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Aims: The work aimed to understand the important changes during glucose metabolism in Saccharomyces cerevisiae under acidified sodium nitrite (ac.NaNO2) mediated nitrosative stress. Methods and Results: Confocal microscopy and fluorescence‐activated cell sorting analysis were performed to investigate the generation of reactive nitrogen and oxygen species, and redox homeostasis under nitrosative stress was also characterized. Quantitative PCR analysis revealed that the expression of ADH genes was upregulated under such condition, whereas the ACO2 gene was downregulated. Some of the enzymes of the tricarboxylic acid cycle were partially inhibited, whereas malate metabolism and alcoholic fermentation were increased under nitrosative stress. Kinetics of ethanol production was also characterized. A network analysis was conducted to validate our findings. In the presence of ac.NaNO2, in vitro protein tyrosine nitration formation was checked by western blotting using pure alcohol dehydrogenase and aconitase. Conclusions: Alcoholic fermentation rate was increased under stress condition and this altered metabolism might be conjoined with the defence machinery to overcome the nitrosative stress. Significance and Impact of the Study: This is the first work of this kind where the role of metabolism under nitrosative stress has been characterized in S. cerevisiae and it will provide a base to develop an alternative method of industrial ethanol production. [ABSTRACT FROM AUTHOR]

Malate dehydrogenase, which facilitates the reversible conversion of malate to oxaloacetate, is essential for energy balance, plant growth, and cold and salt tolerance. However, the genome-wide study of the MDH family has not yet been carried out in tomato (Solanum lycopersicum L.). In this study, 12 MDH genes were identified from the S. lycopersicum genome and renamed according to their chromosomal location. The tomato MDH genes were split into five groups based on phylogenetic analysis and the genes that clustered together showed similar lengths, and structures, and conserved motifs in the encoded proteins. From the 12 tomato MDH genes on the chromosomes, three pairs of segmental duplication events involving four genes were found. Each pair of genes had a Ka/Ks ratio < 1, indicating that the MDH gene family of tomato was purified during evolution. Gene expression analysis exhibited that tomato MDHs were differentially expressed in different tissues, at various stages of fruit development, and differentially regulated in response to abiotic stresses. Molecular docking of four highly expressed MDHs revealed their substrate and co-factor specificity in the reversible conversion process of malate to oxaloacetate. Further, co-localization of tomato MDH genes with quantitative trait loci (QTL) of salt stress-related phenotypes revealed their broader functions in salt stress tolerance. This study lays the foundation for functional analysis of MDH genes and genetic improvement in tomato. [ABSTRACT FROM AUTHOR]

Integrating research into the classroom environment is an influential pedagogical tool to support student learning, increase retention of STEM students, and help students identify as scientists. The evolution of course-based undergraduate research experiences (CUREs) has grown from individual faculty incorporating their research in the teaching laboratory into well-supported systems to sustain faculty engagement in CUREs. To support the growth of protein-centric biochemistry-related CUREs, we cultivated a community of enthusiastic faculty to develop and adopt malate dehydrogenase (MDH) as a CURE focal point. The MDH CURE Community has grown into a vibrant and exciting group of over 28 faculty from various institutions, including community colleges, minority-serving institutions, undergraduate institutions, and research-intensive institutions in just 4 years. This collective has also addressed important pedagogical questions on the impact of CURE collaboration and the length of the CURE experience in community colleges, undergraduate institutions, and research-intensive institutions. This work provided evidence that modular or partial-semester CUREs also support student outcomes, especially the positive impact it had on underrepresented students. We are currently focused on expanding the MDH CURE Community network by generating more teaching and research materials, creating regional hubs for local interaction and increasing mentoring capacity, and offering mentoring and professional development opportunities for new faculty adopters. [ABSTRACT FROM AUTHOR]

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According to Table 4, the maximum succinate production that is identified by Yang et al. [[15]] is 1.16 mmol gDW SP -1 sp hr SP -1 sp whereas the highest succinate production identified by Zhu and Shimizu [[16]] is 1.54 ± 0.23 mmol gDW SP -1 sp hr SP -1 sp . As evidenced in Table 2.3, OptKnock attained the best succinate production with 6.21 mmol gDW SP -1 sp hr SP -1 sp in third knockouts, which is lower than the succinate production rate with 8.1943 mmol gDW SP -1 sp hr SP -1 sp that is identified by BAROOM. Keywords: artificial intelligence; bioinformatics; data science; metabolic engineering; modelling; optimization EN artificial intelligence bioinformatics data science metabolic engineering modelling optimization 1 12 12 10/03/22 20220901 NES 220901 1 Introduction Gene knockout strategy is a typical genetic engineering method for deleting genes in organisms in order to understand their consequences. [Extracted from the article]

