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肺炎克雷伯菌固氮缺陷突变体的互补分析。

Complementation analysis of Klebsiella pneumoniae mutants defective in nitrogen fixation.

作者信息

Dixon R, Kennedy C, Kondorosi A, Krishnapillai V, Merrick M

出版信息

Mol Gen Genet. 1977 Nov 29;157(2):189-98. doi: 10.1007/BF00267397.

Abstract

A series of mutants defective in nitrogen fixation (nif) were isolated in Klebsiella pneumoniae strain M5a1. The nif mutations were either located on plasmid pRD1 or on the K. pneumoniae chromosome. A total of 37 plasmid mutants and 28 chromosomal mutants were employed in complementation tests using the acetylene reduction technique. Most mutants could be assigned to one of seven nif cistrons: nifA, nifB, nifD, nifE, nifF, nifH, and nifK. Complementation analysis of two nif deletion mutants confirmed transductional evidence that these strains carry nifB-A-F deletions. One deletion mutant had, in contrast to previous transductional analysis, a functional nifK cistron and presumably is deleted for nifB-A-F-E. Examination of the biochemical phenotype of several mutants suggests that the nifA product has a regulatory function, and nifK, nifD and nifH are most probably the structural genes for nitrogenase.

摘要

在肺炎克雷伯菌M5a1菌株中分离出一系列固氮(nif)缺陷型突变体。nif突变要么位于质粒pRD1上,要么位于肺炎克雷伯菌染色体上。使用乙炔还原技术,共37个质粒突变体和28个染色体突变体用于互补试验。大多数突变体可归为七个nif顺反子之一:nifA、nifB、nifD、nifE、nifF、nifH和nifK。两个nif缺失突变体的互补分析证实了转导证据,即这些菌株携带nifB - A - F缺失。与之前的转导分析相反,一个缺失突变体具有功能性的nifK顺反子,推测缺失的是nifB - A - F - E。对几个突变体的生化表型检查表明,nifA产物具有调节功能,nifK、nifD和nifH很可能是固氮酶的结构基因。

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