Wolffe A P, Perlman A J, Tata J R
EMBO J. 1984 Dec 1;3(12):2763-70. doi: 10.1002/j.1460-2075.1984.tb02207.x.
We have investigated the effect of heat shock on primary cultures of male and female Xenopus laevis hepatocytes as a function of estrogen-induced vitellogenin gene expression. Coincident with the induction of heat-shock protein (hsp) synthesis, thermal stress abolishes the estrogen activated transcription and accumulation of vitellogenin mRNA, at the same time causing the destabilization of vitellogenin mRNA accumulated by prior treatment with the hormone. Exposure of the cells to estrogen before heat shock allows an immediate resumption of vitellogenin gene transcription on return to 26 degrees C. Heat shock applied to cells from hormonally naive male Xenopus extends the lag period preceding vitellogenin gene transcription upon return to normal temperatures. This transient and reversible paralysis of estrogen responsiveness is paralleled by reversible changes in the amount of nuclear estrogen receptor in the hepatocytes. Heat shock therefore offers a novel approach in the manipulation and analysis of the early stages of steroid hormonal regulation of gene expression.
我们研究了热休克对非洲爪蟾雌雄肝细胞原代培养物的影响,该影响是雌激素诱导卵黄蛋白原基因表达的一个函数。与热休克蛋白(hsp)合成的诱导同时发生的是,热应激消除了雌激素激活的卵黄蛋白原mRNA转录和积累,同时导致先前用该激素处理积累的卵黄蛋白原mRNA不稳定。在热休克前将细胞暴露于雌激素中,可使其在恢复到26摄氏度时立即恢复卵黄蛋白原基因转录。对来自未接触过激素的雄性非洲爪蟾的细胞施加热休克,会延长恢复正常温度后卵黄蛋白原基因转录之前的延迟期。雌激素反应性的这种短暂且可逆的麻痹与肝细胞中核雌激素受体数量的可逆变化平行。因此,热休克为甾体激素基因表达调控早期阶段的操作和分析提供了一种新方法。