We unveil the intimate relationship between protein dynamics and allostery by following the trajectories of model proteins in their conformational and sequence spaces. Starting from a nonallosteric hyperthermophilic malate dehydrogenase, we have tracked the role of protein dynamics in the evolution of the allosteric capacity. Based on a large phylogenetic analysis of the malate (MalDH) and lactate dehydrogenase (LDH) superfamily, we identified two amino acid positions that could have had a major role for the emergence of allostery in LDHs, which we targeted for investigation by site-directed mutagenesis. Wild-type MalDH and the single and double mutants were tested with respect to their substrate recognition profiles. The double mutant displayed a sigmoid-shaped profile typical of homotropic activation in LDH. By using molecular dynamics simulations, we showed that the mutations induce a drastic change in the protein sampling of its conformational landscape, making transiently T-like (inactive) conformers, typical of allosteric LDHs, accessible. Our data fit well with the seminal key concept linking protein dynamics and evolvability. We showed that the selection of a new phenotype can be achieved by a few key dynamics-enhancing mutations causing the enrichment of low-populated conformational substates. [ABSTRACT FROM AUTHOR]

2-Hydroxyglutarate (2HG) is an oncometabolite that can contribute to tumor progression. Two enantiomer forms, L-2HG and D-2HG, arise from independent pathways starting from the precursor α-ketoglutarate (αKG). L-2HG production occurs through the promiscuous activities of malate dehydrogenase (MDH) and lactate dehydrogenase (LDH) under acidic and/or hypoxic conditions. D-2HG frequently accumulates by gain-of-function mutations in the genes encoding two isoforms of isocitrate dehydrogenase (IDH1 and IDH2). Cognate metabolite repair enzymes, L- and D-2-hydroxyglutarate dehydrogenases, oxidize the enantiomers and cause abnormally high 2HG accumulation and disease when mutated. Elevated levels of either oncometabolite affect redox homeostasis, metabolism, and immune system functioning. Moreover, the oncometabolites inhibit several α-ketoglutarate-dependent dioxygenases resulting in epigenetic changes such as DNA and histone hypermethylation as well as deficiencies in DNA repair. L-2HG, and D-2HG in some cases, inhibit degradation of hypoxia-inducible factor (HIF1α), a transcription factor that alters gene expression to adapt to hypoxic conditions, favoring tumorigenesis. Patients with the rare disease 2-hydroxyglutaric aciduria (2HGA) have exceedingly high levels of 2HG, which is neurotoxic, causing developmental delays and brain abnormalities. D-2HG also has specific effects on collagen production and NADPH pools. Recently, D-2HG has been targeted in new chemotherapies aimed at disrupting the gain-of-function IDH1 and IDH2 mutants, resulting in successful clinical trials for several cancers., (© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

This review discusses the intriguing yet controversial concept of metabolons, focusing on the malate dehydrogenase-citrate synthase (MDH-CISY) metabolon as a model. Metabolons are multienzyme complexes composed of enzymes that catalyze sequential reactions in metabolic pathways. Metabolons have been proposed to enhance metabolic pathway efficiency by facilitating substrate channeling. However, there is skepticism about the presence of metabolons and their functionality in physiological conditions in vivo. We address the skepticism by reviewing compelling evidence supporting the existence of the MDH-CISY metabolon and highlighting its potential functions in cellular metabolism. The electrostatic interaction between MDH and CISY and the intermediate oxaloacetate, channeled within the metabolon, has been demonstrated using various experimental techniques, including protein-protein interaction assays, isotope dilution studies, and enzyme coupling assays. Regardless of the wealth of in vitro evidence, further validation is required to elucidate the functionality of MDH-CISY metabolons in living systems using advanced structural and spatial analysis techniques., (© 2024 The Author(s).)

