scholarly journals Intracellular 2-keto-3-deoxy-6-phosphogluconate is the signal for carbon catabolite repression of phenylacetic acid metabolism in Pseudomonas putida KT2440

Microbiology ◽  
2009 ◽  
Vol 155 (7) ◽  
pp. 2420-2428 ◽  
Author(s):  
Juhyun Kim ◽  
Jinki Yeom ◽  
Che Ok Jeon ◽  
Woojun Park

The growth pattern of Pseudomonas putida KT2440 in the presence of glucose and phenylacetic acid (PAA), where the sugar is used in preference to the aromatic compound, suggests that there is carbon catabolite repression (CCR) of PAA metabolism by glucose or gluconate. Furthermore, CCR is regulated at the transcriptional level. However, this CCR phenomenon does not occur in PAA-amended minimal medium containing fructose, pyruvate or succinate. We previously identified 2-keto-3-deoxy-6-phosphogluconate (KDPG) as an inducer of glucose metabolism, and this has led to this investigation into the role of KDPG as a signal compound for CCR. Two mutant strains, the edd mutant (non-KDPG producer) and the eda mutant (KDPG overproducer), grew in the presence of PAA but not in the presence of glucose. The edd mutant utilized PAA even in the presence of glucose, indicating that CCR had been abolished. This observation has additional support from the finding that there is high phenylacetyl-CoA ligase activity in the edd mutant, even in the presence of glucose+PAA, but not in wild-type cells under the same conditions. Unlike the edd mutant, the eda mutant did not grow in the presence of glucose+PAA. Interestingly, there was no uptake and/or metabolism of PAA in the eda mutant cells under the same conditions. Targeted disruption of PaaX, a repressor of the PAA operon, had no effect on CCR of PAA metabolism in the presence of glucose, suggesting that there is another transcriptional repression system associated with the KDPG signal. This is the first study to demonstrate that KDPG is the true CCR signal of PAA metabolism in P. putida KT2440.

Microbiology ◽  
2010 ◽  
Vol 156 (5) ◽  
pp. 1313-1322 ◽  
Author(s):  
Fenja S. Bleichrodt ◽  
Rita Fischer ◽  
Ulrike C. Gerischer

The degradation of many structurally diverse aromatic compounds in Acinetobacter baylyi is accomplished by the β-ketoadipate pathway. In addition to specific induction of expression by certain aromatic compounds, this pathway is regulated by complex mechanisms at multiple levels, which are the topic of this study. Multiple operons feeding into the β-ketoadipate pathway are controlled by carbon catabolite repression (CCR) caused by succinate plus acetate. The pathways under study enable the catabolism of benzoate (ben), catechol (catA), cis,cis-muconate (catB,C,I,J,F,D), vanillate (van), hydroxycinnamates (hca), dicarboxylates (dca), salicylate (sal), anthranilate (ant) and benzyl esters (are). For analysis of CCR at the transcriptional level a luciferase reporter gene cassette was introduced into the operons. The Crc (catabolite repression control) protein is involved in repression of all operons (except for catA), as demonstrated by the analysis of respective crc strains. In addition, cross-regulation was demonstrated for the vanA,B, hca and dca operons. The presence of protocatechuate caused transcriptional repression of the vanA,B- and hca-encoded funnelling pathways (vertical regulation). Thus the results presented extend the understanding both of CCR and of the effects of Crc for all aromatic degradative pathways of A. baylyi and increase the number of operons known to be controlled by two additional mechanisms, cross-regulation and vertical regulation.


2020 ◽  
Vol 8 (11) ◽  
pp. 1782
Author(s):  
Tania Henriquez ◽  
Tom Baldow ◽  
Yat Kei Lo ◽  
Dina Weydert ◽  
Andreas Brachmann ◽  
...  

Bacteria must be able to cope with harsh environments to survive. In Gram-negative bacteria like Pseudomonas species, resistance-nodulation-division (RND) transporters contribute to this task by pumping toxic compounds out of cells. Previously, we found that the RND system TtgABC of Pseudomonas putida KT2440 confers resistance to toxic metal chelators of the bipyridyl group. Here, we report that the incubation of a ttgB mutant in medium containing 2,2’-bipyridyl generated revertant strains able to grow in the presence of this compound. This trait was related to alterations in the pp_2827 locus (homolog of mexS in Pseudomonas aeruginosa). The deletion and complementation of pp_2827 confirmed the importance of the locus for the revertant phenotype. Furthermore, alteration in the pp_2827 locus stimulated expression of the mexEF-oprN operon encoding an RND efflux pump. Deletion and complementation of mexF confirmed that the latter system can compensate the growth defect of the ttgB mutant in the presence of 2,2’-bipyridyl. To our knowledge, this is the first report on a role of pp_2827 (mexS) in the regulation of mexEF-oprN in P. putida KT2440. The results expand the information about the significance of MexEF-OprN in the stress response of P. putida KT2440 and the mechanisms for coping with bipyridyl toxicity.


