Browsing by Subject "Metabolic adaptation"

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Genomic adaptation of Burkholderia anthina to glyphosate uncovers a novel herbicide resistance mechanism
(2023) Schwedt, Inge; Collignon, Madeline; Mittelstädt, Carolin; Giudici, Florian; Rapp, Johanna; Meißner, Janek; Link, Hannes; Hertel, Robert; Commichau, Fabian M.
Glyphosate (GS) specifically inhibits the 5-enolpyruvyl-shikimate-3-phosphate (EPSP) synthase that converts phosphoenolpyruvate (PEP) and shikimate-3-phosphate to EPSP in the shikimate pathway of bacteria and other organisms. The inhibition of the EPSP synthase depletes the cell of the EPSP-derived aromatic amino acids as well as of folate and quinones. A variety of mechanisms (e.g., EPSP synthase modification) has been described that confer GS resistance to bacteria. Here, we show that the Burkholderia anthina strain DSM 16086 quickly evolves GS resistance by the acquisition of mutations in the ppsR gene. ppsR codes for the pyruvate/ortho-Pi dikinase PpsR that physically interacts and regulates the activity of the PEP synthetase PpsA. The mutational inactivation of ppsR causes an increase in the cellular PEP concentration, thereby abolishing the inhibition of the EPSP synthase by GS that competes with PEP for binding to the enzyme. Since the overexpression of the Escherichia coli ppsA gene in Bacillus subtilis and E. coli did not increase GS resistance in these organisms, the mutational inactivation of the ppsR gene resulting in PpsA overactivity is a GS resistance mechanism that is probably unique to B. anthina.
Physiological and metabolic adaptation of Beta vulgaris and Suaeda maritima to salinity and hypoxia
(2022) Behr, Jan Helge; Zörb, Christian
Soils with high salinity are often also affected by waterlogging with hypoxic conditions in the root zone, which severely reduces plant growth and crop yield. The combination of salinity and hypoxia generates an intense stress for the plant: On the one hand, hypoxic conditions at the root level cause a severe energy deficit due to the inhibition of oxidative phosphorylation, on the other hand, energy-consuming tolerance mechanisms have to be maintained to cope with salt stress. To better understand the tolerance mechanisms to combined saline and hypoxic conditions, the metabolic and physiological adaptation capacity of the model halophyte Suaeda maritima, typically found in flooded saline soils, and the closely related sugar beet (Beta vulgaris L.) were analysed. Salt tolerant plants are characterised by their ability to tolerate high Na+ and Cl- concentrations without being damaged by ion toxicity. The basis of this tolerance is primarily osmotic adaptation, the compartmentalisation of ions in cell organelles and the ability to replace K+ with Na+ in important cellular processes. Li+ has similar physico-chemical properties to Na+ and K+, but forms complexes with organic and inorganic anions more readily than other alkali metals. Therefore, Li+ can displace metals during the uptake and translocation by the plant and at enzymatic binding sites, which impairs enzyme activity and can lead to toxic effects. The effects of different cations with similar physicochemical properties on their accumulation pattern at high and low osmolarity were investigated to determine whether Li+ toxicity could be mitigated by competitive uptake of K+ and Na+. Hydroponic culture experiments with increasing salt concentration demonstrated the ability of S. maritima and B. vulgaris to tolerate high salt concentrations by maintaining ion homeostasis and high tissue tolerance to Na+ accumulation. An increased Na+/K+ ratio under hypoxic conditions indicates that an energy shortage caused by oxygen depletion in the root impairs Na+ exclusion and K+ uptake, thereby increasing the ionic imbalance under hypoxic conditions. The metabolic profile showed a tissue-specific response to salinity and hypoxia: The root metabolism is mainly influenced by hypoxia, inhibiting oxidative phosphorylation, while at the same time glycolysis is enhanced to maintain ATP production. The enhanced accumulation of amino acids and TCA cycle intermediates suggests that a partial flow of the TCA cycle fuelled by the GABA shunt may play a crucial role in the recovery of reduction equivalents for ATP production by glycolysis, thereby sustaining energy-intensive cellular processes under hypoxic conditions. As a consequence to the high Na+ accumulation in the shoots, the metabolic profile of young and mature leaves is mainly influenced by salt stress, which triggers the accumulation of compatible solutes for osmotic adjustment and ROS scavenging mechanisms. To achieve tolerance to high salinity, energy consumption rises. Hence, the biomass increase of B. vulgaris stagnates at 200 mM NaCl. In contrast, S. maritima shows its optimal growth at the same salinity range, which reflects the higher adaptability of the halophyte to saline conditions. Different mechanisms in the shoot and root lead to an accumulation of proline, which contributes to the increased tolerance to combined salinity and hypoxia, as proline stabilises membranes and proteins under salt stress and scavenges increased ROS formation induced by hypoxia. High ion accumulation in combination with hypoxic conditions enhances ROS formation in the shoots, leading to light-induced pigment degradation in S. maritima, which is mitigated by enhanced proline biosynthesis in the chloroplasts. In contrast, proline accumulation in the root is not exclusively the result of enhanced proline biosynthesis, but of inhibited proline degradation due to the low availability of reduction equivalents when salinity and hypoxia are combined. The accumulation of Li+ is relatively low in comparison to Na+ and K+, as B. vulgaris strongly limits the Li+ uptake via the transpiration stream to avoid toxic Li+ concentrations in the leaves. High concentrations of Li+ combined with Na+/K+, increase Li+ accumulation in leaves and cause growth inhibition as well as the formation of necrotic tissue, indicating low tissue tolerance to Li+ and severe stress. The application of equimolar concentrations of Na+ and K+ has no effect on Li+ accumulation and ion toxicity, suggesting that Li+ uptake is independent of Na+ and K+ cation channels and that Li+ toxicity is not mainly caused by the displacement of K+ at enzymatic binding sites.