Nuclear inheritance of a gene affecting mitochondrial gene expression |
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Authors: | Zaki A Sherif Linda M Jefferson Carolyn D Whitfield-Broome |
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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 |
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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 Gal−32TGRTK+ 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 Gal−32TGRTK+ 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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