Zoological Institute, University of Zürich-Irchel, CH-8057 Zürich, Switzerland.
EMBO J. 1983;2(4):485-91. doi: 10.1002/j.1460-2075.1983.tb01451.x.
Sex determination and dosage compensation in Drosophila are implemented by the ratio of X-chromosomes to sets of autosomes (X:A ratio). Our aim was to change this X:A ratio during development, and to assess the response of the affected cells in sexually dimorphic structures. For this purpose, clones of XO constitution were produced in female embryos and larvae of two genotypes in which almost the entire euchromatic arm of one X-chromosome was translocated to the third chromosome. Genotype I was heterozygous for the X-linked recessive mutations Sxl, genotype II was homozygous for Sxl. The Sxl gene (sex-lethal) is involved in mediating sex determination and dosage compensation. In genotype I (Sxl), male clones could be generated up to 48 h in genitalia and analia, up to 72 h in the sex comb region and up to 96 h in 5th and 6th tergites. In genotype II (Sxl), male clones only appeared in the tergites, and only up to 24 h. The difference in these results is ascribed to the presence of Sxl in genotype I: when homozygous, this mutation causes XX clones to differentiate male structures; most of the male clones produced in genotype I must therefore be XX. In contrast, male clones produced in genotype II must be XO. Since these were only found when generated in embryos we conclude that the X:A ratio expresses itself autonomously in clones by setting the state of activity of the Sxl gene around blastoderm stage. Once this is achieved, the X:A signal is no longer needed, and the state of activity of the Sxl gene determines sex and dosage compensation.
性别的确定和剂量补偿在果蝇中是通过 X 染色体与常染色体组数的比值(X:A 比值)来实现的。我们的目的是在发育过程中改变这个 X:A 比值,并评估受影响的细胞在性二态结构中的反应。为此,我们在两种基因型的雌性胚胎和幼虫中产生了 XO 组成的克隆,其中一条 X 染色体的整个常染色体臂几乎都被转移到了第三号染色体上。基因型 I 是 X 连锁隐性突变 Sxl 的杂合子,基因型 II 是 Sxl 的纯合子。Sxl 基因(性别致死)参与介导性别决定和剂量补偿。在基因型 I(Sxl)中,雄性克隆可以在生殖器和肛区产生长达 48 小时,在性梳区产生长达 72 小时,在第 5 和第 6 个背板上产生长达 96 小时。在基因型 II(Sxl)中,雄性克隆仅在背板上出现,且仅持续 24 小时。这些结果的差异归因于基因型 I 中 Sxl 的存在:当纯合时,这种突变导致 XX 克隆分化为雄性结构;因此,在基因型 I 中产生的大多数雄性克隆必须是 XX。相比之下,在基因型 II 中产生的雄性克隆必须是 XO。由于这些克隆仅在胚胎中产生,我们得出结论,X:A 比值通过在胚胎期左右 Sxl 基因的活性状态来自主表达在克隆中。一旦达到这个状态,X:A 信号就不再需要,Sxl 基因的活性状态决定了性别和剂量补偿。