scholarly journals Differential Distribution of Mouse Mammary Tumor Virus-Related Sequences in the DNA’s of Rats2

1979 ◽  
Vol 62 (5) ◽  
pp. 1279-1286
Author(s):  
W. Drohan ◽  
J. Schlom
Keyword(s):  
Mammary Tumor ◽  
Dna Sequences ◽  
Mouse Mammary Tumor Virus ◽  
Germ Line ◽  
Embryo Cell ◽  
Differential Distribution ◽  
Mammary Tumor Virus ◽  
Laboratory Rats ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Abstract Radioactively labeled mouse mammary tumor virus (MuMTV) 60-70S RNA, obtained from virions grown In both murine and feline cells, was employed In molecular hybridization experiments to detect MuMTV-related sequences In the DNA’s of rats (Rattus norveglcus). With the use of relaxed conditions of hybridization and assay for RNA-DNA duplexes, all strains of laboratory rats and feral rats examined were shown to possess endogenous MuMTV-related DNA sequences In the low repetitive range. These sequences were related to approximately 20% of the MuMTV genome and exhibited a melting temperature (Tm) approximately 5° C lower than MuMTV-specific proviral sequences In murine (Mus musculus) DNA’s. Certain colonies of the F344 strain of rat (Fischer) contained animals whose DNA’s possessed additional MuMTV-related sequences. These sequences were related to the non-germ-line-transmitted, tumorassociated (TA) sequences of the highly oncogenic MuMTV (C3H). They were found In the DNA of some F344 rats and a cloned established F344 rat embryo cell line at a frequency of approximately one copy per haploid genome and exhibited a Tm 9° C lower than that of hybrid duplexes formed between radioactive MuMTV TA-sequence RNA and C3H mouse mammary tumor DNA. The DNA’s of rats, therefore, contained two sets of sequences that were related to sequences of the MuMTV genome: One set was germ-line transmitted, whereas the other set appeared to be transmitted in some rats via a non-germ line or infectious process.

scholarly journals Nucleosome-mediated disruption of transcription factor-chromatin initiation complexes at the mouse mammary tumor virus long terminal repeat in vivo.

1994 ◽  
Vol 14 (1) ◽  
pp. 32-41 ◽  
Author(s):  
H L Lee ◽  
T K Archer
Keyword(s):  
Mammary Tumor ◽  
Dna Sequences ◽  
Mouse Mammary Tumor Virus ◽  
Binding Protein ◽  
Tata Binding Protein ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Nuclear Factor 1

Glucocorticoid induction of mouse mammary tumor virus (MMTV) is short lived, returning to base levels within 24 h despite the continued presence of hormone. MMTV DNA sequences assembled as chromatin require hormone for binding by nuclear factor 1 (NF1) and octamer proteins (OCT). However, in the same cells, NF1 and OCT factors are bound to transiently introduced DNA in the absence of hormone. In contrast, recruitment of the TATA-binding protein and a novel DNA-binding protein, which we have designated FDT, for factor downstream of the TATA-binding protein, is hormone dependent for both stable and transient templates. Furthermore, transient DNA templates, but not nucleosomal templates, retain these transcription factors over the course of 24 h. This finding suggests that MMTV chromatin structure contributes to activation and cessation of transcription in vivo.

Mammary preneoplasia and tumorigenesis in the BALB/c mouse: structure and modification of mouse mammary tumor virus DNA sequences

1987 ◽  
Vol 7 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Miguel A. Gama-Sosa ◽  
Trudy Breznik ◽  
Janet S. Butel ◽  
Daniel Medina ◽  
J.Craig Cohen
Keyword(s):  
Mammary Tumor ◽  
Dna Sequences ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

scholarly journals Dexamethasone increases the number of RNA polymerase II molecules transcribing integrated mouse mammary tumor virus DNA and flanking mouse sequences.

