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大肠杆菌核糖体蛋白基因的体外表达:翻译的自体抑制

In vitro expression of Escherichia coli ribosomal protein genes: autogenous inhibition of translation.

作者信息

Yates J L, Arfsten A E, Nomura M

出版信息

Proc Natl Acad Sci U S A. 1980 Apr;77(4):1837-41. doi: 10.1073/pnas.77.4.1837.

Abstract

Escherichia coli ribosomal protein L1 (0.5 micro M) was found to inhibit the synthesis of both proteins of the L11 operon, L11 and L1, but not the synthesis of other proteins directed by lambda rifd 18 DNA. Similarly, S4 (1 micro M) selectively inhibited the synthesis of three proteins of the alpha operon, S13, S11, and S4, directed by lambda spcI DNA or a restriction enzyme fragment obtained from this DNA. S8 (3.6 micro M) also showed preferential inhibitory effects on the synthesis of some proteins encoded in the spc operon, L24 and L5 (and probably S14 and S8), directed by lambda spcl DNA or a restriction enzyme fragment carrying the genes for these proteins. The inhibitory effect of L1 was observed only with L1 and not with other proteins examined, including S4 and S8. Similarly, the effect of S4 was not observed with L1 or S8, and that of S8 was not seen with L1 or S4. Inhibition was shown to take place at the level of translation rather than transcription. Thus, at least some ribosomal proteins (L1 S4, and S8) have the ability to cause selective translational inhibition of the synthesis of certain ribosomal proteins whose genes are in the same operon as their own. These results support the hypothesis that certain free ribosomal proteins not assembled into ribosomes act as "autogenous" feedback inhibitors to regulate the synthesis of ribosomal proteins.

摘要

发现大肠杆菌核糖体蛋白L1(0.5微摩尔)可抑制L11操纵子中L11和L1这两种蛋白质的合成,但不抑制由λrifd 18 DNA指导的其他蛋白质的合成。同样,S4(1微摩尔)选择性抑制由λspcI DNA或从该DNA获得的限制性酶切片段指导的α操纵子中三种蛋白质S13、S11和S4的合成。S8(3.6微摩尔)对由λspcl DNA或携带这些蛋白质基因的限制性酶切片段指导的spc操纵子中编码的某些蛋白质(L24和L5,可能还有S14和S8)的合成也表现出优先抑制作用。仅在L1存在时观察到L1的抑制作用,而在包括S4和S8在内的其他检测蛋白质中未观察到。同样,在L1或S8存在时未观察到S4的作用,在L1或S4存在时也未观察到S8的作用。抑制作用显示发生在翻译水平而非转录水平。因此,至少一些核糖体蛋白(L1、S4和S8)有能力对某些核糖体蛋白的合成产生选择性翻译抑制,这些核糖体蛋白的基因与其自身基因位于同一操纵子中。这些结果支持这样的假说,即某些未组装到核糖体中的游离核糖体蛋白作为“自体”反馈抑制剂来调节核糖体蛋白的合成。

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