Multiple regulatory domains in the mouse mammary tumor virus long terminal repeat revealed by analysis of fusion genes in transgenic mice

1988 ◽  
Vol 8 (1) ◽  
pp. 473-479
Author(s):  
T A Stewart ◽  
P G Hollingshead ◽  
S L Pitts
Keyword(s):  
Transgenic Mice ◽  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Terminal Repeat ◽  
Growth Hormone Gene ◽  
Fusion Genes ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Transcription initiated within the mouse mammary tumor virus (MTV) long terminal repeat (LTR) is regulated by glucocorticoids, androgens, and estrogen. However, expression of the virus in vivo and transcription of MTV LTR fusion genes in transgenic mice are not readily interpretable solely in terms of the influence of these hormones. To investigate whether there is a regulatory role for sequences within the LTR but outside the region known to be responsible for glucocorticoid induction, we have produced transgenic mice carrying genes in which various regions of the LTR have been linked to the human growth hormone gene. Analysis of expression of the fusion genes in these transgenic mice has demonstrated that the 5' end of the LTR can profoundly influence transcription initiated within the MTV LTR.

scholarly journals Multiple regulatory domains in the mouse mammary tumor virus long terminal repeat revealed by analysis of fusion genes in transgenic mice.

1988 ◽  
Vol 8 (1) ◽  
pp. 473-479 ◽  
Author(s):  
T A Stewart ◽  
P G Hollingshead ◽  
S L Pitts
Keyword(s):  
Transgenic Mice ◽  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Terminal Repeat ◽  
Growth Hormone Gene ◽  
Fusion Genes ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Transcription initiated within the mouse mammary tumor virus (MTV) long terminal repeat (LTR) is regulated by glucocorticoids, androgens, and estrogen. However, expression of the virus in vivo and transcription of MTV LTR fusion genes in transgenic mice are not readily interpretable solely in terms of the influence of these hormones. To investigate whether there is a regulatory role for sequences within the LTR but outside the region known to be responsible for glucocorticoid induction, we have produced transgenic mice carrying genes in which various regions of the LTR have been linked to the human growth hormone gene. Analysis of expression of the fusion genes in these transgenic mice has demonstrated that the 5' end of the LTR can profoundly influence transcription initiated within the MTV LTR.

scholarly journals Superantigen Expression Is Driven by Both Mouse Mammary Tumor Virus Long Terminal Repeat-Associated Promoters in Transgenic Mice

2000 ◽  
Vol 74 (6) ◽  
pp. 2900-2902 ◽  
Author(s):  
Brian Salmons ◽  
Thomas Miethke ◽  
Stefan Wintersperger ◽  
Mathias Müller ◽  
Gottfried Brem ◽  
...  
Keyword(s):  
Life Cycle ◽  
Transgenic Mice ◽  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Terminal Repeat ◽  
Mammary Tumor Virus ◽  
Virus Life Cycle ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

ABSTRACT In addition to the usual retroviral promoter, the mouse mammary tumor virus (MMTV) long terminal repeat carries a second promoter located in the U3 region. Here we show that both of these promoters are independently able to give rise to superantigen activity in transgenic mice. The ability of multiple MMTV promoters to drive superantigen expression underscores its importance in the virus life cycle.

scholarly journals The Wnt-1 (int-1) oncogene promoter and its mechanism of activation by insertion of proviral DNA of the mouse mammary tumor virus.

1990 ◽  
Vol 10 (8) ◽  
pp. 4170-4179 ◽  
Author(s):  
R Nusse ◽  
H Theunissen ◽  
E Wagenaar ◽  
F Rijsewijk ◽  
A Gennissen ◽  
...  
Keyword(s):  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Terminal Repeat ◽  
Upstream Sequence ◽  
Start Site ◽  
Mammary Tumor Virus ◽  
Proviral Dna ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Wnt-1 (int-1) is a cellular oncogene often activated by insertion of proviral DNA of the mouse mammary tumor virus. We have mapped the 5' end and the promoter area of the Wnt-1 gene by nuclease protection and primer extension assays. In differentiating P19 embryonal carcinoma cells, in which Wnt-1 is naturally expressed, two start sites of transcription were found, one preceded by two TATA boxes and one preceded by several GC boxes. In P19 cells, a 1-kilobase upstream sequence of Wnt-1 was able to confer differentiation-specific expression on a heterologous gene. We have investigated how Wnt-1 transcription was affected by mouse mammary tumor virus proviral integrations in various configurations near the promoters of the gene. One provirus has been inserted in the 5' nontranslated part of Wnt-1, in the same transcriptional orientation, and has functionally replaced the Wnt-1 promoters. Wnt-1 transcription in this tumor starts in the right long terminal repeat of the provirus, with considerable readthrough transcription from the left long terminal repeat. Another provirus has been inserted in the orientation opposite that of Wnt-1 into a GC box, disrupting the first Wnt-1 transcription start site but not the downstream start site. Most insertions have not structurally altered the Wnt-1 transcripts and have enhanced the activity of the normal two promoters.

scholarly journals The Position and Length of the Steroid-Dependent Hypersensitive Region in the Mouse Mammary Tumor Virus Long Terminal Repeat Are Invariant despite Multiple Nucleosome B Frames

1998 ◽  
Vol 18 (6) ◽  
pp. 3633-3644 ◽  
Author(s):  
Gilberto Fragoso ◽  
William D. Pennie ◽  
Sam John ◽  
Gordon L. Hager
Keyword(s):  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Restriction Enzymes ◽  
Terminal Repeat ◽  
Receptor Binding Site ◽  
Mammary Tumor Virus ◽  
Steroid Dependent ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

ABSTRACT Stimulation of the mouse mammary tumor virus with steroids results in the generation of a DNase I-hypersensitive region (HSR) spanning the hormone responsive element (HRE) in the long terminal repeat. Restriction enzymes were used to characterize the accessibility of various sites within the HSR of mouse mammary tumor virus long terminal repeat-reporter constructions in four different cell lines. The glucocorticoid-dependent HSR was found to span minimally 187 bases, a stretch of DNA longer than that associated with histones in the core particle. Although the 5′-most receptor binding site within the HRE is downstream of −190, hypersensitive sites were found further upstream to at least −295. The relationship in the accessibility between pairs of sites in the vicinity of the HSR was further examined in one cell line by a two-enzyme restriction access assay. In the uninduced state, the accessibilities at these sites were found to be independent of each other. In contrast, when stimulated with hormone, the accessibilities at these sites were observed to become linked. That is, once a distinct promoter was activated, all of the sites within the HSR of that molecule became accessible. The HSR formed along an invariant stretch of DNA sequence despite the multiplicity of nucleosome frames in the nucleosome B region, where the HRE is located. The results indicate that the macroscopic length of the HSR does not arise from core length-remodeling events in molecules containing Nuc-B in alternative positions.

A Mouse Mammary Tumor Virus-Like Long Terminal Repeat Superantigen in Human Breast Cancer

2004 ◽  
Vol 64 (12) ◽  
pp. 4105-4111 ◽  
Author(s):  
Yue Wang ◽  
Jian-Dong Jiang ◽  
Dongping Xu ◽  
Yan Li ◽  
Chunfeng Qu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Human Breast Cancer ◽  
Terminal Repeat ◽  
Human Breast ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus
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