Identification and molecular cloning of Moloney mouse sarcoma virus-specific sequences from uninfected mouse cells.

Jones, Molly Morgan; Bosselman, R A; Hoorn, Frans A. van der; Berns, Anton; Fan, Hua; Verma, Inder M.

doi:10.1073/pnas.77.5.2651

Cited by 54 publications

(26 citation statements)

References 18 publications

(13 reference statements)

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“…1 and 3a) are in good agreement with published data on protein and RNA expression (15,31). The absence of detectable hybridization of a vmos-specific probe (oncogene of Moloney murine sarcoma virus; XbaI-HindIII fragment) (26) to any RNA sample served to show that nonspecific hybridization is negligible in the dot-blot technique used in this study (data not shown) (31).…”

supporting

confidence: 80%

Transcription of c-onc genes c-rasKi and c-fms during mouse development.

Müller¹,

Slamon²,

Adamson³

et al. 1983

Mol. Cell. Biol.

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168

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We investigated the expression of cellular sequences c-rasKi and c-fms, which are homologous to the oncogenes of Kirsten rat sarcoma virus and the McDonough strain offeline sarcoma virus, during murine development and in a variety of mouse tissues. The c-rasKi gene was found to be transcribed into two mRNA species of approximately 2.0 and 4.4 kilobases, whereas a single c-fms-related transcript of approximately 3.7 kilobases was identified. The c-rasKi gene appeared to be expressed ubiquitously, since similar levels of transcripts were observed in embryos, fetuses, extraembryonal structures, and a variety of postnatal tissues. In contrast, significant expression of c-fms was found to be confined to the placenta and extraembryonal membranes (i.e., combined yolk sac and amnion). The concentration of c-fms transcripts in the placenta increased approximately 15-fold (relative to day-7 to day-9 conceptuses) during development before reaching a plateau at day 14 to 15 of gestation. The time course of cfms expression in the extraembryonal membranes appeared to parallel the stagespecific pattern observed in the placenta. The level of c-fms transcripts in the extraembryonal tissues reached a level which was approximately 20-to 50-fold greater than that in the fetus. These findings suggest that the c-fms gene product may play a role in differentiation of extraembryonal structures or in transport processes occurring in these tissues. Our results indicate that the c-onc genes analyzed in the present study exert essentially different functions durin-g mouse development.The acutely oncogenic retroviruses contain sequences in their genomes which are required for induction of neoplasia in vivo and for morphological and malignant transformation of cultured cells in vitro (3, 50). These sequences, termed viral oncogenes (v-onc), apparently originated from the normal vertebrate genome (3,50). The precise mechanism of acquisition of these cellular sequences remains obscure, but it presumably involves recombination between the genome of a replication-competent retrovirus and the host genome (3, 50). To date, 16 different cellular homologs of retroviral oncogenes have been identified

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supporting

confidence: 80%

Transcription of c-onc genes c-rasKi and c-fms during mouse development.

Müller¹,

Slamon²,

Adamson³

et al. 1983

Mol. Cell. Biol.

Self Cite

168

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“…Filters were hybridised overnight to a DNA probe labelled by random priming with 32P-dCTP (Feinberg & Vogelstein, 1983) at 42°C in 50% formamide, washed at 65°C in 0.1 x standard saline citrate (1 x SSC: 0.15 M NaCl, 0.015 M Na citrate), and 1% sodium dodecyl sulfate (SDS) for 1 h, and exposed to Kodak X-Omat S films (Kodak, Rochester, NY) at -80°C with intensifying screens. The 450bp v-mos probe used in this study was derived by PstI digestion from the pMSV-31 plasmid (Jones et al, 1980).…”

Section: Tumour Inductionmentioning

confidence: 99%

In vitro differentiation of rhabdomyosarcomas induced by nickel or by Moloney murine sarcoma virus

Nanni

Azzarello²,

Tessarollo³

et al. 1991

Br J Cancer

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Summary In vitro cultures and clonal derivatives have been established from rat rhabdomyosarcomas induced by Moloney-Murine Sarcoma Virus (MSV) or by nickel sulfide; differentiation ability has been studied as expression of desmin, embryonic and adult myosin isoforms, a-actin isoforms and cellular fusion. The two rhabdomyosarcoma models showed different levels of myogenic differentiation. Multinucleated myotube-like structures were frequently observed in cultures derived from nickel-induced tumours. Desmin was present in 50-80% of cells and embryonic myosin in up to 10%. In MSV-tumour-derived cultures and in their metastases or clonal derivatives two cell types are present in different ratios: spindle-shaped cells, adherent to plastic surfaces, and rounded cells, loosely attached or floating free in the medium. These cultures showed features of myogenic differentiation (10-80% desmin-positive cells), but embryonic myosin expression and production of multinucleated myotube-like structures were very rare events. Cultures from autochthonous lymph node and lung metastatic cells showed similar patterns of differentiation. Retinoic acid increased differentiated features (myotube formation and embryonic myosin expression) only in nickel-induced rhabdomyosarcoma cells. The two models described here mimic the heterogeneity in differentiation pattern found among human rhabdomyosarcomas. Myogenic differentiation ability was retained at a good level by nickelinduced tumours, whereas it was strongly impaired in MSV-induced tumours.

