Abstract:Metabolism is the foundation of all living organisms and is at the core of numerous if not all biological processes. The ability of an organism to modulate its metabolism is a central characteristic needed to proliferate, to be dormant and to survive any assault.
Pseudomonas fluorescens
is bestowed with a uniquely versatile metabolic framework that enables the microbe to adapt to a wide range of conditions including disparate nutrients and toxins. In this mini-review we elaborate on the various metabolic r… Show more
“…The results of the present study strengthen the notion that network-wide adaption of metabolic fluxes [ 62 , 66 ] accompanies (and plausibly, enables) the phenomenon traditionally described—at a genetic and regulatory level—as the general stress response [ 52 , 53 , 67 , 68 ]. Metabolic adaption to oxidative stress has been revisited by Christodoulou et al [ 30 ], demonstrating that reserve flux capacity in the PP pathway empowers E .…”
Section: Discussionsupporting
confidence: 86%
“…putida deploys a survival strategy that seems to differ from that reported for the close relative species P . fluorescens , where production of α-ketoacids and ATP formation via converging metabolic mechanisms prevails under oxidative stress [ 68 , 73 ]—yet the observed responses are dependent on the carbon substrates used for both species. Fig.…”
As a frequent inhabitant of sites polluted with toxic chemicals, the soil bacterium and plant-root colonizer Pseudomonas putida can tolerate high levels of endogenous and exogenous oxidative stress. Yet, the ultimate reason of such phenotypic property remains largely unknown. To shed light on this question, metabolic network-wide routes for NADPH generation—the metabolic currency that fuels redox-stress quenching mechanisms—were inspected when P. putida KT2440 was challenged with a sub-lethal H2O2 dose as a proxy of oxidative conditions. 13C-tracer experiments, metabolomics, and flux analysis, together with the assessment of physiological parameters and measurement of enzymatic activities, revealed a substantial flux reconfiguration in oxidative environments. In particular, periplasmic glucose processing was rerouted to cytoplasmic oxidation, and the cyclic operation of the pentose phosphate pathway led to significant NADPH-forming fluxes, exceeding biosynthetic demands by ~50%. The resulting NADPH surplus, in turn, fueled the glutathione system for H2O2 reduction. These properties not only account for the tolerance of P. putida to environmental insults—some of which end up in the formation of reactive oxygen species—but they also highlight the value of this bacterial host as a platform for environmental bioremediation and metabolic engineering.
“…The results of the present study strengthen the notion that network-wide adaption of metabolic fluxes [ 62 , 66 ] accompanies (and plausibly, enables) the phenomenon traditionally described—at a genetic and regulatory level—as the general stress response [ 52 , 53 , 67 , 68 ]. Metabolic adaption to oxidative stress has been revisited by Christodoulou et al [ 30 ], demonstrating that reserve flux capacity in the PP pathway empowers E .…”
Section: Discussionsupporting
confidence: 86%
“…putida deploys a survival strategy that seems to differ from that reported for the close relative species P . fluorescens , where production of α-ketoacids and ATP formation via converging metabolic mechanisms prevails under oxidative stress [ 68 , 73 ]—yet the observed responses are dependent on the carbon substrates used for both species. Fig.…”
As a frequent inhabitant of sites polluted with toxic chemicals, the soil bacterium and plant-root colonizer Pseudomonas putida can tolerate high levels of endogenous and exogenous oxidative stress. Yet, the ultimate reason of such phenotypic property remains largely unknown. To shed light on this question, metabolic network-wide routes for NADPH generation—the metabolic currency that fuels redox-stress quenching mechanisms—were inspected when P. putida KT2440 was challenged with a sub-lethal H2O2 dose as a proxy of oxidative conditions. 13C-tracer experiments, metabolomics, and flux analysis, together with the assessment of physiological parameters and measurement of enzymatic activities, revealed a substantial flux reconfiguration in oxidative environments. In particular, periplasmic glucose processing was rerouted to cytoplasmic oxidation, and the cyclic operation of the pentose phosphate pathway led to significant NADPH-forming fluxes, exceeding biosynthetic demands by ~50%. The resulting NADPH surplus, in turn, fueled the glutathione system for H2O2 reduction. These properties not only account for the tolerance of P. putida to environmental insults—some of which end up in the formation of reactive oxygen species—but they also highlight the value of this bacterial host as a platform for environmental bioremediation and metabolic engineering.
“…The regulation of reduced nicotinamide nucleotides NADH and NADPH under oxidative stress has been reported in other microorganisms [ 66 , 67 ]. In Pseudomonas fluorescence NADPH-generating enzymes were highly upregulated during menadione-induced oxidative stress while NADH-generating enzymes were down regulated [ 67 ].…”
While haloarchaea are highly resistant to oxidative stress, a comprehensive understanding of the processes regulating this remarkable response is lacking. Oxidative stress-responsive small non-coding RNAs (sRNAs) have been reported in the model archaeon, Haloferax volcanii, but targets and mechanisms have not been elucidated. Using a combination of high throughput and reverse molecular genetic approaches, we elucidated the functional role of the most up-regulated intergenic sRNA during oxidative stress in H. volcanii, named Small RNA in Haloferax Oxidative Stress (SHOxi). SHOxi was predicted to form a stable secondary structure with a conserved stem-loop region as the potential binding site for trans-targets. NAD-dependent malic enzyme mRNA, identified as a putative target of SHOxi, interacted directly with a putative 'seed' region within the predicted stem loop of SHOxi. Malic enzyme catalyzes the oxidative decarboxylation of malate into pyruvate using NAD + as a cofactor. The destabilization of malic enzyme mRNA, and the decrease in the NAD + /NADH ratio, resulting from the direct RNA-RNA interaction between SHOxi and its trans-target was essential for the survival of H. volcanii to oxidative stress. These findings indicate that SHOxi likely regulates redox homoeostasis during oxidative stress by the post-transcriptional destabilization of malic enzyme mRNA. SHOximediated regulation provides evidence that the fine-tuning of metabolic cofactors could be a core strategy to mitigate damage from oxidative stress and confer resistance. This study is the first to establish the regulatory effects of sRNAs on mRNAs during the oxidative stress response in Archaea.
“…Microbes have activated defensive strategies and evolved several adaptation mechanisms for survival [7], such as accumulation on a cell wall, transportation across the cell membrane, a permeable membrane, intracellular sequestration, and enzymatic detoxifications [5,8]. The capability of organisms to modulate their metabolism is a central characteristic required for proliferation, hibernation, and survival [9]. The metabolic mechanism of microbial resistance to heavy metal could be elucidated in detail from different perspectives, which we shall describe next.…”
Heavy metal pollution in the Antarctic has gone beyond our imagination. Copper toxicity is a selective pressure on Planococcus sp. O5. We observed relatively broad tolerance in the polar bacterium. The heavy metal resistance pattern is Pb2+ > Cu2+ > Cd2+ > Hg2+ > Zn2+. In the study, we combined biochemical and metabolomics approaches to investigate the Cu2+ adaptation mechanisms of the Antarctic bacterium. Biochemical analysis revealed that copper treatment elevated the activity of antioxidants and enzymes, maintaining the bacterial redox state balance and normal cell division and growth. Metabolomics analysis demonstrated that fatty acids, amino acids, and carbohydrates played dominant roles in copper stress adaptation. The findings suggested that the adaptive mechanisms of strain O5 to copper stress included protein synthesis and repair, accumulation of organic permeable substances, up-regulation of energy metabolism, and the formation of fatty acids.
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