Specific interaction of cellular factors with the B enhancer of polyoma virus.

Piette, Jacques; Kryszke, Marie-Hélène; Yaniv, Moshe

doi:10.1002/j.1460-2075.1985.tb03987.x

Cited by 124 publications

(99 citation statements)

References 64 publications

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“…The properties of these elements are consistent with the hypothesis that differentiated cells contain positive trans-acting proteins (differentiators) that interact with the specific cis-acting sequences to stimulate the expression of the associated genes. This idea is also consistent with the observations and concepts of other workers (8)(9)(10)(11)(12).…”

supporting

confidence: 93%

Regulation of rat insulin 1 gene expression: evidence for negative regulation in nonpancreatic cells.

Nir¹,

Walker²,

Rutter³

1986

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

171

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Two cis-acting elements, the enhancer and the promoter,, independently contribute to the cell-specific expression of the rat insulin 1 gene. The activities of these elements are presumably mediated by trans-acting factors. We have performed intracellular competition experiments that suggest the presence of a negative factor(s) that represses the enhancer activity in cells that do not express the insulin gene.In these experiments fibroblast cells (COS-7) were transfected with two plasmids: a test plasmid containing the gene for chlorampheiiicol acetyltransferase under the control of the thymidine kinase promoter and the insulin enhancer; and a competitor plasmid containing insulin enhancer sequences and the simian virus 40 origin of replication to permit its replication in the recipient cells. The presence of the competitor plasmid led to a 5-to 6-fold -increase in chloramphenicol acetyltransferase activity as compared with the activity detected when insulin enhancer was absent from either the competitor or the test plasmid. A 5-fold increase in chloramphenicol acetyltransferase activity was also seen when the rat amylase enhancer was present on the competitor plasmid; in contrast the simian virus 40 enhancer exerted no effect. Efficient derepression required additional sequences downstream from those essential for enhancer activity. We propose that the activity ofthe rat insulin 1 enhancer is modulated by a negative tbans-acting factor(s) that is active in cells not expressing insulin but is overridden by the dominant positive trans-acting factor(s) present in insulinproducing cells.During cellular differentiation, cell types acquire the ability to stably express a characteristic set of genes. The. molecular mechanisms by which this occurs are poorly understood. Several genes whose expression is restricted to a specific subset of cells contain cis-acting sequences required for efficient transcription in the appropriate differentiated cells (1-6). We have demonstrated (7) that 5' flanking DNA sequences of the rat insulin 1 gene contain two such cellspecific elements. The properties of these elements are consistent with the hypothesis that differentiated cells contain positive trans-acting proteins (differentiators) that interact with the specific cis-acting sequences to stimulate the expression of the associated genes. This idea is also consistent with the observations and concepts of other workers (8-12). On the other hand, "extinction" of the differentiated phenotype after fusion of differentiated cells with fibroblasts is frequently observed (13). We have also noted that specific sequence deletions in the insulin gene 5' flanking sequences can lead to increases in expression in nondifferentiated cells (unpublished observations). These results are consistent with a role for repressor-like molecules in nonexpressing cells.

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supporting

confidence: 93%

Regulation of rat insulin 1 gene expression: evidence for negative regulation in nonpancreatic cells.

Nir¹,

Walker²,

Rutter³

1986

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

171

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“…Isolation of nuclear proteins from adult rat brain and from 3T6 and PC12 cells was performed as described (Piette et al, 1985). Nuclear extracts from adult rat liver and kidney were purified according to Gorski et al (1986) and DNase I footprinting and gel shift assays carried out as previously reported (Cereghini et a]., 1987;Raymondjean et al, 1988).…”

Section: Dnase I Protection and Band-shift Assaysmentioning

confidence: 99%

Determinants of the brain‐specific expression of the rat aldolase C gene: ex vivo and in vivo analysis

Thomas¹,

Makeh²,

Briand³

et al. 1993

European Journal of Biochemistry

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A 115‐bp promoter fragment of the aldolase C gene is sufficient for conferring neural cell specificity on a reporter gene, in cultured PC12 cells and in transgenic mice. In vitro DNase I protection experiments detected two footprints on the promoter, termed boxes A/A', and B. The 5′ A/A' box contains overlapping Sp1 and Krox20/Krox24 binding sites; it binds Sp1 in fibroblasts (box A') and a different complex in brain (box A). Any deletion or mutation of this box that impairs protein recognition also suppresses promoter activity. The replacement of box A/A' by a Sp1 consensus binding site results in the loss of the brain specificity of expression in transgenic mice. Further 3′, box B is composed of a 5′ direct repeat and a 3′ GC box consisting of overlapping Sp1 and Krox20/Krox24 binding sites. Mutation of the direct repeat subregion appears to be more deleterious for the promoter activity than mutation of the G+C‐rich subregion.

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“…Infected ceils were separated into cytoplasmic and nuclear fractions, and nuclei were extracted sequentially with buffers containing increasing concentrations of NaC1 by a modification of the method described by Piette et al (1985). Infected cell monolayers were washed with cold PBS and scraped into 1 ml PBS.…”

Section: Fractionation Of Cells Infected With Vaccinia Virus Recombinmentioning

confidence: 99%

Characterization of the varicella-zoster virus gene 61 protein

Stevenson

Colman²,

Davison³

1992

Journal of General Virology

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Specific interaction of cellular factors with the B enhancer of polyoma virus.

Cited by 124 publications

References 64 publications

Regulation of rat insulin 1 gene expression: evidence for negative regulation in nonpancreatic cells.

Regulation of rat insulin 1 gene expression: evidence for negative regulation in nonpancreatic cells.

Determinants of the brain‐specific expression of the rat aldolase C gene: ex vivo and in vivo analysis

Characterization of the varicella-zoster virus gene 61 protein

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