Differential regulation of fixN-reiterated genes in Rhizobium etli by a novel fixL-fixK-cascade
Differential regulation of fixN-reiterated genes in Rhizobium etli by a novel fixL-fixK-cascade
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DOI：
10.1094/mpmi.2000.13.12.1283
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发表时间：
2000-12-01
影响因子：
3.5
通讯作者：
Romero, D
中科院分区：
文献类型：
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作者：
Girard, L;Brom, S;Romero, D
根瘤菌科固氮调节的复杂性包括调节成分的重复以及物种之间每个成分的不同作用。对于Rhizobium etli CFN42，我们报道共生质粒（pCFN42d）包含一个关键调节基因（fixKd）和共生细胞色素氧化酶基因（fixNOQPd），在这里我们讨论这些基因（fixKf和fixNOQPf）重复的发生以及在先前被认为神秘的质粒（pCFN42f）上发现不寻常的fixL同源物，推导出的结构FixL多肽暗示了如R，leguminosarum中所述的二元调节系统的接收器和发射器模块的融合。 viciae VF39，基因融合分析，加上每个调控元件的突变，表明FixKf的自由表达完全依赖于FixL，相反，在测试条件下未检测到FixKd的合成。 FixKf 蛋白是两次 fixN 重复的微氧表达所必需的，而 FixKd 蛋白似乎是可有可无的。有趣的是，fixN重复的表达表现出对FixL的差异依赖性，其中在不存在FixL的情况下fixNf的转录被抑制，但fixNd的表达仍然显示出显着水平。这表明存在独立于 FixL 的机制来表达 fixNd 重复。令人惊讶的是，fixL、FixKd 或 fixKf（单独或组合）的突变并没有改变共生有效性。然而，fixNd（但不包括fixNf）的突变受到严重影响，表明这些重复在固氮中的不同作用。
Among the complexities in the regulation of nitrogen fixation in the Rhizobiaceae are reiteration of regulatory components as well as variant roles for each component between species. For Rhizobium etli CFN42, we reported that the symbiotic plasmid (pCFN42d) contains a key regulatory gene (fixKd) and genes for a symbiotic cytochrome oxidase (fixNOQPd), Here we discuss the occurrence of reiteration of these genes (fixKf and fixNOQPf) and the finding of an unusual fixL homolog on a plasmid previously considered cryptic (pCFN42f), The structure of the deduced FixL polypeptide is suggestive of a fusion of the receiver and transmitter modules of a two-component regulatory system as described in R, leguminosarum by. viciae VF39, Gene fusion analysis, coupled with mutation of each regulatory element, revealed that free-living expression of FixKf was dependent fully on FixL, In contrast, synthesis of FixKd was not detected under the conditions tested. The FixKf protein is needed for microaerobic expression of both fixN reiterations, whereas the FixKd protein appears to be dispensable. Interestingly, expression of the fixN reiterations exhibits a differential dependence for FixL, where transcription of fixNf was suppressed in the absence of FixL but expression of fixNd still showed significant levels. This suggests the existence of a FixL-independent mechanism for expression of the fixNd reiteration. Surprisingly, mutations in fixL, FixKd, or fixKf (either singly or in combination) did not alter symbiotic effectiveness. A mutation in fixNd (but not in fixNf) was, however, severely affected, indicating a differential role for these reiterations in nitrogen fixation.