Abstract
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).
MeSH Terms
Aminolevulinic Acid/pharmacology
Bone Marrow/metabolism
Cell Line
Dimethyl Sulfoxide/pharmacology
Female
Genetic Linkage
Heme/biosynthesis
Hemin/pharmacology
Hemoglobins/biosynthesis
Hybrid Cells/metabolism
Leukemia, Erythroblastic, Acute/metabolism
RNA, Messenger/biosynthesis
X Chromosome
Chemicals
Hemoglobins
RNA, Messenger
Heme
Hemin
Aminolevulinic Acid
Dimethyl Sulfoxide
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Benoff S
Bruce S A
Skoultchi A I
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