Mutations in rpoBC suppress the defects of a Sinorhizobium meliloti relA mutant.
Mutations in rpoBC suppress the defects of a Sinorhizobium meliloti relA mutant.
复制标题
rpoBC 突变抑制苜蓿中华根瘤菌 relA 突变体的缺陷。
DOI:
10.1128/jb.185.18.5602-5610.2003
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发表时间:
2003
影响因子:
3.2
通讯作者:
Long,SharonR
中科院分区:
文献类型:
--
作者:
Wells,DerekH;Long,SharonR
The nitrogen-fixing symbiosis betweenSinorhizobium melilotiandMedicago sativarequires complex physiological adaptation by both partners. One method by which bacteria coordinately control physiological adaptation is the stringent response, which is triggered by the presence of the nucleotide guanosine tetraphosphate (ppGpp). ppGpp, produced by the RelA enzyme, is thought to bind to and alter the ability of RNA polymerase (RNAP) to initiate and elongate transcription and affect the affinity of the core enzyme for various sigma factors. AnS. meliloti relAmutant which cannot produce ppGpp was previously shown to be defective in the ability to form nodules. This mutant also overproduces a symbiotically necessary exopolysaccharide called succinoglycan (38). The work presented here encompasses the analysis of suppressor mutants, isolated from host plants, that suppress the symbiotic defects of therelAmutant. All suppressor mutations are extragenic and map to eitherrpoBorrpoC, which encode the β and β′ subunits of RNAP. Phenotypic, structural, and gene expression analyses reveal that suppressor mutants can be divided into two classes; one is specific in its effect on stringent response-regulated genes and shares striking similarity with suppressor mutants ofEscherichia colistrains that lack ppGpp, and another reduces transcription of all genes tested in comparison to that in therelAparent strain. Our findings indicate that the ability to successfully establish symbiosis is tightly coupled with the bacteria's ability to undergo global physiological adjustment via the stringent response.