Parker-Thornburg J, Bonner J J
Institute for Molecular and Cellular Biology, Indiana University, Bloomington 47405.
Cell. 1987 Dec 4;51(5):763-72. doi: 10.1016/0092-8674(87)90099-7.
We have isolated a number of mutations in D. melanogaster that result in the constitutive expression of the heat shock response in a tissue-specific manner. These mutations induce alcohol dehydrogenase (ADH) when the ADH structural gene is fused to the promoter for the 70 kd heat shock protein (hsp70) gene. Flies carrying these mutations, the hsp70-Adh fusion, and a deletion in their endogenous Adh genes are ethanol tolerant and exhibit elevated ADH levels. Several of the tissue-specific mutations have also been shown to induce an hsp26-Adh fusion gene in trans. The mutation Act88FKM75, a G----A transition in the indirect flight muscle-specific actin gene, also exhibits this phenotype. Comparisons with the Act88FKM75 mutation suggest that the tissue-specific mutations induce the heat shock response by disrupting the physiology of the cells in which the variant gene product is expressed.
我们在黑腹果蝇中分离出了一些突变,这些突变导致热休克反应以组织特异性方式组成型表达。当乙醇脱氢酶(ADH)结构基因与70kd热休克蛋白(hsp70)基因的启动子融合时,这些突变会诱导ADH表达。携带这些突变、hsp70-Adh融合基因以及其内源Adh基因缺失的果蝇对乙醇具有耐受性,并且ADH水平升高。一些组织特异性突变还被证明能反式诱导hsp26-Adh融合基因。突变Act88FKM75是间接飞行肌特异性肌动蛋白基因中的一个G→A转换,也表现出这种表型。与Act88FKM75突变的比较表明,组织特异性突变通过破坏表达变异基因产物的细胞的生理功能来诱导热休克反应。