Open AccessSynergism between distinct enhanson domains in viral induction of the human beta interferon gene.
Author(s) -
Jean-François Leblanc,
Lucie Cohen,
M. Rodrigues,
John Hiscott
Publication year - 1990
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.10.8.3987
Subject(s) - biology , plasmid , microbiology and biotechnology , reporter gene , activator (genetics) , promoter , transfection , transcription (linguistics) , gene , beta (programming language) , interferon , gene expression , virology , genetics , computer science , programming language , linguistics , philosophy
This study demonstrates distinct virus-inducible enhanson properties for three regions of the human beta interferon (IFN-beta) promoter; maximum virus inducibility required syngerism among all three enhansons. Expression of the IRF-1 transcription factor differentially increased the expression of plasmids containing (AAGTGA)4 or PRDIII (-94 to -78) motifs but was inefficient in the induction of the intact IFN-beta promoter. The human T-cell lymphotropic virus type I Tax protein was a strong positive activator of PRDII (-64 to -55)-containing plasmids but was also unable to stimulate the IFN-beta promoter. Induction of the intact IFN-beta promoter linked to a reporter plasmid was achieved in lymphoid and epithelioid cellular backgrounds by a triple transfection with IRF-1 and Tax expression plasmids or a combination of IRF-1 and phorbol ester, indicating that at least two trans-activating events and the association of two proteins on the promoter template are required for IFN-beta activation.