Mutation of the c-fos gene dyad symmetry element inhibits serum inducibility of transcription in vivo and the nuclear regulatory factor binding in vitro.
In vitro mutagenesis of a 61-base-pair DNA sequence element that is necessary for induction of the c-fos proto-oncogene by growth factors revealed that a small region of dyad symmetry within the sequence element is critical for c-fos transcriptional activation. The same c-fos dyad symmetry element was found to bind a nuclear protein in vitro, causing a specific mobility shift of this c-fos regulatory sequence. An analysis of insertion and deletion mutants established a strict correlation between the ability of the dyad symmetry element to promote serum activation of c-fos transcription and in vitro nuclear protein binding. These experiments suggest that the DNA mobility shift assay detects a nuclear protein that mediates growth factor stimulation of c-fos expression. In vitro competition experiments indicate that the c-fos regulatory factor also binds to sequences within another growth factor-inducible gene, the beta-actin gene.
D000818:Animals; D001483:Base Sequence; D004247:DNA / Q000235:genetics; D005786:Gene Expression Regulation; D006801:Humans; D051379:Mice; D009154:Mutation; D009698:Nucleoproteins / Q000235:genetics*; D000090063:Proto-Oncogene Mas; D011519:Proto-Oncogenes; D014157:Transcription Factors / Q000235:genetics*; D014158:Transcription, Genetic
C000715470:MAS1 protein, human; D009698:Nucleoproteins; D000090063:Proto-Oncogene Mas; D014157:Transcription Factors; D004247:DNA