EGTA处理引起海胆胚胎热休克蛋白的合成

Maria C. Roccheri , Karoly Onorato, Cinzia Tipa, Caterina Casano
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引用次数: 9

摘要

卵泡后期的卵泡胚,当温度从生理温度(20°C)升高到31°C时,会合成大量热休克蛋白(hsps),并表现出对大宗蛋白合成的严重抑制。通过单电泳和双向电泳,我们发现EGTA(乙二醇-双[β-氨基乙醚]四乙酸)处理在海胆胚胎中诱导了大量蛋白质合成和整套热休克蛋白合成的显著抑制。此外,egta处理的海胆胚胎能够在致命的温度(35°C)下存活,变得耐热。由于与不同的钙螯合剂EDTA(乙二胺四乙酸)或在无钙培养基中孵育均未诱导热休克蛋白合成,因此我们得出结论,EGTA引起的应激反应与其钙螯合剂功能无关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
EGTA Treatment Causes the Synthesis of Heat Shock Proteins in Sea Urchin Embryos

Paracentrotus lividus embryos, at post-blastular stage, when subjected to a rise in temperature from physiologic (20°C) to 31°C, synthesize a large group of heat shock proteins (hsps), and show a severe inhibition of bulk protein synthesis. We show, by mono- and two-dimensional electrophoresis, that also EGTA (ethylene glycol-bis[β-aminoethyl ether] tetraacetic acid) treatment induces in sea urchin embryos both marked inhibition of bulk protein synthesis and the synthesis of the entire set of hsps. Furthermore, EGTA-treated sea urchin embryos are able to survive at a temperature otherwise lethal (35°C) becoming thermotolerant. Because incubation with a different calcium-chelator, EDTA (ethylenediaminetetraacetic acid), or in calcium-free medium did not induce hsps synthesis we conclude that the stress response caused by EGTA is not related to its calcium chelator function.

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