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Nucleic Acids Research, 1992, Vol. 20, No. 12 2997-3003
© 1992

MOLECULAR BIOLOGY

Post-transcriptional regulation of transferrin receptor mRNA by IFN{gamma}

Marie-Françoise Bourgeade, Flora Silbermann, Lukas Kühn1, Ugo Testa2, Cesare Peschle2, Sylvie Mémet, Ming Nguy Thang and Françoise Besançon

U245 INSERM, Batiment INSERM, Hopital St Antoine 184 rue du Faubourg St Antoine, 75012 Paris, France 1Swiss Institute For Experimental Cancer Research CH-1066 Epalinges, Switzerland 2Istituto Superiore Di Sanita 00161 Rome, Italy

Received April 3, 1992. Accepted May 15, 1992.

IFN{gamma} inhibits the rise in transferrin receptor mRNA level which is normally observed when stationary WISH cells are stimulated to proliferate. This effect is not attributable to a change in the transcription rate of the transferrin receptor gene or in the cytoplasmic stability of the mRNA. The IFN{gamma}-induced reduction of the transferrin receptor mRNA content is already present at the nuclear level to an extent comparable to that observed in whole cells. Thus, IFN{gamma} does not impair the passage of this mRNA from the nuclear to the cytoplasmic compartment but probably interferes with a nuclear post-transcriptional event during the processing of the immature transferrin receptor mRNA. Two different levels of regulation of transferrin receptor mRNA have been previously reported. Iron modulates the cytoplasmic stability of this mRNA through the binding of a specific cytoplasmic factor, whereas cell growth variation influences the transcription of this gene. Our results suggest the existence of another mechanism of regulation for transferrin receptor gene expression not so far considered. Furthermore, the distinction between the mechanism of regulation exerted by IFN{gamma} and that exerted by cell proliferation on transferrin receptor gene expression suggests that, in WISH cells, the IFN-lnduced transferrin receptor decay is not a consequence of cell growth arrest but rather one of the causes of the antiproliferative effect of IFN through iron deprivation.


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