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Nuclear inheritance of a gene affecting mitochondrial gene expression
Authors:Zaki A Sherif  Linda M Jefferson  Carolyn D Whitfield-Broome
Institution:(1) Department of Biochemistry and Molecular Biology, Howard University Cancer Center, Howard University College of Medicine, 520 W Street, N.W., 20059 Washington, D.C.;(2) Present address: Department of Otolaryngology, Georgetown University Medical Center, Lombardi E416 Research Building, 3970 Reservoir Road, N.W., 20007 Washington, D.C.;(3) Present address: Prince George's Hospital Center, 3001 Hospital Drive Center, 20785 Cheverly, Maryland
Abstract:Due to a deficiency in mitochondrial protein synthesis, Chinese hamster lung (CHL) cell mutant Gal 32 does not grow in galactose or fructose. This report examines the nuclear or cytoplasmic inheritance of this single, recessive mutation. In a control experiment, fusion of Gal+TGsTK cells with Gal32TGRTK+ cells resulted in tetraploid hybrids (as verified by karyotyping) that were selected in hypoxanthine/aminopterin/thymidine medium. The majority (2/3) of the control hybrids grew in galactose as expected since Gal is dominant over Gal. Fusion of Rhodamine 6-G treated Gal+TGSTK cells with Gal32TGRTK+ cells resulted in Rhodamine 6-G-tetraploid hybrids that were selected in hypoxanthine/aminopterin/thymidine medium. The majority (7/12) of the Rhodamine 6-G-hybrids grew in galactose as expected for a nuclearly encoded gene considering that Rhodamine 6-G interferes with transmission of mtDNA but not nuclear DNA. Therefore, these results are compelling in their demonstration of the nuclear origin of the Gal 32 mutation.
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