Cell culture factors influencing in vitro expression of mouse mammary tumor virus

In Vitro ◽  
1976 ◽  
Vol 12 (10) ◽  
pp. 693-701 ◽  
Author(s):  
D. L. Fine ◽  
L. O. Arthur ◽  
L. J. T. Young
Keyword(s):  
Cell Culture ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumor Virus ◽  
In Vitro Expression ◽  
Factors Influencing ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

scholarly journals Transforming Growth Factor β Enhances the Glucocorticoid Response of the Mouse Mammary Tumor Virus Promoter through Smad and GA-Binding Proteins

2004 ◽  
Vol 78 (5) ◽  
pp. 2201-2211 ◽  
Author(s):  
Koldo Aurrekoetxea-Hernández ◽  
Elena Buetti
Keyword(s):  
Growth Factor ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Regulatory Elements ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

ABSTRACT Tissue-specific transcription is advantageously investigated by using viral promoters, which are selected for compact regulatory elements. Mouse mammary tumor virus (MMTV) has adapted to specialized cell types and targets initially B lymphocytes. We previously showed that, in B-cell lines, glucocorticoid-induced MMTV transcription requires an ETS family factor, GA-binding protein (GABP), bound in tandem to the MMTV DNA next to the glucocorticoid receptor (GR). We now report that transforming growth factor β (TGF-β) superinduces this response up to 10-fold through binding of its effectors, Smads, between the GABP-binding motifs. The basal level was unaffected. The TGF-β-glucocorticoid cooperation also depended on GR and GABP binding, was transferable to another promoter, and occurred both with transiently transfected and with integrated templates. Smad3 associated in vitro with GR, with GABPα (via the MH2 domain), and with GABPβ, Smad4 only with GABPα. Interactions of Smad3 with GABP (when coexpressed or endogenous to B cells) were shown by coprecipitation and by mammalian two-hybrid assay. This composite DNA element integrates three signaling pathways deriving from TGF-β, glucocorticoid hormones, and a unique ETS factor, and may allow MMTV to exploit factors from the milk. It may as well indicate novel possibilities for cellular regulatory networks.

scholarly journals Transcription factor access is mediated by accurately positioned nucleosomes on the mouse mammary tumor virus promoter.

1991 ◽  
Vol 11 (2) ◽  
pp. 688-698 ◽  
Author(s):  
T K Archer ◽  
M G Cordingley ◽  
R G Wolford ◽  
G L Hager
Keyword(s):  
Mammary Tumor ◽  
Transcription Initiation ◽  
Mouse Mammary Tumor Virus ◽  
Initiation Complex ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Nuclear Factor 1

A fragment of the mouse mammary tumor virus (MMTV) promoter was reconstituted from pure histones into a dinucleosome with uniquely positioned octamer cores. Core boundaries for the in vitro-assembled dinucleosome corresponded to the observed in vivo phasing pattern for long terminal repeat nucleosomes A and B. Nuclear factor 1 (NF1), a constituent of the MMTV transcription initiation complex, was excluded from the assembled dinucleosome, whereas the glucocorticoid receptor was able to bind. During transcription of MMTV in vivo, displacement of nucleosome B was necessary to permit assembly of the initiation complex. These results indicate that the nucleoprotein structure of the promoter can provide differential access to sequence-specific DNA-binding proteins and that active chromatin remodeling can occur during transcription activation.

scholarly journals In Vitro System for Production of Mouse Mammary Tumor Virus

1974 ◽  
Vol 28 (6) ◽  
pp. 1040-1046
Author(s):  
D. L. Fine ◽  
L. O. Arthur ◽  
J. K. Plowman ◽  
E. A. Hillman ◽  
F. Klein
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumor Virus ◽  
In Vitro System ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

scholarly journals Alterations in chromatin structure associated with glucocorticoid-induced expression of endogenous mouse mammary tumor virus genes

1985 ◽  
Vol 5 (5) ◽  
pp. 1104-1110
Author(s):  
D O Peterson
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Rna Synthesis ◽  
Dnase I ◽  
Type I ◽  
Mammary Tumor Virus ◽  
Proviral Dna ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

Alterations in the chromatin structure of endogenous mouse mammary tumor virus genes accompany glucocorticoid induction of viral RNA synthesis in the C57BL/6 T lymphoma cell line T1M1. These alterations are defined by the appearance of sites of DNase I hypersensitivity within proviral DNA in isolated nuclei, as well as by changes in the moderate nuclease sensitivity of entire proviral transcription units. Induced hypersensitive sites, termed type I, appear with a time course comparable to that required for induction of the rate of viral RNA synthesis and are maintained only in the continuous presence of hormone. Two such sites map to analogous positions in the 5' and 3' long terminal repeats of proviral DNA within, or very near, sequences that have been shown to comprise positions of specific binding of the glucocorticoid receptor in vitro and that are required for hormone-inducible transcription in vivo. A third type I site maps to another position of in vitro receptor binding near the 3' long terminal repeat. Some sites of DNase I hypersensitivity, termed type II, appear not to be markedly hormone dependent; two such sites are present in corresponding positions in each long terminal repeat. Comparison of the moderate DNase I sensitivity of mouse mammary tumor virus proviral DNA suggests that the three different endogenous units in T1M1 cells can be maintained in distinct chromatin conformations that are determined by factors related to the site of provirus insertion. It seems possible that altered chromatin conformations may reflect, or actually encode, important mechanistic features of these hormone-responsive genes.

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