Control of Reversion of Moloney Murine Sarcoma Virus Transformed Cells

2015 ◽  
pp. 537-543
Author(s):  
P. J. Fischinger ◽  
S. Nomura ◽  
P. T. Peebles
Keyword(s):  
Transformed Cells ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Moloney Murine Sarcoma Virus ◽  
Murine Sarcoma

scholarly journals Alternate utilization of two regulatory domains within the Moloney murine sarcoma virus long terminal repeat.

1985 ◽  
Vol 5 (8) ◽  
pp. 1959-1968 ◽  
Author(s):  
B J Graves ◽  
S P Eisenberg ◽  
D M Coen ◽  
S L McKnight
Keyword(s):  
Long Terminal Repeat ◽  
Transcriptional Activation ◽  
Substantial Effect ◽  
Positive Control ◽  
Terminal Repeat ◽  
Temporal Shift ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Moloney Murine Sarcoma Virus ◽  
Murine Sarcoma

The Moloney murine sarcoma virus long terminal repeat (LTR) harbors two distinct positive activators of transcription, namely, a distal signal and an enhancer. In this report we demonstrate that infection by herpes simplex virus (HSV) can markedly affect the utilization of these two Moloney murine sarcoma virus transcription signals. We investigated the HSV-mediated trans-acting effects with two goals in mind: first, to gain insight into LTR function, and second, to probe the mechanisms used by HSV to establish its own transcription cascade. In mock-infected cells, LTR-mediated expression was heavily dependent on the Moloney murine sarcoma virus enhancer but was effectively distal signal independent. HSV infection mobilized the use of the LTR distal signal and concomitantly alleviated enhancer dependence. Indeed, enhancer function may actually be inhibited by HSV trans-acting factors. These results suggest that the two positive control signals of the Moloney murine sarcoma virus LTR facilitate transcriptional activation by two different pathways. We further observed that the identity of the structural gene driven by the LRT, as well as the state of integration of a transfected template, can exert a substantial effect on the response of a template to HSV infection. According to these findings, we propose a tentative model to account for the initial temporal shift of the HSV transcriptional cascade.

Properties of clonal lines of murine sarcoma virus transformed cells

Virology ◽  
1969 ◽  
Vol 38 (1) ◽  
pp. 174-179 ◽  
Author(s):  
George J. Todaro ◽  
Stuart A. Aaronson
Keyword(s):  
Transformed Cells ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Clonal Lines ◽  
Murine Sarcoma

Direct identification of palmitic acid as the lipid attached to p21ras

1986 ◽  
Vol 6 (1) ◽  
pp. 116-122
Author(s):  
J E Buss ◽  
B M Sefton
Keyword(s):  
Palmitic Acid ◽  
Sodium Dodecyl ◽  
Transformed Cells ◽  
Direct Identification ◽  
Ras Protein ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Layer Chromatography ◽  
Murine Sarcoma

p21v-H-ras, the transforming protein of Harvey murine sarcoma virus, contains a covalently attached lipid. Using thin-layer chromatography, we identified the acyl group as the 16-carbon saturated fatty acid palmitic acid. No myristic acid was detected in fatty acids released from in vivo-labeled p21v-H-ras. The p21v-K-ras protein encoded by Kirsten sarcoma virus was also palmitylated. The processing and acylation of p21v-K-ras however differed from that of p21v-H-ras. Three forms of [3H]palmitic acid-labeled p21ras proteins were detected in Kirsten sarcoma virus-transformed cells. This contrasted with Harvey sarcoma virus, in which two forms of p21v-H-ras contained palmitic acid. Analysis by partial proteolysis of p21v-H-ras labeled with [3H]palmitic acid suggested that all of the lipid found in intact p21v-H-ras was located in the C-terminal region. On sodium dodecyl sulfate-polyacrylamide gels, p21v-H-ras labeled with [3H]palmitic acid migrated slightly ahead of the majority of p21v-H-ras. Of the mature forms of p21v-H-ras, apparently only a subpopulation contains palmitic acid.