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“…3 and in the text, the results of which are shown in lanes A, B, and C, respectively. Lane A contained 10 times less RNA than the other lanes. The nuclease S1 mapping experiments were performed as described (10) Our data show the presence of cis-acting inhibitory sequences 2 kb upstream of c-mos(rat) that act on RNA levels in vivo.…”

mentioning

confidence: 99%

“…Lane A contained 10 times less RNA than the other lanes. The nuclease S1 mapping experiments were performed as described (10) Our data show the presence of cis-acting inhibitory sequences 2 kb upstream of c-mos(rat) that act on RNA levels in vivo. In contrast, the inhibitory sequences found 3' of c-fos(human) appeared to act at the level of translation (14,23).…”

mentioning

confidence: 99%

Sequences upstream of c-mos(rat) that block RNA accumulation in mouse cells do not inhibit in vitro transcription.

Hoorn¹,

Müller²,

Pizer³

1985

Mol. Cell. Biol.

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An unusual feature of the c-mos oncogene is the lack of expression in mouse tissues. Recombinant plasmids that contain the strong adenovirus late promoter and different amounts of cellular DNA 5' to c-mos(rat) were constructed and tested in transfection and transcription assays. The cellular sequences inhibit RNA accumulation in mouse but not human cells and do not inhibit in vitro transcription of the plasmid DNAs.A feature unique to the c-mos oncogene (3) is the absence of expression in tissues from adult mice or mouse embryos (8,11,16). Since methylation of v-mos, the transforming gene of Moloney murine sarcoma virus (M-MSV), reduced the transforming capacity of the gene (12), the failure to express c-mos was originally attributed to the hypermethylated state of the c-mos gene in tissues (8). Recently, evidence was published for the presence of cellular DNA sequences upstream of c-mos(mouse) which inhibited its transforming capacity (26). As the assays used by Wood et al. to detect these inhibitory mouse sequences were based on the absence of focus formation after transfection (26), it was not clear whether the inhibition was at the level of RNA transcription, RNA processing, or translation, and we decided to examine directly the effect of these DNA sequences on RNA synthesis.We previously showed a high degree of homology between the c-mos genes of mice and rats and between their 5' flanking sequences (22). Because of these similarities, we chose to investigate the effect of the putative inhibitory sequences on the expression of c-mos(rat) and constructed the vectors shown in Fig. 1. They all contain c-mos(rat). Further, they contain the adenovirus 2 major late promoter (AdMLP) on a 455-base-pair (bp) XhoI-HindIII fragment which also contains the first leader exon and the adenovirus IVa2 promoter (19). However, we were unable to detect any activity of the adenovirus IVa2 promoter in the experiments described below, in agreement with earlier observations by Fire et al. (4). All vectors also contain different amounts of rat DNA that normally precedes c-mos(rat), placed between the AdMLP and the c-mos gene. Thus clones pAL,CMR-1, -2, and -3 contain, respectively, 850, 2,100 and 3,250 bp of rat DNA flanking the c-mos(rat) gene. The sequences around the HpaI site, harboring the putative inhibitory sequences, are present in clones pAL,CMR-2 and -3 but absent from pAL1CMR-1 and were shown previously to contain extensive homology to the similar region in mouse DNA (22). In vitro transcription (2, 5) was used to test the ability of the RNA polymerase II to start at the AdMLP and transcribe efficiently through the putative inhibitory sequences to the c-mos gene. Clones pAL1CMR-1 and -2 were digested with * Corresponding author.SmaI and HpaI, whereas pAL1CMR-3 was digested with SmaI and HindIII (Fig. 1). Thus, any transcription starting at the retroviral promoter in the long terminal repeat (LTR), which might interfere with initiation of transcription at the AdMLP, would generate a 30-nucleotide run-off transcript for e...

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Identification and molecular cloning of Moloney mouse sarcoma virus-specific sequences from uninfected mouse cells.

Cited by 54 publications

References 18 publications

Transcription of c-onc genes c-rasKi and c-fms during mouse development.

Transcription of c-onc genes c-rasKi and c-fms during mouse development.

In vitro differentiation of rhabdomyosarcomas induced by nickel or by Moloney murine sarcoma virus

Sequences upstream of c-mos(rat) that block RNA accumulation in mouse cells do not inhibit in vitro transcription.

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