缺乏热休克因子2的小鼠胚胎成纤维细胞的表型特征
Phenotypic characterization of mouse embryonic fibroblasts lacking heat shock factor 2.
作者信息
Paslaru Liliana, Morange M, Mezger Valérie
机构信息
Department of Biochemistry, "Carol Davila" University of Medicine and Pharmacy, Fundeni Hospital, Bucharest, Romania.
出版信息
J Cell Mol Med. 2003 Oct-Dec;7(4):425-35. doi: 10.1111/j.1582-4934.2003.tb00245.x.
In murine cells, the heat shock response is regulated by a transcription factor, HSF1, which triggers the transcription of heat shock genes. HSF2 has been shown to be involved in meiosis and mouse brain development. We characterized the effects of the absence of HSF2 in mouse embryonic fibroblasts (MEFs). The temperature threshold of the heat shock response appeared lowered in Hsf2(-/-) MEFS as monitored by the synthesis of heat shock protein HSP70. In contrast to unstressed wild type MEFS, HSP70 and HSF1 are localized in the nucleus of unstressed Hsf2(-/-) MEFS, a characteristic of stressed cells. HSF1 is not activated for DNA-binding at unstressed temperature in Hsf2(-/-) MEFS. Therefore, the absence of HSF2 induces some but not all of the characteristics of the stress response. In addition, Hsf2(-/-) MEFS exhibited proliferation defects, altered morphology, remodeling of the fibronectin network.
在鼠细胞中，热休克反应由转录因子HSF1调控，HSF1触发热休克基因的转录。已表明HSF2参与减数分裂和小鼠大脑发育。我们对小鼠胚胎成纤维细胞（MEF）中缺失HSF2的影响进行了表征。通过热休克蛋白HSP70的合成监测发现，Hsf2(-/-) MEF中热休克反应的温度阈值似乎降低了。与未受应激的野生型MEF不同，HSP70和HSF1定位于未受应激的Hsf2(-/-) MEF的细胞核中，这是受应激细胞的一个特征。在未受应激温度下，Hsf2(-/-) MEF中的HSF1未被激活用于结合DNA。因此，HSF2的缺失诱导了应激反应的一些但不是所有特征。此外，Hsf2(-/-) MEF表现出增殖缺陷、形态改变、纤连蛋白网络重塑。
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