THE GENETIC BASIS OF DOSAGE COMPENSATION OF ALCOHOL DEHYDROGENASE-1 IN MAIZE

ABSTRACT The levels of alcohol dehydrogenase (ADH) do not exhibit a structural gene-dosage effect in a one to four dosage series of the long arm of chromosome one (1L) (BIRCHLER19 79). This phenomenon, termed dosage compensation, has been studied in more detail. Experiments are described in which individuals aneuploid for shorter segments were examined for the level of ADH in order to characterize the genetic nature of the compensation. The relative ADH expression in segmental trisomics and tetrasomics of region IL 0.72–0.90, which includes the Adh locus, approaches the level expected from a strict gene dosage effect. Region IL 0.20–0.72 produces a negative effect upon ADH in a similar manner to that observed with other enzyme levels when IL as a whole is varied (BIRCHLEF1I9 79). These and other comparisons have led to the concept that the compensation of ADH results from the cancellation of the structural gene effect by the negative aneuploid effect. The example of ADH is discussed as a model for certain other cases of dosage compensation in higher eukaryotes.

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THE STRUCTURAL GENE FOR α-MANNOSIDASE-1 IN DICTYOSTELIUM DISCOIDEUM

Genetics ◽

10.1093/genetics/84.2.159 ◽

1976 ◽

Vol 84 (2) ◽

pp. 159-174

Author(s):

S J Free ◽

R T Schimke ◽

W F Loomis

Keyword(s):

Linkage Group ◽

Dictyostelium Discoideum ◽

Structural Gene ◽

Gene Dosage ◽

Dosage Effect ◽

Substrate Affinity ◽

Developmentally Regulated ◽

Group Vi ◽

Gene Dosage Effect

ABSTRACT We have isolated 4 independent mutations affecting α-mannosidase-1, a a developmentally regulated activity in Dictyostelium discoideum. Three of these result in a thermolabile α-mannosidase-1 activity. One mutation also affects the substrate affinity (Km) of the activity. In diploids these mutations show a gene dosage effect and are all alleles. The structural gene for α-mannosidase-1, as defined by these mutations, defines a new linkage group, linkage group VI. α-Mannosidase-1 is probably a homopolymer with subunits of 54,000 daltons.

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Analysis of autosomal dosage compensation involving the alcohol dehydrogenase locus in Drosophila melanogaster.

Genetics ◽

10.1093/genetics/124.3.677 ◽

1990 ◽

Vol 124 (3) ◽

pp. 677-686 ◽

Cited By ~ 2

Author(s):

J A Birchler ◽

J C Hiebert ◽

K Paigen

Keyword(s):

Alcohol Dehydrogenase ◽

Structural Gene ◽

Dosage Compensation ◽

Messenger Rna ◽

Gene Dosage ◽

Regulatory Region ◽

Fusion Construct ◽

Promoter Sequences ◽

Alcohol Dehydrogenase Activity ◽

Sufficient Magnitude

Abstract An example of autosomal dosage compensation involving the expression of the alcohol dehydrogenase (Adh) locus is described. Flies trisomic for a quarter of the length of the left arm of chromosome two, including Adh, have diploid levels of enzyme activity and alcohol dehydrogenase messenger RNA. Subdivision of the compensating trisomic into smaller ones revealed a region that exerts an inverse regulatory effect on alcohol dehydrogenase activity and messenger RNA levels and a smaller region surrounding the structural gene that exhibits a direct gene dosage response. The two opposing effects are of sufficient magnitude that they cancel when simultaneously present resulting in the observed compensation in the larger aneuploid. An Adh promoter-white structural gene fusion construct is affected by the inverse regulatory region indicating that the effect is mediated through the Adh promoter sequences. The role of autosomal dosage compensation in understanding aneuploid syndromes and karyotype evolution in Drosophila species is discussed.

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