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We have investigated, with and without the influence of X-inactivation, the relationship between autosomal gene-dosage and gene-product in a mammalian system, the mouse. The gene was mitochondrial malic enzyme (Mod-2), shown to lie on Chromosome 7 between the albino (c) and shaker-1 (sh-1) loci, and the enzyme was its product, mitochondrial malic enzyme (MOD-2). Gene duplication, with and without the influence of X-inactivation, was achieved using a translocation that involves the insertion of a portion of Chr 7, including Mod-2, into the X, T(X;7)1Ct. A 1:1 relationship for Mod-2 dosage and MOD-2 activity was found in heart mitochondria. Evidence of X-inactivation of Mod-2 was noted in heart and kidney preparations from females carrying a Mod-2 duplication (one copy of Mod-2 in the X and two copies of Mod-2 on Chr 7). We conclude that the expression of an autosomal locus attached to X-chromatin depends upon whether the translocation is in a balanced or unbalanced state.
E M Eicher, and
D I Coleman
February 1978,
Nature,
E M Eicher, and
D I Coleman
December 1970,
Biochemical genetics,
E M Eicher, and
D I Coleman
December 1979,
Proceedings of the National Academy of Sciences of the United States of America,
E M Eicher, and
D I Coleman
January 1979,
The Journal of biological chemistry,
E M Eicher, and
D I Coleman
August 1979,
Biochemical genetics,
E M Eicher, and
D I Coleman
June 1986,
Neurology,
E M Eicher, and
D I Coleman
November 1991,
The Journal of biological chemistry,
E M Eicher, and
D I Coleman
October 1975,
Annals of human genetics,
E M Eicher, and
D I Coleman
June 1983,
Neurology,
E M Eicher, and
D I Coleman
January 1978,
Human heredity,
