HSFs and regulation of Hsp70.1 (Hspa1b) in oocytes and preimplantation embryos: new insights brought by transgenic and knockout mouse models
HSFs and regulation of Hsp70.1 (Hspa1b) in oocytes and preimplantation embryos: new insights brought by transgenic and knockout mouse models
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DOI：
10.1007/s12192-010-0239-1
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发表时间：
2011-05-01
影响因子：
3.8
通讯作者：
Christians, Elisabeth
中科院分区：
文献类型：
--
作者：
Le Masson, Florent;Christians, Elisabeth
编码热休克蛋白（Hsps）的基因在热应激后由于热休克转录因子（HSF）的激活而被诱导，热休克转录因子（HSF）与位于热休克蛋白启动子序列内的热休克元件（HSE）相互作用。这种细胞和保护性反应（热休克反应（HSR））是众所周知的，并在进化上保守。然而，HSR并不在多细胞生物体的生命期间产生的所有细胞中起作用，例如，小鼠早期胚胎利用小鼠转基因和基因敲除模型，我们研究了反式（HSF 1和2）和顺式（HSE）调控元件在Hsp70.1（Hspa1b）从卵母细胞到囊胚的几个发育步骤中的作用。我们的研究证实，即使在没有任何压力的情况下，HSF 1调节卵母细胞和早期胚胎中的Hsp70.1。我们的数据强调的作用，母亲和父亲的热休克蛋白70.1的发育调节表达时观察合子基因组激活发生。此外，在这种无应激的发育条件下，与HSE的亲和力和结合可能比应激反应更宽松。最后，提交胚泡不同的压力条件下，我们表明，热休克蛋白表达和细胞存活所需的HSF2的差异。综上所述，我们的研究结果表明，热休克的反式和顺式调控元件的作用演变沿着早期胚胎发育的连续步骤。
Gene encoding heat shock protein (Hsps) are induced following a thermal stress thanks to the activation of heat shock transcription factor (HSF) which interacts with heat shock elements (HSE) located within the sequence of Hsp promoters. This cellular and protective response (heat shock response (HSR)) is well known and evolutionarily conserved. Nevertheless, HSR does not function in all the cells produced during the life of a multicellular organism, e.g., early mouse embryos. Taking advantage of mouse transgenic and knockout models, we investigated the roles of trans (HSF 1 and 2) and cis (HSE) regulatory elements in the control of Hsp70.1 (Hspa1b) through several developmental steps from oocytes to blastocysts. Our studies confirm that, even in absence of any stress, HSF1 regulates Hsp70.1 in oocytes and early embryos. Our data emphasize the role of maternal and paternal HSFs in the developmentally regulated expression of Hsp70.1 observed when the zygotic genome activation occurs. Furthermore, in this unstressed developmental condition, affinity and binding to HSEs might be more permissive than in the stress response. Finally, submitting blastocyst to different stress conditions, we show that HSF2 is differentially required for Hsp expression and cell survival. Taken together, our findings indicate that the role of heat shock trans and cis regulatory elements evolve along the successive steps of early embryonic development.