Faculty Research 1990 - 1999

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

Document Type

Article

Publication Date

1990

Keywords

Animal, Chromosomes, Cloning-Molecular, Diploidy, Dosage-Compensation-(Genetics), Drosophila-Melanogaster: en, ge, DNA: an, Female, Gene-Expression-Regulation-Enzymologic, Genes-Structural, Male, Phenotype, Promoter-Regions-(Genetics), RNA-Messenger: an, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-NON-P-H-S, SUPPORT-U-S-GOVT-P-H-S, Transcription-Genetic, Translocation-(Genetics), Trisomy

First Page

677

Last Page

686

JAX Source

Genetics 1990 Mar; 124(3):677-86.

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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