Department of Biology, Indiana University, Bloomington, Indiana 47401.
Genetics. 1981 Mar;97(3-4):625-37. doi: 10.1093/genetics/97.3-4.625.
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.
酒精脱氢酶（ADH）的水平在染色体 1 长臂（1L）的一至四倍剂量系列中没有表现出结构基因剂量效应（Birchler 1979）。这种现象被称为剂量补偿，已经进行了更详细的研究。本文描述了检查较短片段非整倍体个体的 ADH 水平的实验，以表征补偿的遗传性质。包含 Adh 基因座的 1L 0.72-0.90 区域的部分三体和四体的相对 ADH 表达接近严格基因剂量效应所预期的水平。1L 整体变化时，区域 1L 0.20-0.72 以类似于观察到其他酶水平的方式对 ADH 产生负效应（Birchler 1979）。这些和其他比较导致了这样的概念，即 ADH 的补偿是由负非整倍体效应抵消结构基因效应的结果。ADH 被作为高等真核生物中某些其他剂量补偿情况的模型进行了讨论。
