DNA binding of heat shock factor to the heat shock element is insufficient for transcriptional activation in murine erythroleukemia cells.
DNA binding of heat shock factor to the heat shock element is insufficient for transcriptional activation in murine erythroleukemia cells.
复制标题
热休克因子与热休克元件的 DNA 结合不足以在鼠红白血病细胞中进行转录激活。
DOI：
10.1128/mcb.10.4.1600-1608.1990
复制
发表时间：
1990
影响因子：
5.3
通讯作者：
Kingston,RE
中科院分区：
文献类型：
--
作者：
Hensold,JO;Hunt,CR;Calderwood,SK;Housman,DE;Kingston,RE
热休克反应是最保守的调控基因表达的例子之一，存在于所有细胞生物体中。温度升高或其他细胞应激对热休克基因的转录激活是通过热休克因子(HSF)与热诱导基因启动子中存在的保守核苷酸序列(热休克元件)结合而介导的。尽管这种反应高度保守，但胚胎发育阶段的特点是没有热休克反应。小鼠红白血病(Mel)细胞也缺乏这种反应，我们在这里报告了这些基因中最保守的基因之一hsp70的这种缺陷的详细特征。令人惊讶的是，尽管诱导了一种具有小鼠HSF结合特异性的蛋白质，但该基因没有发生热诱导的转录激活。然而，MEL HSF与3T3细胞中的HSF在表观尺寸上略有不同，后者表现出正常的热休克反应。这些数据表明，热激活哺乳动物的HSF至少需要两个独立的步骤：改变结合活性，然后进一步修饰，激活转录。MEL细胞不会对热休克做出反应，因为它们缺乏执行这种二次修改的能力。这些细胞提供了一个有用的系统来表征哺乳动物的热休克激活。
The heat shock response is among the most highly conserved examples of regulated gene expression, being present in all cellular organisms. Transcriptional activation of heat shock genes by increased temperature or other cellular stresses is mediated by the binding of a heat shock factor (HSF) to a conserved nucleotide sequence (the heat shock element) present in the promoter of heat-inducible genes. Despite the high degree of conservation of this response, embryonic stages of development are characterized by the absence of a heat shock response. Murine erythroleukemia (MEL) cells also lack this response, and we report here a detailed characterization of this defect for one of the most highly conserved of these genes,hsp70.Surprisingly, heat-induced transcriptional activation of this gene does not occur, despite the induction of a protein with the binding specificity of murine HSF. However, the MEL HSF differs slightly in apparent size from the HSF in 3T3 cells, which exhibit a normal heat shock response. These data suggest that activation of mammalian HSF by heat requires at least two separate steps: an alteration of binding activity followed by further modification that activates transcription. MEL cells do not respond to heat shock because they lack the ability to perform this secondary modification. These cells provide a useful system for characterizing heat shock activation in mammals.