Malate dehydrogenase (MDH) enzymes play critical roles in cellular metabolism, facilitating the reversible conversion of malate to oxaloacetate using NAD+/NADH as a cofactor. The two human isoforms of MDH have roles in the citric acid cycle and the malate-aspartate shuttle, and thus both are key enzymes in aerobic respiration as well as regenerating the pool of NAD+ used in glycolysis. This review highlights the potential of MDH as a therapeutic drug target in various diseases, including metabolic and neurological disorders, cancer, and infectious diseases. The most promising molecules for targeting MDH have been examined in the context of human malignancies, where MDH is frequently overexpressed. Recent studies have led to the identification of several antagonists, some of which are broad MDH inhibitors while others have selectivity for either of the two human MDH isoforms. Other promising compounds have been studied in the context of parasitic MDH, as inhibiting the function of the enzyme could selectively kill the parasite. Research is ongoing with these chemical scaffolds to develop more effective small-molecule drug leads that would have great potential for clinical applications., (© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

Malate dehydrogenase (MDH) is a ubiquitous and central enzyme in cellular metabolism, found in all kingdoms of life, where it plays vital roles in the cytoplasm and various organelles. It catalyzes the reversible NAD+-dependent reduction of L-malate to oxaloacetate. This review describes the reaction mechanism for MDH and the effects of mutations in and around the active site on catalytic activity and substrate specificity, with a particular focus on the loop that encloses the active site after the substrates have bound. While MDH exhibits selectivity for its preferred substrates, mutations can alter the specificity of MDH for each cosubstrate. The kinetic characteristics and similarities of a variety of MDH isozymes are summarized, and they illustrate that the KM values are consistent with the relative concentrations of the substrates in cells. As a result of its existence in different cellular environments, MDH properties vary, making it an attractive model enzyme for studying enzyme activity and structure under different conditions., (© 2024 The Author(s).)

In this review, we examine the protein-protein interactions of cytosolic malate dehydrogenase (MDH), an under-studied area in cellular metabolism. We provide a comprehensive overview of MDH involvement in metabolism, especially its interactions with metabolic partners and dynamics of changing metabolism. We present an analysis of the biophysical nature of these interactions and the current methods used to study them. Our review includes an assessment of computational docking studies, which offer initial hypotheses about potential MDH interaction partners. Furthermore, we provide a summary of the sparse yet insightful experimental evidence available, establishing a foundation for future research. By integrating biophysical analysis and methodological advancements, this paper aims to illuminate the intricate network of interactions involving cytosolic MDH and their metabolic implications. This work not only contributes to our understanding of MDH's role in metabolism but also highlights the potential impact of these interactions in metabolic disorders., (© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

Malate dehydrogenase (MDH) catalyzes the interconversion of oxaloacetate and malate coupled to the oxidation/reduction of coenzymes NAD(P)H/NAD(P)+. While most animals have two isoforms of MDH located in the cytosol and mitochondria, all major groups of land plants have at least six MDHs localized to the cytosol, mitochondria, plastids, and peroxisomes. This family of enzymes participates in important reactions in plant cells including photosynthesis, photorespiration, lipid metabolism, and NH4+ metabolism. MDH also helps to regulate the energy balance in the cell and may help the plant cope with various environmental stresses. Despite their functional diversity, all of the plant MDH enzymes share a similar structural fold and act as dimers. In this review, we will introduce readers to our current understanding of the plant MDHs, including their evolution, structure, and function. The focus will be on the MDH enzymes of the model plant Arabidopsis thaliana., (© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

Malate dehydrogenase (MDH) is an essential enzyme in the tricarboxylic acid cycle that functions in cellular respiration and redox homeostasis. Recent studies indicate that MDH facilitates metabolic plasticity in tumor cells, catalyzing the formation of an oncometabolite, contributing to altered epigenetics, and maintaining redox capacity to support the rewired energy metabolism and biosynthesis that enables cancer progression. This minireview summarizes current findings on the unique supporting roles played by MDH in human cancers and provides an update on targeting MDH in cancer chemotherapy., (© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