1984 ◽  
Vol 4 (6) ◽  
pp. 1057-1062 ◽  
Author(s):  
J M Firzlaff ◽  
H Diggelmann
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Mammary Tumor ◽  
Dna Sequences ◽  
Mouse Mammary Tumor Virus ◽  
Hormone Treatment ◽  
Mrna Levels ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

In mouse Ltk- cells that were transfected with recombinant bacteriophage DNA containing a complete proviral copy of an integrated endogenous mouse mammary tumor virus (MMTV) with its flanking cellular sequences, the newly acquired MMTV proviruses were transcribed in a glucocorticoid-responsive fashion. After hormone treatment of selected cell clones in culture we isolated the nuclei, elongated the nascent RNA chains in vitro, and determined the number of RNA polymerase II molecules on the transcribed MMTV DNA as well as on the flanking mouse DNA sequences. We found that the specific increase in the polymerase loading after hormone treatment is proportional to the increase in the amount of stable MMTV mRNA. When the DNA sequences which are responsible for hormone-receptor binding and for the increased MMTV mRNA levels were deleted, no increase in RNA polymerase II loading on MMTV DNA was observed. Nuclear RNA chains which were transcribed in response to hormone treatment were detected not only from the transfected MMTV DNA but also from the mouse DNA sequences adjacent to the 3' end of the provirus.

Mouse mammary tumor virus DNA sequences in tumorigenic and nontumorigenic cells from a mammary adenocarcinoma

Virology ◽  
1982 ◽  
Vol 118 (1) ◽  
pp. 117-127 ◽  
Author(s):  
Vincent L. Morris ◽  
Douglas A. Gray ◽  
Richard F. Jones ◽  
Edwin C.M. Lee Chan ◽  
Charles M. McGrath
Keyword(s):  
Mammary Tumor ◽  
Dna Sequences ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Adenocarcinoma ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

scholarly journals Nucleosome-mediated disruption of transcription factor-chromatin initiation complexes at the mouse mammary tumor virus long terminal repeat in vivo

1994 ◽  
Vol 14 (1) ◽  
pp. 32-41
Author(s):  
H L Lee ◽  
T K Archer
Keyword(s):  
Mammary Tumor ◽  
Dna Sequences ◽  
Mouse Mammary Tumor Virus ◽  
Binding Protein ◽  
Tata Binding Protein ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Nuclear Factor 1

Glucocorticoid induction of mouse mammary tumor virus (MMTV) is short lived, returning to base levels within 24 h despite the continued presence of hormone. MMTV DNA sequences assembled as chromatin require hormone for binding by nuclear factor 1 (NF1) and octamer proteins (OCT). However, in the same cells, NF1 and OCT factors are bound to transiently introduced DNA in the absence of hormone. In contrast, recruitment of the TATA-binding protein and a novel DNA-binding protein, which we have designated FDT, for factor downstream of the TATA-binding protein, is hormone dependent for both stable and transient templates. Furthermore, transient DNA templates, but not nucleosomal templates, retain these transcription factors over the course of 24 h. This finding suggests that MMTV chromatin structure contributes to activation and cessation of transcription in vivo.

Dexamethasone increases the number of RNA polymerase II molecules transcribing integrated mouse mammary tumor virus DNA and flanking mouse sequences

1984 ◽  
Vol 4 (6) ◽  
pp. 1057-1062
Author(s):  
J M Firzlaff ◽  
H Diggelmann
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Mammary Tumor ◽  
Dna Sequences ◽  
Mouse Mammary Tumor Virus ◽  
Hormone Treatment ◽  
Mrna Levels ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

In mouse Ltk- cells that were transfected with recombinant bacteriophage DNA containing a complete proviral copy of an integrated endogenous mouse mammary tumor virus (MMTV) with its flanking cellular sequences, the newly acquired MMTV proviruses were transcribed in a glucocorticoid-responsive fashion. After hormone treatment of selected cell clones in culture we isolated the nuclei, elongated the nascent RNA chains in vitro, and determined the number of RNA polymerase II molecules on the transcribed MMTV DNA as well as on the flanking mouse DNA sequences. We found that the specific increase in the polymerase loading after hormone treatment is proportional to the increase in the amount of stable MMTV mRNA. When the DNA sequences which are responsible for hormone-receptor binding and for the increased MMTV mRNA levels were deleted, no increase in RNA polymerase II loading on MMTV DNA was observed. Nuclear RNA chains which were transcribed in response to hormone treatment were detected not only from the transfected MMTV DNA but also from the mouse DNA sequences adjacent to the 3' end of the provirus.

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