A Centrifugal Compressor Seal

Adams, Maurice; Raimondi, A. A.

doi:10.1080/05698197708982845

Cited by 37 publications

(72 citation statements)

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“…1). The translocated c-myc exons are transcribed as efficiently in these cells as in human lymphoblastoid cell controls, whereas expression of the unrearranged genes is depressed more than 20-fold (1,3,5,33,40).…”

Section: Methodsmentioning

confidence: 99%

Opposite replication polarity of the germ line c-myc gene in HeLa cells compared with that of two Burkitt lymphoma cell lines.

Leffak¹,

James²

1989

Mol. Cell. Biol.

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To study the cell type specificity of the direction of replication of the human c-myc genes and the relationship of replication polarity to transcriptional activity, we analyzed the directions of replication of the c-myc genes in two Burkitt lymphoma cell lines, CA46 and ST486, and in HeLa cells. On the basis of in vitro runoff replication of forks initiated in intact cells, we found that transcribed c-myc genes in the germ line configuration in HeLa cells were replicated in the direction of transcription from origins in the 5'-flanking DNA, while the repressed, unrearranged c-myc genes of CA46 and ST486 cells were replicated in the antitranscriptional direction. In contrast, the transcribed c-myc genes of CA46 cells were replicated in the transcriptional direction, while the translocated, amplified c-myc genes of ST486 cells showed no preferred polarity of replication. The data also provided evidence for the existence of an endogenous barrier to DNA polymerases in the flanking DNA immediately 5' to the HeLa c-myc genes.The replication of eucaryotic chromosomes is controlled through the selection of sites for the initiation of DNA synthesis (2,6,7,10,12,14,19,21,24,32,39) and through the temporal programming of the activity at these sites (10,12,19,23). Combined with evidence for the existence of proteins which recognize the replication origins of viral minichromosomes (11,17,28,44), these results suggest that chromosome replication can be regulated in trans by DNA sequence-specific protein binding.That the activity of eucaryotic genes is related to the replication of chromatin is supported by several observations that transcribed genes are replicated early in the S phase of the cell cycle (8,9,16,18) and by the demonstration that the efficient transcription of certain transfected genes requires the replication of their chromatin template (13, 42). Moreover, Miller and Nasmyth (31) have demonstrated that passage through the S phase is necessary for repression of the silent mating type loci in Saccharomyces cerevisiae. Smithies (37) has proposed that the processes of replication and transcription are linked such that transcriptionally active genes are replicated from upstream origins, whereas inactive genes are replicated from either upstream or downstream origins. Consistent with this proposal, we have shown that the avian histone H5 genes are replicated in the transcriptional direction in embryonic erythrocytes, where they are expressed, but in the antitranscriptional direction in lymphoblastoid cells and chicken embryo fibroblasts, where they are quiescent (43). In comparison, the avian alpha-pi and alpha-D globin genes are replicated in the transcriptional direction both in cells in which they are active (erythrocytes) and in cells in which they are inactive (lymphoblastoid cells and fibroblasts) (26; Y. I. Lindstrom and M. Leffak, manuscript in preparation).To investigate further the relationship between replication polarity and transcriptional activity, we used the in vitro runoff replication (IVR) assay (2...

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Section: Methodsmentioning

confidence: 99%

Opposite replication polarity of the germ line c-myc gene in HeLa cells compared with that of two Burkitt lymphoma cell lines.

Leffak¹,

James²

1989

Mol. Cell. Biol.

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“…Among ras oncogenes isolated from cell lines of spontaneously arising tumors, many lesions affecting the structure of the encoded p21 gene products have been reported (for example, see references 40,43, and 44). However, in the case of myc oncogenes, the nature of the activating mechanism has been less clear, in that several of the reported myc oncogenes isolated from transducing retroviruses or translocated chromosomal segments have been shown to contain altered or deleted regulatory segments as well as mutations affecting the structure of the myc protein (1,5,6,21,31,45,49).…”

mentioning

confidence: 99%

Behavior of myc and ras oncogenes in transformation of rat embryo fibroblasts.

Land¹,

Chen²,

Morgenstern³

et al. 1986

Mol. Cell. Biol.

250

148

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The requirements for transformation of rat embryo fibroblasts (REFs) by transfected ras and myc oncogenes were explored. Under conditions of dense monolayer culture, neither oncogene was able to transform REFs on its own. However, the introduction of a ras oncogene together with a selectable neomycin resistance marker into REFs allowed killing of the normal nontransfected cells and the outgrowth of colonies of ras transformants, 10% of which survived crisis and became tumorigenic. These cells expressed >10-fold-higher levels of ras p21 than tumorigenic cells cotransfected with ras and myc oncogenes. The myc oncogene similarly was unable to induce tumorigenic conversion of REFs unless especially refractile colonies of oncogene-bearing cells, produced by use of a cotransfected selectable marker, were picked and subcultured. Tumorigenic conversion of REFs by single transfected oncogenes appears to require special culture conditions and high levels of gene expression.In previous reports, we and others have described experiments which suggested that multiple oncogenes are required to mediate the transformation of normal cells into tumorigenic cells (8,13,14,16,18,20,23,26,32,(35)(36)(37)50). The normal cells used in our own experiments were rat embryo fibroblasts (REFs), which were found to be incom-. pletely transformed to tumorigenicity by a ras or myc oncogene when introduced by transfection. These data suggested that a single oncogene could not impart the tumorigenic phenotype to REFs. However, when two oncogenes such as ras and myc were concomitantly introduced into REFs, these cells were able to yield fibrosarcomas after injection into young syngeneic rats or nude mice.Such results indicated that oncogenes like ras and myc act in distinct and complementary ways on cellular phenotype. Moreover, this cooperation suggested as assay in which yet other oncogenes could be tested for the ability to act in place of myc or ras in transforming cells. In this way, it was learned that the polyomavirus middle T oncogene can stand in place of ras in a cotransfection assay. Conversely, the large T oncogenes of polyomavirus and simian virus 40 (N-terminal fragment) as well as the Ela antigen of adenovirus, the N-myc oncogene, and the p53 tumor antigen gene could replace myc in the cotransfection test (8,13,14,16,26,35,37,50). These results made it possible to define two functional classes of oncogenes. The first class includes the three ras oncogenes as well as the polyomavirus middle T oncogene. The second encompasses the myc, N-myc, p53, polyomavirus large T, SV40 large T (N-terminal-proximal), and adenovirus Ela oncogenes.In the present report, we further explore the consequences of these functional assignments. We describe several properties that distinguish these two oncogene types from one another and the conditions under which the requirement for MATERIALS AND METHODS Plasmids. pEJ6.6 is a plasmid carrying the Ha-ras oncogene from the EJIT24 human bladder carcinoma cell line (39). Plasmid pHO6T1 carries the same Ha-ras ...

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“…For example, chronic myelogenous leukemia uniformly juxtaposes the Bcr and Abl genes (26,55). Burkitt's lymphoma pairs the myc and immunoglobulin (Ig) loci (2,18,58), while follicular lymphoma contains a bcl-2-Ig fusion gene (3,15,59). However, T-cell acute lymphoblastic leukemias (T-ALL) introduce a variety of different chromosomal partners into their T-cell receptor (TCR) loci.…”

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confidence: 99%