GM-CSF and oncogene mRNA stabilities are independently regulated in trans in a mouse monocytic tumor.
Regulation of mRNA turnover has emerged as an important control point in lymphokine and oncogene expression. We have studied a monocytic tumor in which activation of GM-CSF expression results from the constitutive stabilization of the normally short-lived GM-CSF mRNA. Linkage of the germ-line 3' untranslated region of the GM-CSF gene to a neo reporter gene demonstrated that mRNA stabilization is mediated by a tumor-specific trans-acting factor(s), rather than by an alteration of the GM-CSF gene itself. Significantly, similar fusions of the c-myc and c-fos 3' untranslated regions to neo yielded mRNAs that turned over rapidly in all cells, including the tumor cells. These results demonstrate that AU-rich mRNA turnover signals are recognized differentially in trans within the same cell.
Schuler
G D
GD
Department of Molecular Biology, Lewis Thomas Laboratory, Princeton University, New Jersey 08540.
Cole
M D
MD
D000818:Animals; D001483:Base Sequence; D003115:Colony-Stimulating Factors / Q000235:genetics*; D003609:Dactinomycin / Q000494:pharmacology; D005786:Gene Expression Regulation; D008040:Genetic Linkage; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D006133:Growth Substances / Q000235:genetics*; D006207:Half-Life; D007941:Leukemia P388 / Q000235:genetics; D051379:Mice; D008969:Molecular Sequence Data; D009857:Oncogenes; D012333:RNA, Messenger / Q000494:pharmacology*; D014158:Transcription, Genetic
D003115:Colony-Stimulating Factors; D006133:Growth Substances; D012333:RNA, Messenger; D003609:Dactinomycin; D016178:Granulocyte-Macrophage Colony-Stimulating Factor