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共生体诱导宿主基因表达改变的证据:变形虫中SAM合成酶的不可逆丧失。

Evidence for symbiont-induced alteration of a host's gene expression: irreversible loss of SAM synthetase from Amoeba proteus.

作者信息

Choi J Y, Lee T W, Jeon K W, Ahn T I

机构信息

Department of Biology Education, Seoul National University, Korea.

出版信息

J Eukaryot Microbiol. 1997 Sep-Oct;44(5):412-9. doi: 10.1111/j.1550-7408.1997.tb05717.x.

Abstract

Symbiont-bearing xD amoebae no longer produce a 45-kDa cytoplasmic protein that functions as S-adenosylmethionine synthetase in symbiont-free D amoebae. The absence of the protein in xD amoebae is attributable to xD amoeba's failure to transcribe the corresponding gene as a result of harboring bacterial symbionts. However, xD amoebae have about half the level of enzyme activity found in D amoebae, indicating that they use an alternative source for the enzyme. xD amoebae originated from D amoebae by bacterial infection and now depend on their symbionts for survival. xD amoebae exhibit irreversible nucleolar abnormalities when their symbionts are removed, suggesting that X-bacteria supply the needed enzyme. A monoclonal antibody against the 45-kDa protein was produced and used as a probe in cloning its corresponding cDNA. The product of the cDNA was found to have S-adenosylmethionine synthetase activity. These results show how symbiotic X-bacteria may become essential cellular components of amoeba by supplementing a genetic defect for an amoeba's house-keeping gene that is brought about by an action of X-bacteria themselves. This is the first reported example in which symbionts alter the host's gene expression to block the production of an essential protein.

摘要

携带共生体的xD变形虫不再产生一种45 kDa的细胞质蛋白,该蛋白在无共生体的D变形虫中作为S-腺苷甲硫氨酸合成酶发挥作用。xD变形虫中该蛋白的缺失归因于xD变形虫由于携带细菌共生体而未能转录相应基因。然而,xD变形虫的酶活性水平约为D变形虫的一半,这表明它们使用了该酶的替代来源。xD变形虫起源于被细菌感染的D变形虫,现在依赖其共生体生存。当去除xD变形虫的共生体时,它们会出现不可逆的核仁异常,这表明X细菌提供了所需的酶。制备了一种针对45 kDa蛋白的单克隆抗体,并将其用作克隆其相应cDNA的探针。发现该cDNA的产物具有S-腺苷甲硫氨酸合成酶活性。这些结果表明,共生的X细菌如何通过补充由X细菌自身作用导致的变形虫管家基因的遗传缺陷,成为变形虫必不可少的细胞成分。这是首次报道共生体改变宿主基因表达以阻止必需蛋白产生的例子。

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