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Nuclear inheritance of a gene affecting mitochondrial gene expression

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-...

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Bibliographic Details
Published in:Somatic cell and molecular genetics 1996-11, Vol.22 (6), p.443-451
Main Authors: Sherif, Z A, Jefferson, L M, Whitfield-Broome, C D
Format: Article
Language:English
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Summary: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.
ISSN:0740-7750
1572-9931
DOI:10.1007/BF02369436