Malate dehydrogenase (MDH) is a key enzyme in mammalian metabolic pathways in cytosolic and mitochondrial compartments. Regulation of MDH through phosphorylation remains an underexplored area. In this review we consolidate evidence supporting the potential role of phosphorylation in modulating the function of mammalian MDH. Parallels are drawn with the phosphorylation of lactate dehydrogenase, a homologous enzyme, to reveal its regulatory significance and to suggest a similar regulatory strategy for MDH. Comprehensive mining of phosphorylation databases, provides substantial experimental (primarily mass spectrometry) evidence of MDH phosphorylation in mammalian cells. Experimentally identified phosphorylation sites are overlaid with MDH's functional domains, offering perspective on how these modifications could influence enzyme activity. Preliminary results are presented from phosphomimetic mutations (serine/threonine residues changed to aspartate) generated in recombinant MDH proteins serving as a proof of concept for the regulatory impact of phosphorylation. We also examine and highlight several approaches to probe the structural and cellular impact of phosphorylation. This review highlights the need to explore the dynamic nature of MDH phosphorylation and calls for identifying the responsible kinases and the physiological conditions underpinning this modification. The synthesis of current evidence and experimental data aims to provide insights for future research on understanding MDH regulation, offering new avenues for therapeutic interventions in metabolic disorders and cancer., (© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

Malate dehydrogenase (MDH) is pivotal in mammalian tissue metabolism, participating in various pathways beyond its classical roles and highlighting its adaptability to cellular demands. This enzyme is involved in maintaining redox balance, lipid synthesis, and glutamine metabolism and supports rapidly proliferating cells' energetic and biosynthetic needs. The involvement of MDH in glutamine metabolism underlines its significance in cell physiology. In contrast, its contribution to lipid metabolism highlights its role in essential biosynthetic processes necessary for cell maintenance and proliferation. The enzyme's regulatory mechanisms, such as post-translational modifications, underscore its complexity and importance in metabolic regulation, positioning MDH as a potential target in metabolic dysregulation. Furthermore, the association of MDH with various pathologies, including cancer and neurological disorders, suggests its involvement in disease progression. The overexpression of MDH isoforms MDH1 and MDH2 in cancers like breast, prostate, and pancreatic ductal adenocarcinoma, alongside structural modifications, implies their critical role in the metabolic adaptation of tumor cells. Additionally, mutations in MDH2 linked to pheochromocytomas, paragangliomas, and other metabolic diseases emphasize MDH's role in metabolic homeostasis. This review spotlights MDH's potential as a biomarker and therapeutic target, advocating for further research into its multifunctional roles and regulatory mechanisms in health and disease., (© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

Metabolism within an organism is regulated by various processes, including post-translational modifications (PTMs). These types of chemical modifications alter the molecular, biochemical, and cellular properties of proteins and allow the organism to respond quickly to different environments, energy states, and stresses. Malate dehydrogenase (MDH) is a metabolic enzyme that is conserved in all domains of life and is extensively modified post-translationally. Due to the central role of MDH, its modification can alter metabolic flux, including the Krebs cycle, glycolysis, and lipid and amino acid metabolism. Despite the importance of both MDH and its extensively post-translationally modified landscape, comprehensive characterization of MDH PTMs, and their effects on MDH structure, function, and metabolic flux remains underexplored. Here, we review three types of MDH PTMs - acetylation, ADP-ribosylation, and methylation - and explore what is known in the literature and how these PTMs potentially affect the 3D structure, enzymatic activity, and interactome of MDH. Finally, we briefly discuss the potential involvement of PTMs in the dynamics of metabolons that include MDH., (© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

College science programs exhibit high rates of student attrition, especially among Students of Color, women, members of the LGBTQ+ community, and those with disabilities. Many of the reasons students choose to leave or feel pushed out of science can be mitigated through participation in faculty-mentored research. However, faculty resources are limited, and not every student has access to faculty mentoring due to systemic or structural barriers. By bringing authentic scientific research into the classroom context, course-based undergraduate research experiences (CUREs) expand the number of students who participate in research and provide benefits similar to faculty-mentored research. Instructors also benefit from teaching CUREs. Using a systematic review of 14 manuscripts concerning the Malate Dehydrogenase CUREs Community (MCC) and malate dehydrogenase (MDH) CUREs, we demonstrate that CUREs can be implemented flexibly, are authentic research experiences, generate new scientific discoveries, and improve student outcomes. Additionally, CURE communities offer substantial advantages to faculty wishing to implement CUREs., (© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

