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Nucleic Acids Research, 1989, Vol. 17, No. 14 5509-5516
© 1989

MOLECULAR BIOLOGY

Increased erythrold-specific expression of a mutated HPFH {gamma}-globin promoter requires the erythroid factor NFE-1

Silvia Nicolis1, Antonella Ronchi1, Nicoletta Malgarctti1, Roberto Mantovani1, Barbara Giglioni2 and Sergio Ottolenghi1,2

1Dipartimento di Genetica e di Biologia dei Microrganismi, Universita degli Studi di Milano Milan 2Centro per lo Studio della Patologia cellulare del CNR Milan, Italy

Received May 3, 1989. Revised June 23, 1989. Accepted June 23, 1989.

The -175 T{blacktriangleright}C mutation in the promoter of the A{gamma}- Gor {gamma}-globin gene causes a 50-100 fold increase of the expression of the respective gene in adult erythroid cells (Hereditary Persistence of Fetal Hemoglobin). We show here that this mutation increases 3-9 fold the expression of a {gamma}-CAT reporter plasmid transfected into the erythroid cells K562, but not that of the same plasmid in non erythroid cells. The overexpression of the mutant is abolished by the mutation of the binding site for the erythroid specific factor NFE1; inactivation of the adjacent binding site for the ubiquitous factor OTF1 does not cause overexpression of the normal {gamma}-globin promoter. Previous results demonstrated that the -175 mutation slightly increases the in vitro binding of NFE1 and almost abolishes that of OTF1; the present functional data indicate that altered binding of NFE1, but not of OTF1, is responsible for the observed overexpression of the mutated promoter.


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