Open AccessNegative control of hemoglobin production in somatic cell hybrids due to heme deficiency.
Author(s) -
Susan Benoff,
Sarah A. Bruce,
Arthur I. Skoultchi
Publication year - 1978
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.75.9.4354
Subject(s) - hemoglobin , dimethyl sulfoxide , heme , globin , somatic cell , bone marrow , biology , biochemistry , microbiology and biotechnology , cell fusion , chemistry , cell , gene , enzyme , immunology , organic chemistry
In somatic cell hybrids formed by the fusion of mouse erythroleukemic cells with mouse primary bone marrow cells, retention of the X chromosome contributed by the bone marrow parent is correlated with inhibition of hemoglobin accumulation in response to dimethyl sulfoxide. The inhibition of hemoglobin accumulation is not due to the absence of globin mRNA. Dimethyl sulfoxide-treated hybrid cells accumulate polyribosomal globin mRNA to levels comparable to those of the parental erythroleukemic cells under the same conditions. Heme, or its precursor delta-aminolevulinc acid, can overcome the effects of the bone marrow X chromosome and induce hemoglobin accumulation in the dimethyl sulfoxide-treated hybrid cells. The data suggest that the X chromosome contributed by the bone marrow cells inhibits hemoglobin production by inhibiting inducible heme biosynthesis, most probably at the step catalyzed by delta-aminolevulinic acid synthetase (EC 2.3.1.37).