Ischemia-reperfusion (I-R) injury is the most common cause of acute kidney injury. In experiments involving primary human renal proximal tubular epithelial cells (RPTECs) exposed to anoxia-reoxygenation, we explored the hypothesis that mitochondrial malate dehydrogenase-2 (MDH-2) inhibition redirects malate metabolism from the mitochondria to the cytoplasm, towards the malate-pyruvate cycle and reversed malate-aspartate shuttle. Colorimetry, fluorometry, and western blotting showed that MDH2 inhibition accelerates the malate-pyruvate cycle enhancing cytoplasmic NADPH, thereby regenerating the potent antioxidant reduced glutathione. It also reversed the malate-aspartate shuttle and potentially diminished mitochondrial reactive oxygen species (ROS) production by transferring electrons, in the form of NADH, from the mitochondria to the cytoplasm. The excessive ROS production induced by anoxia-reoxygenation led to DNA damage and protein modification, triggering DNA damage and unfolded protein response, ultimately resulting in apoptosis and senescence. Additionally, ROS induced lipid peroxidation, which may contribute to the process of ferroptosis. Inhibiting MDH-2 proved effective in mitigating ROS overproduction during anoxia-reoxygenation, thereby rescuing RPTECs from death or senescence. Thus, targeting MDH-2 holds promise as a pharmaceutical strategy against I-R injury., (© 2024 Wiley Periodicals LLC.)

Soluble sugars and organic acids are the most abundant components in ripe fruits, and they play critical roles in the development of fruit flavor and taste. Some loquat cultivars have high acid content which seriously affect the quality of fruit and reduce the value of commodity. Consequently, studying the physiological mechanism of sugar-acid metabolism in loquat can clarify the mechanism of their formation, accumulation and degradation in the fruit. Minerals application has been reported as a promising way to improve sugar-acid balance of the fruits. In this study, loquat trees were foliar sprayed with 0.1, 0.2 and 0.3% borax, and changes in soluble sugars and organic acids were recorded. The contents of soluble sugars and organic acids were determined using HPLC-RID and UPLC-MS, respectively. The activities of enzymes responsible for the metabolism of sugars and acids were quantified and expressions of related genes were determined using quantitative real-time PCR. The results revealed that 0.2% borax was a promising treatment among other B applications for the increased levels of soluble sugars and decreased acid contents in loquats. Correlation analysis showed that the enzymes i.e., SPS, SS, FK, and HK were may be involved in the regulation of fructose and glucose metabolism in the fruit pulp of loquat. While the activity of NADP-ME showed negative and NAD-MDH showed a positive correlation with malic acid content. Meanwhile, EjSPS1, EjSPS3, EjSS3, EjHK1, EjHK3, EjFK1, EjFK2, EjFK5, and EjFK6 may play an important role in soluble sugars metabolism in fruit pulp of loquat. Similarly, EjPEPC2, EjPEPC3, EjNAD-ME1, EjNAD-MDH1, EjNAD-MDH5-8, EjNAD-MDH10, and EjNAD-MDH13 may have a vital contribution to malic acid biosynthesis in loquat fruits. This study provides new insights for future elucidation of key mechanisms regulating soluble sugars and malic acid biosynthesis in loquats.

