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第一类与第三类利福平耐药突变之间相互作用的遗传学证据。

Genetic evidence for the interaction between cluster I and cluster III rifampicin resistant mutations.

作者信息

Singer M, Jin D J, Walter W A, Gross C A

机构信息

Department of Bacteriology, University of Wisconsin-Madison 53706.

出版信息

J Mol Biol. 1993 May 5;231(1):1-5. doi: 10.1006/jmbi.1993.1251.

Abstract

Rifampicin-resistant (Rifr) mutations of Escherichia coli map to the central portion of the rpoB gene, which encodes the beta subunit of RNA polymerase. These mutations are located in three distinct clusters, designated I, II and III. Three intragenic suppressors of the cluster III Rifr mutation, rpoB3406(RH687), restore the ability of the mutant strain to grow at low and high temperatures and map to a single locus in cluster I. These suppressors are identical to two previously characterized Rifr alleles, rpoB3401(RC529) and rpoB3402(RS529). None of the other 14 previously identified Rifr mutations that we have characterized confers this phenotype. We suggest that this allele-specific suppression results from interaction between Cluster I and Cluster III of the beta subunit.

摘要

大肠杆菌的耐利福平(Rifr)突变定位于rpoB基因的中部,该基因编码RNA聚合酶的β亚基。这些突变位于三个不同的簇中,分别命名为I、II和III。簇III Rifr突变rpoB3406(RH687)的三个基因内抑制子恢复了突变菌株在低温和高温下生长的能力,并定位于簇I中的一个单一基因座。这些抑制子与两个先前鉴定的Rifr等位基因rpoB3401(RC529)和rpoB3402(RS529)相同。我们鉴定的其他14个先前确定的Rifr突变均未表现出这种表型。我们认为这种等位基因特异性抑制是由β亚基的簇I和簇III之间的相互作用导致的。

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