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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) (Birchler 1979). 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 1L 0.72-0.90, which includes the Adh locus, approaches the level expected from a strict gene dosage effect. Region 1L 0.20-0.72 produces a negative effect upon ADH in a similar manner to that observed with other enzyme levels when 1L as a whole is varied (Birchler 1979). 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.
James A. Birchler (Sun,) studied this question.