Chang K A, Kuroda M I
Department of Cell Biology, Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, USA.
Genetics. 1998 Oct;150(2):699-709. doi: 10.1093/genetics/150.2.699.
Dosage compensation in Drosophila is the mechanism by which X-linked gene expression is made equal in males and females. Proper regulation of this process is critical to the survival of both sexes. Males must turn the male-specific lethal (msl)-mediated pathway of dosage compensation on and females must keep it off. The msl2 gene is the primary target of negative regulation in females. Preventing production of MSL2 protein is sufficient to prevent dosage compensation; however, ectopic expression of MSL2 protein in females is not sufficient to induce an insurmountable level of dosage compensation, suggesting that an additional component is limiting in females. A candidate for this limiting factor is MSL1, because the amount of MSL1 protein in females is reduced compared to males. We have identified two levels of negative regulation of msl1 in females. The predominant regulation is at the level of protein stability, while a second regulatory mechanism functions at the level of protein synthesis. Overcoming these control mechanisms by overexpressing both MSL1 and MSL2 in females results in 100% female-specific lethality.
果蝇中的剂量补偿是一种机制，通过该机制使雄性和雌性中X连锁基因的表达相等。正确调节这一过程对两性的生存至关重要。雄性必须开启雄性特异性致死（msl）介导的剂量补偿途径，而雌性必须使其关闭。msl2基因是雌性中负调控的主要靶点。阻止MSL2蛋白的产生足以防止剂量补偿；然而，在雌性中异位表达MSL2蛋白不足以诱导无法克服的剂量补偿水平，这表明雌性中存在另一种限制因素。这种限制因子的一个候选者是MSL1，因为与雄性相比，雌性中MSL1蛋白的量减少了。我们已经确定了雌性中msl1的两个负调控水平。主要的调控发生在蛋白质稳定性水平，而第二种调控机制在蛋白质合成水平起作用。通过在雌性中过表达MSL1和MSL2来克服这些控制机制会导致100%的雌性特异性致死率。
