of human adenovirus are located in only a small region of the left end of the viral genome (5, 10, 29, 32, 34, 37, 39, 40). The transforming genes of the highly oncogenic adenovirus 12 (Adl2) are located in the left end of Adl2 DNA (early region 1A [ElA] and E1B). Rat cells transformed by the EcoRI-C (0 through 16.4 map units) (CY cells), HindIII-G (0 through 6.8 map units) (GY cells), and AccI-H fragments (0 through 4.7 map units) (HY cells) were established (34, 37, 40). CY and GY cells showed the phenotype of completely transformed cells, showing foci in culture, forming large colonies in ...

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“…It has been suggested that ElA acts by inactivating a cellular repressor of transcription (13,14,16,20,21). This has been used to explain the ability of ElA mutants to synthesize early mRNA and protein at high multiplicity in HeLa cells (16,20,27).…”

Section: Discussionmentioning

confidence: 99%

Control Functions of Adenovirus Transformation Region E1A Gene Products in Rat and Human Cells

Bellett

David

et al. 1985

Molecular and Cellular Biology

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Altered control of the rat cell cycle induced by adenovirus requires expression of transformation region E1A, but not of E1B, E2A, E2B, or late genes. We show here that neither E3 nor E4 is required, so the effect results directly from an E1A product. Mutants with defects in the 289-amino-acid (aa) E1A product had little or no effect on the rat cell cycle even at 1,000 IU per cell. A mutant (pm975) lacking the 243-aa E1A product altered cell cycle progression, but less efficiently than did wild-type virus. The 289-aa E1A protein is therefore essential for cell cycle effects; the 243-aa protein is also necessary for the full effect but cannot act alone. Mutants with altered 289-aa E1A proteins showed different extents of leak expression of viral early region E2A as the multiplicity was increased; each leaked more in human than in rat cells. dl312, with no E1A products, failed to produce E2A mRNA or protein at 1,000 IU per cell in rat cells but did so in some experiments in human cells. There appears to be a very strict dependence of viral early gene expression on E1A in rat cells, whereas dependence on E1A is more relaxed in HeLa cells, perhaps due to a cellular E1A-like function. Altered cell cycle control is more dependent on E1A function than is early viral gene expression.

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Control of Adenovirus Gene Expression: Cellular Gene Products Restrict Expression of Adenovirus Host Range Mutants in Nonpermissive Cells

Cited by 24 publications

References 31 publications

Differential activation of RNA polymerase III-transcribed genes by the polyomavirus enhancer and the adenovirus E1A gene products

Differential activation of RNA polymerase III-transcribed genes by the polyomavirus enhancer and the adenovirus E1A gene products

Expression of the E4 gene is required for establishment of soft-agar colony-forming rat cell lines transformed by the adenovirus 12 E1 gene

Control Functions of Adenovirus Transformation Region E1A Gene Products in Rat and Human Cells

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