Showing papers by "Peter Herrlich published in 1983"

Subfragments of the large terminal repeat cause glucocorticoid-responsive expression of mouse mammary tumor virus and of an adjacent gene

Abstract: After transfection of mouse mammary tumor virus (MMTV) proviral DNA into cultured cells, the DNA is transcribed in a glucocorticoid-sensitive fashion. The large terminal repeat (LTR) region of MMTV is 1,328 nucleotides long and contains the regulatory information necessary for the hormonal response. We have constructed a MMTV LTR-thymidine kinase (tk) chimeric gene and have tested the biological activity of molecules containing various deletions in the LTR after transformation of LTK- APRT- mouse cells. In the TK+ transformants, both a LTR- tk chimeric RNA and an authentic tk RNA are correctly initiated and transcribed. The synthesis of the chimeric RNA as well as that of the tk RNA is hormonally regulated. A plasmid containing 202 nucleotides of LTR DNA 5' to the RNA initiation site is fully sensitive to glucocorticoids; 50 nucleotides still cause a residual inducibility.

Regulation of MHC class II invariant chain expression: induction of synthesis in human and murine plasmocytoma cells by arresting replication.

Abstract: The expression of the H2 Ia-associated invariant chain (Ii) has been determined by pulse labeling cells with [35S]methionine and resolving the proteins. Expression is maximal in noncycling peripheral B lymphocytes and is reduced upon maturation of B lymphocytes to plasma cells. B cell-derived cell lines behave correspondingly: IgM+ non-secretor cell lines synthesize Ii while plasmocytoma cells do not. Pre-B cell lines are also negative. In all Ii-negative cell lines, the synthesis of Ii is selectively induced by treating the cells with inhibitors of replication.

A deletion mutant of mouse mammary tumour virus, lacking 516 nucleotides of the 5' long terminal repeat sequence, can be expressed in a hormone-responsive fashion.

Abstract: Summary In vitro manipulation of proviral DNA of mouse mammary tumour virus (MMTV) was used to construct mutants with defined deletions at the 5′ end of the proviral gene. In the mutants 516, 1400 and 2000 nucleotides were removed from the 5′ end. The deleted proviral DNA was tested for transcription and glucorticoid hormone regulation of viral RNA expression upon cotransfection into rat XC tk- cells with a thymidine kinase gene. Intact proviral DNA contained in the plasmid vector pBR322 and the deletion mutant pGR16Δ516, missing 516 nucleotides of the 5′ long terminal repeat (LTR) sequence, were transcribed in a hormone responsive fashion and produced RNA species of 35S and 24S. Deletion of the entire LTR sequence abolished MMTV transcription and the hormonal effect.