Nicoloff Hervé, Elagöz Aram, Arsène-Ploetze Florence, Kammerer Benoît, Martinussen Jan, Bringel Françoise
Laboratoire de Dynamique, Evolution et Expression de Génomes de Microorganismes, Université Louis Pasteur/CNRS FRE 2326, 28 rue Goethe, F-67083 Strasbourg, France.
J Bacteriol. 2005 Mar;187(6):2093-104. doi: 10.1128/JB.187.6.2093-2104.2005.
Carbamoyl phosphate is a precursor for both arginine and pyrimidine biosynthesis. In Lactobacillus plantarum, carbamoyl phosphate is synthesized from glutamine, ATP, and carbon dioxide by two sets of identified genes encoding carbamoyl phosphate synthase (CPS). The expression of the carAB operon (encoding CPS-A) responds to arginine availability, whereas pyrAaAb (encoding CPS-P) is part of the pyrR1BCAaAbDFE operon coding for the de novo pyrimidine pathway repressed by exogenous uracil. The pyr operon is regulated by transcription attenuation mediated by a trans-acting repressor that binds to the pyr mRNA attenuation site in response to intracellular UMP/phosphoribosyl pyrophosphate pools. Intracellular pyrimidine triphosphate nucleoside pools were lower in mutant FB335 (carAB deletion) harboring only CPS-P than in the wild-type strain harboring both CPS-A and CPS-P. Thus, CPS-P activity is the limiting step in pyrimidine synthesis. FB335 is unable to grow in the presence of uracil due to a lack of sufficient carbamoyl phosphate required for arginine biosynthesis. Forty independent spontaneous FB335-derived mutants that have lost regulation of the pyr operon were readily obtained by their ability to grow in the presence of uracil and absence of arginine; 26 harbored mutations in the pyrR1-pyrB loci. One was a prototroph with a deletion of both pyrR1 and the transcription attenuation site that resulted in large amounts of excreted pyrimidine nucleotides and increased intracellular UTP and CTP pools compared to wild-type levels. Low pyrimidine-independent expression of the pyr operon was obtained by antiterminator site-directed mutagenesis. The resulting AE1023 strain had reduced UTP and CTP pools and had the phenotype of a high-CO2-requiring auxotroph, since it was able to synthesize sufficient arginine and pyrimidines only in CO2-enriched air. Therefore, growth inhibition without CO2 enrichment may be due to low carbamoyl phosphate pools from lack of CPS activity.
氨甲酰磷酸是精氨酸和嘧啶生物合成的前体。在植物乳杆菌中,氨甲酰磷酸由谷氨酰胺、ATP和二氧化碳通过两组已鉴定的编码氨甲酰磷酸合成酶(CPS)的基因合成。carAB操纵子(编码CPS-A)的表达对精氨酸的可用性作出反应,而pyrAaAb(编码CPS-P)是pyrR1BCAaAbDFE操纵子的一部分,该操纵子编码由外源尿嘧啶抑制的从头嘧啶途径。pyr操纵子由转录衰减调节,转录衰减由一种反式作用阻遏物介导,该阻遏物响应细胞内UMP/磷酸核糖焦磷酸库与pyr mRNA衰减位点结合。仅含有CPS-P的突变体FB335(carAB缺失)中的细胞内嘧啶三磷酸核苷库低于同时含有CPS-A和CPS-P的野生型菌株。因此,CPS-P活性是嘧啶合成中的限制步骤。由于缺乏精氨酸生物合成所需的足够氨甲酰磷酸,FB335在尿嘧啶存在下无法生长。通过它们在尿嘧啶存在和精氨酸不存在下生长的能力,很容易获得40个独立的自发FB335衍生突变体,这些突变体失去了pyr操纵子的调控;26个在pyrR1-pyrB位点存在突变。其中一个是原养型,其pyrR1和转录衰减位点均缺失,与野生型水平相比,导致大量嘧啶核苷酸分泌,细胞内UTP和CTP库增加。通过抗终止子定点诱变获得了pyr操纵子低嘧啶非依赖性表达。所得的AE1023菌株的UTP和CTP库减少,具有高二氧化碳需求营养缺陷型的表型,因为它仅在富含二氧化碳的空气中才能合成足够的精氨酸和嘧啶。因此,没有二氧化碳富集时的生长抑制可能是由于缺乏CPS活性导致氨甲酰磷酸库较低。