BACKGROUND: Quercetin (Q), tea polyphenols (TP), and rutin (R) are widely used plant‐derived active ingredients. They possess antioxidant, anti‐inflammatory, and anti‐tumor properties, and can reduce the muscle damage caused by mycotoxins. However, few studies have examined the protective mechanisms of quercetin, tea polyphenols, and rutin on muscle quality. To elucidate their protective mechanisms, shrimp were exposed to both T‐2 toxin and these three antioxidants for 20 days in a dose‐escalating trial. The changes in the protein composition of shrimp muscle were measured. The target proteins associated with T‐2 and antioxidants were screened and identified by non‐labeled quantitative proteomics. RESULTS: The T‐2 toxin induced abnormal expression of 21 target proteins, leading to the deterioration of muscle proteins in shrimp. The three antioxidants ameliorated the T‐2 toxin‐induced damage to muscle proteins by increasing the sarcoplasmic and myofibrillar protein content and decreasing the alkali‐soluble protein content. Quercetin had the strongest protective effect. The protective processes of these antioxidants involved the upregulation of target proteins involved in carbohydrate metabolism (enolase, malate dehydrogenase), protein translation (elongation factor 1‐alpha and eukaryotic translation initiation factor 2 subunit alpha), and cytoskeleton component (actin 2, fast‐type skeletal muscle actin 1). Quercetin regulated the largest number of target proteins, making it the best protective agent against T‐2 toxin. CONCLUSION: The T‐2 toxin (4.80–24.30 mg/kg feed) induced changes in target proteins and muscle composition of shrimp, leading to a deterioration in muscle proteins. Quercetin (2.00–32.00 g/kg feed) had significant protective effects against this deterioration in muscle protein in shrimp. © 2022 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Streptococcus mutans (S. mutans) is one of the primary pathogens responsible for dental caries. Streptococcus gordonii (S. gordonii) is one of the early colonizers of dental plaque and can compete with S. mutans for growth. In the present analysis, we explored key target genes against S. gordonii in S. mutans using 80 S. mutans clinical isolates with varying capabilities against S. gordonii. A principal coordinate analysis revealed significant genetic diversity differences between antagonistic and non-antagonistic groups. Genomic comparisons revealed 33 and 61 genes that were, respectively, positively and negatively correlated with S. mutans against S. gordonii, with RNA-sequencing (RNAseq) highlighting 11 and 43 genes that were, respectively, upregulated and downregulated in the antagonistic group. Through a combination of these results and antiSMASH analysis, we selected 16 genes for qRT-PCR validation in which the expression levels of SMU_137 (malate dehydrogenase, mleS), SMU_138 (malate permease, mleP), SMU_139 (oxalate decarboxylase, oxdC), and SMU_140 (glutathione reductase) were consistent with RNA-seq results. SMU_1315c-1317c (SMU_1315c transport-related gene) and SMU_1908c- 1909c were, respectively, downregulated and upregulated in the antagonistic group. The expression patterns of adjacent genes were closely related, with correlation coefficient values greater than 0.9. These data reveal new targets (SMU_137-140, SMU_1315c-1317c, and SMU_1908c-1909c) for investigating the critical gene clusters against S. gordonii in S. mutans clinical isolates. [ABSTRACT FROM AUTHOR]

The present study assessed the toxic effect of super-paramagnetic iron oxide nanoparticles (SPIONs) on haemato-immunological responses, antioxidant capacity, oxidative stress, and metabolic enzyme activities in Labeo rohita fingerlings, as well as the possible ameliorative effect of dietary vitamin E. The experiment was conducted for 30 days (15-day exposure and recovery each) under static bioassay. The LC50 concentration of SPIONs was estimated by 96-h exposure which was 3253.20 mg/L. The fishes were distributed in two groups and exposed to three levels 1/50th, 1/25th, and 1/10th of SPION-LC50 concentration. Group 1: fed with control diet and referred to as CS0, CS/50, CS/25, and CS/10, while group 2: fed vitamin E supplemented diet and referred to as ES0, ES/50, ES/25, and ES/10. Significant alterations were observed in haemato-immunological responses, malondialdehyde (MDA), and oxidative and metabolic enzymes activity even after supplementation of vitamin E. The exposure to SPIONs altered haemato-immunological parameters, MDA accumulation, and tissue enzyme activity, i.e., superoxide dismutase (SOD), catalase (CAT), glutathione s-transferases (GST), xanthine oxidase (XO), lactate dehydrogenase (LDH), and malate dehydrogenase (MDH) in a dose-dependent manner. However, they relapsed to the level of control in S/50 exposed group at the end of the recovery period. The dietary vitamin E shows significant toxicity mitigating effect during the recovery period. Thus, SPIONs can be used up to a concentration of 65.06 mg/L in the culture water of Labeo rohita and its toxicity at higher doses can be partially ameliorated by feeding of vitamin E (at 250 mg/kg feed) for 15 days during post exposure period. Highlights: • The toxicity of SPIONs increased with increasing concentration of nanoparticle. • The lethal concentration (LC50) of SPIONs was 3253.20 mg/L. • At the end of the recovery period, dietary supplementation of vitamin E ameliorate toxic effect of SPIONs. • The physiological change caused due to the toxic effect of 65.04 mg/L SPIONs can be completely recovered in 15 days by dietary supplementation of vitamin E at 250 mg/kg in L. rohita. [ABSTRACT FROM AUTHOR]

