Open AccessInduction of c-fos mRNA and AP-1 DNA-binding activity by cAMP in cooperation with either the adenovirus 243- or the adenovirus 289-amino acid E1A protein.
Author(s) -
Daniel A. Engel,
Ulrich Müller,
Richard Gedrich,
Julie S. Eubanks,
Thomas Shenk
Publication year - 1991
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.88.9.3957
Subject(s) - activator (genetics) , microbiology and biotechnology , messenger rna , biology , transcription (linguistics) , adenoviridae , gene , amino acid , creb1 , transcription factor , binding protein , gene expression , chemistry , biochemistry , creb , genetic enhancement , philosophy , linguistics
Products of the adenovirus E1A gene can act synergistically with cAMP to activate transcription of several viral early genes and the cellular genes c-fos and jun-B. Transcription factor AP-1-binding activity is also induced by the combined action of E1A and cAMP. Mouse S49 cells were infected with adenovirus variants expressing either the 243- or 289-amino acid E1A protein and treated with the cAMP analog dibutyryl-cAMP. Significant E1A-dependent induction of c-fos mRNA and AP-1-binding activity was observed in cells expressing either E1A protein. These effects absolutely required the presence of cAMP. In contrast, the 243-amino acid protein was a poor activator of the viral early genes E2 and E4 compared with the 289-amino acid protein. These data suggest that the 243- and 289-amino acid E1A proteins both interact functionally with the cAMP signaling system to activate transcription of a cellular gene and AP-1-binding activity. The mechanism involved in this process is probably different from the mechanism of transcriptional activation of viral genes.