2000 ◽  
Vol 182 (4) ◽  
pp. 1144-1149 ◽  
Author(s):  
Kathryn L. Hester ◽  
Jodi Lehman ◽  
Fares Najar ◽  
Lin Song ◽  
Bruce A. Roe ◽  
...  

ABSTRACT Crc (catabolite repression control) protein of Pseudomonas aeruginosa has shown to be involved in carbon regulation of several pathways. In this study, the role of Crc in catabolite repression control has been studied in Pseudomonas putida. The bkd operons of P. putida and P. aeruginosa encode the inducible multienzyme complex branched-chain keto acid dehydrogenase, which is regulated in both species by catabolite repression. We report here that this effect is mediated in both species by Crc. A 13-kb cloned DNA fragment containing the P. putida crc gene region was sequenced. Crc regulates the expression of branched-chain keto acid dehydrogenase, glucose-6-phosphate dehydrogenase, and amidase in both species but not urocanase, although the carbon sources responsible for catabolite repression in the two species differ. Transposon mutants affected in their expression of BkdR, the transcriptional activator of thebkd operon, were isolated and identified as crcand vacB (rnr) mutants. These mutants suggested that catabolite repression in pseudomonads might, in part, involve control of BkdR levels.


2021 ◽  
Author(s):  
Shiny Martis B ◽  
Michel Droux ◽  
William Nasser ◽  
Sylvie Reverchon ◽  
Sam Meyer

The catabolism of pectin from the plant cell walls plays a crucial role in the virulence of the phytopathogen Dickeya dadantii. In particular, the timely expression of pel genes encoding major pectate lyases is essential to circumvent the plant defense systems and induce a massive pectinolytic activity during the maceration phase. While previous studies identified the role of a positive feedback loop specific to the pectin degradation pathway, here we show that the pel> expression pattern is controlled by a metabolic switch between glucose and pectin. We develop a dynamical and quantitative regulatory model of this process integrating the two main regulators CRP and KdgR related to these two sources of carbon, and reproducing the concentration profiles of the associated metabolites, cAMP and KDG respectively, quantified using a new HPLC method. The model involves only 5 adjustable parameters, and recapitulates the dynamics of these metabolic pathways during bacterial growth together with the regulatory events occurring at the promoters of two major pel genes, pelE and pelD. It highlights their activity as an instance of carbon catabolite repression occurring at the transcriptional regulatory level, and directly related to the virulence of D. dadantii. The model also shows that quantitative differences in the binding properties of common regulators at these two promoters resulted in a qualitative different role of pelD and pelE in the metabolic switch, and also likely in conditions of infection, explaining their evolutionary conservation as separate genes in this species.


2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Adriana Julián-Sánchez ◽  
Adeli P. Castrejón-Gonzaga ◽  
Gabriel Moreno-Hagelsieb ◽  
Rosario A. Muñoz-Clares ◽  
Héctor Riveros-Rosas

2001 ◽  
Vol 266 (2) ◽  
pp. 199-206 ◽  
Author(s):  
L. Petruschka ◽  
G. Burchhardt ◽  
C. Müller ◽  
C. Weihe ◽  
H. Herrmann

2013 ◽  
Vol 79 (7) ◽  
pp. 2416-2423 ◽  
Author(s):  
Rita A. Luu ◽  
Benjamin J. Schneider ◽  
Christie C. Ho ◽  
Vasyl Nesteryuk ◽  
Stacy E. Ngwesse ◽  
...  

ABSTRACTThe phenylacetic acid (PAA) degradation pathway is a widely distributed funneling pathway for the catabolism of aromatic compounds, including the environmental pollutants styrene and ethylbenzene. However, bacterial chemotaxis to PAA has not been studied. The chemotactic strainPseudomonas putidaF1 has the ability to utilize PAA as a sole carbon and energy source. We identified a putative PAA degradation gene cluster (paa) inP. putidaF1 and demonstrated that PAA serves as a chemoattractant. The chemotactic response was induced during growth with PAA and was dependent on PAA metabolism. A functionalcheAgene was required for the response, indicating that PAA is sensed through the conserved chemotaxis signal transduction system. AP. putidaF1 mutant lacking the energy taxis receptor Aer2 was deficient in PAA taxis, indicating that Aer2 is responsible for mediating the response to PAA. The requirement for metabolism and the role of Aer2 in the response indicate thatP. putidaF1 uses energy taxis to detect PAA. We also revealed that PAA is an attractant forEscherichia coli; however, a mutant lacking a functional Aer energy receptor had a wild-type response to PAA in swim plate assays, suggesting that PAA is detected through a different mechanism inE. coli. The role of Aer2 as an energy taxis receptor provides the potential to sense a broad range of aromatic growth substrates as chemoattractants. Since chemotaxis has been shown to enhance the biodegradation of toxic pollutants, the ability to sense PAA gradients may have implications for the bioremediation of aromatic hydrocarbons that are degraded via the PAA pathway.


Sign in / Sign up

Export Citation Format

Share Document