Alternate utilization of two regulatory domains within the Moloney murine sarcoma virus long terminal repeat

1985 ◽  
Vol 5 (8) ◽  
pp. 1959-1968
Author(s):  
B J Graves ◽  
S P Eisenberg ◽  
D M Coen ◽  
S L McKnight
Keyword(s):  
Long Terminal Repeat ◽  
Transcriptional Activation ◽  
Substantial Effect ◽  
Positive Control ◽  
Terminal Repeat ◽  
Temporal Shift ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Moloney Murine Sarcoma Virus ◽  
Murine Sarcoma

The Moloney murine sarcoma virus long terminal repeat (LTR) harbors two distinct positive activators of transcription, namely, a distal signal and an enhancer. In this report we demonstrate that infection by herpes simplex virus (HSV) can markedly affect the utilization of these two Moloney murine sarcoma virus transcription signals. We investigated the HSV-mediated trans-acting effects with two goals in mind: first, to gain insight into LTR function, and second, to probe the mechanisms used by HSV to establish its own transcription cascade. In mock-infected cells, LTR-mediated expression was heavily dependent on the Moloney murine sarcoma virus enhancer but was effectively distal signal independent. HSV infection mobilized the use of the LTR distal signal and concomitantly alleviated enhancer dependence. Indeed, enhancer function may actually be inhibited by HSV trans-acting factors. These results suggest that the two positive control signals of the Moloney murine sarcoma virus LTR facilitate transcriptional activation by two different pathways. We further observed that the identity of the structural gene driven by the LRT, as well as the state of integration of a transfected template, can exert a substantial effect on the response of a template to HSV infection. According to these findings, we propose a tentative model to account for the initial temporal shift of the HSV transcriptional cascade.

The long terminal repeat of an endogenous intracisternal A-particle gene functions as a promoter when introduced into eucaryotic cells by transfection

1984 ◽  
Vol 4 (10) ◽  
pp. 2128-2135
Author(s):  
K K Lueders ◽  
J W Fewell ◽  
E L Kuff ◽  
T Koch
Keyword(s):  
Long Terminal Repeat ◽  
Promoter Activity ◽  
Terminal Repeat ◽  
Flanking Sequence ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Mouse Cells ◽  
Moloney Murine Sarcoma Virus ◽  
Intracisternal A Particle ◽  
Murine Sarcoma

We describe experiments designed to determine whether an endogenous intracisternal A-particle (IAP) gene randomly selected from a mouse embryo library has the potential to be transcriptionally active. Assays for IAP gene transcription were done with permanently transformed rat cells and transiently transfected monkey and mouse cells. The rat cells, which had integrated IAP gene copies, contained IAP RNA. A start site within the IAP 5' long terminal repeat (LTR) was localized by S1 mapping. The promoter activity of the IAP LTR was also measured in cells 48 h after the introduction of recombinant plasmids in which bacterial chloramphenicol acetyl transferase (CAT) encoding sequences were under the control of the LTR. The IAP LTR promoted CAT activity in mouse and monkey cells. In mouse L-cells, the levels of CAT activity were 10 to 25% of those promoted by an analogous recombinant containing the Moloney murine sarcoma virus LTR as the promoter. In contrast to the Moloney murine sarcoma virus LTR, the IAP LTR was five- to eightfold more active in monkey cells than in mouse cells. The 5' and 3' LTRs were equally active, and promoter activity was dependent on having the orientation of the LTRs with respect to the CAT gene the same as their orientation with respect to the IAP gene. A 5'-flanking sequence containing a member of the highly repetitive R-sequence family increased CAT activity in COS cells 11-fold when present along with the LTR. Our results indicate that the LTR of an endogenous mouse IAP gene can function as an efficient promoter in heterologous as well as homologous cells.

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