ArticleJournal of bacteriology2002
Control of inducer accumulation plays a key role in succinate-mediated catabolite repression in Sinorhizobium meliloti.
Article in Journal of bacteriology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Implications of carbon catabolite repression for plant-microbe interactions.Plant communications · 2022Pooled it
- Perspective Approaches to "Trojan Horse" Strategy Development for Combating Bacterial Pathogens.Pharmaceuticals (Basel, Switzerland) · 2026Review
- A signaling complex of adenylate cyclase CyaC of Sinorhizobium meliloti with cAMP and the transcriptional regulators Clr and CycR.BMC microbiology · 2023Article
- Inorganic Phosphate Solubilization by Rhizosphere BacteriumFrontiers in microbiology · 2020Article
- Engineering a vitamin BBMC biotechnology · 2018Article
- Article
- Loss of malic enzymes leads to metabolic imbalance and altered levels of trehalose and putrescine in the bacterium Sinorhizobium meliloti.BMC microbiology · 2016Article
- Chemotaxis signaling systems in model beneficial plant-bacteria associations.Plant molecular biology · 2016Review
- Analysis of a taurine-dependent promoter in Sinorhizobium meliloti that offers tight modulation of gene expression.BMC microbiology · 2014Article
- Biochemical characterization of a nitrogen-type phosphotransferase system reveals that enzyme EI(Ntr) integrates carbon and nitrogen signaling in Sinorhizobium meliloti.Journal of bacteriology · 2014Article
- Characterization of a two-component regulatory system that regulates succinate-mediated catabolite repression in Sinorhizobium meliloti.Journal of bacteriology · 2010Article
- HPrK regulates succinate-mediated catabolite repression in the gram-negative symbiont Sinorhizobium meliloti.Journal of bacteriology · 2009Article
- Construction and expression of sugar kinase transcriptional gene fusions by using the Sinorhizobium meliloti ORFeome.Applied and environmental microbiology · 2008Article
- Sinorhizobium meliloti mutants lacking phosphotransferase system enzyme HPr or EIIA are altered in diverse processes, including carbon metabolism, cobalt requirements, and succinoglycan production.Journal of bacteriology · 2008Article
- How phosphotransferase system-related protein phosphorylation regulates carbohydrate metabolism in bacteria.Microbiology and molecular biology reviews : MMBR · 2006Review
- Comprehensive metabolite profiling of Sinorhizobium meliloti using gas chromatography-mass spectrometry.Functional & integrative genomics · 2004Article
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The symbiotic, nitrogen-fixing bacterium Sinorhizobium meliloti favors succinate and related dicarboxylic acids as carbon sources. As a preferred carbon source, succinate can exert catabolite repression upon genes needed for the utilization of many secondary carbon sources, including the alpha-galactosides raffinose and stachyose. We isolated lacR mutants in a genetic screen designed to find S. meliloti mutants that had abnormal succinate-mediated catabolite repression of the melA-agp genes, which are required for the utilization of raffinose and other alpha-galactosides. The loss of catabolite repression in lacR mutants was seen in cells grown in minimal medium containing succinate and raffinose and grown in succinate and lactose. For succinate and lactose, the loss of catabolite repression could be attributed to the constitutive expression of beta-galactoside utilization genes in lacR mutants. However, the inactivation of lacR did not cause the constitutive expression of alpha-galactoside utilization genes but caused the aberrant expression of these genes only when succinate was present. To explain the loss of diauxie in succinate and raffinose, we propose a model in which lacR mutants overproduce beta-galactoside transporters, thereby overwhelming the inducer exclusion mechanisms of succinate-mediated catabolite repression. Thus, some raffinose could be transported by the overproduced beta-galactoside transporters and cause the induction of alpha-galactoside utilization genes in the presence of both succinate and raffinose. This model is supported by the restoration of diauxie in a lacF lacR double mutant (lacF encodes a beta-galactoside transport protein) grown in medium containing succinate and raffinose. Biochemical support for the idea that succinate-mediated repression operates by preventing inducer accumulation also comes from uptake assays, which showed that cells grown in raffinose and exposed to succinate have a decreased rate of raffinose transport compared to control cells not exposed to succinate.
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