Guard‐cell‐type aluminium‐activated malate transporters (ALMTs) are involved in stomatal closure by exporting anions from guard cells. However, their physiological and electrophysiological functions are yet to be explored. Here, we analysed the physiological and electrophysiological properties of the ALMT channels in Arabidopsis and tomato (Solanum lycopersicum). SlALMT11 was specifically expressed in tomato guard cells. External malate‐induced stomatal closure was impaired in ALMT‐suppressed lines of tomato and Arabidopsis, although abscisic acid did not influence the stomatal response in SlALMT11‐knock‐down tomato lines. Electrophysiological analyses in Xenopus oocytes showed that SlALMT11 and AtALMT12/QUAC1 exhibited characteristic bell‐shaped current‐voltage patterns dependent on extracellular malate, fumarate, and citrate. Both ALMTs could transport malate, fumarate, and succinate, but not citrate, suggesting that the guard‐cell‐type ALMTs are dicarboxylic anion channels activated by extracellular organic acids. The truncation of acidic amino acids, Asp or Glu, from the C‐terminal end of SlALMT11 or AtALMT12/QUAC1 led to the disappearance of the bell‐shaped current‐voltage patterns. Our findings establish that malate‐activated stomatal closure is mediated by guard‐cell‐type ALMT channels that require an acidic amino acid in the C‐terminus as a candidate voltage sensor in both tomato and Arabidopsis. Summary statement: Apoplastic malate induces stomatal closure mediated by ALMT‐type anion channels (SlALMT11 and AtALMT12/QUAC1) of which voltage gating requires an acidic amino acid at the C‐terminal end. [ABSTRACT FROM AUTHOR]

Summary: An important method to improve photosynthesis in C3 crops, such as rice and wheat, is to transfer efficient C4 characters to them. Here, cytosolic carbonic anhydrase (CA: βCA3) of the C4Flaveria bidentis (Fb) was overexpressed under the control of 35S promoter in Arabidopsis thaliana, a C3 plant, to enhance its photosynthetic efficiency. Overexpression of CA resulted in a better supply of the substrate HCO3‐ for the endogenous phosphoenolpyruvate carboxylase in the cytosol of the overexpressers, and increased its activity for generating malate that feeds into the tricarboxylic acid cycle. This provided additional carbon skeleton for increased synthesis of amino acids aspartate, asparagine, glutamate, and glutamine. Increased amino acids contributed to higher protein content in the transgenics. Furthermore, expression of FbβCA3 in Arabidopsis led to a better growth due to expression of several genes leading to higher chlorophyll content, electron transport, and photosynthetic carbon assimilation in the transformants. Enhanced CO2 assimilation resulted in increased sugar and starch content, and plant dry weight. In addition, transgenic plants had lower stomatal conductance, reduced transpiration rate, and higher water‐use efficiency. These results, taken together, show that expression of C4CA in the cytosol of a C3 plant can indeed improve its photosynthetic capacity with enhanced water‐use efficiency. [ABSTRACT FROM AUTHOR]

Propionic acid (PA) predominantly accumulates in tissues and biological fluids of patients affected by propionic acidemia that may manifest chronic renal failure along development. High urinary excretion of maleic acid (MA) has also been described. Considering that the underlying mechanisms of renal dysfunction in this disorder are poorly known, the present work investigated the effects of PA and MA (1–5 mM) on mitochondrial functions and cellular viability in rat kidney and cultured human embryonic kidney (HEK-293) cells. Mitochondrial membrane potential (∆ψm), NAD(P)H content, swelling and ATP production were measured in rat kidney mitochondrial preparations supported by glutamate or glutamate plus malate, in the presence or absence of Ca2+. MTT reduction and propidium iodide (PI) incorporation were also determined in intact renal cells pre-incubated with MA or PA for 24 h. MA decreased Δψm and NAD(P)H content and induced swelling in Ca2+-loaded mitochondria either respiring with glutamate or glutamate plus malate. Noteworthy, these alterations were fully prevented by cyclosporin A plus ADP, suggesting the involvement of mitochondrial permeability transition (mPT). MA also markedly inhibited ATP synthesis in kidney mitochondria using the same substrates, implying a strong bioenergetics impairment. In contrast, PA only caused milder changes in these parameters. Finally, MA decreased MTT reduction and increased PI incorporation in intact HEK-293 cells, indicating a possible association between mitochondrial dysfunction and cell death in an intact cell system. It is therefore presumed that the MA-induced disruption of mitochondrial functions involving mPT pore opening may be involved in the chronic renal failure occurring in propionic acidemia. [ABSTRACT FROM AUTHOR]

The activity of oxidoreductases, malate dehydrogenase and lactate dehydrogenase (MDH, 1.1.1.37; LDH, 1.1.1.27), as well as parameters of adenylate system—[ATP], [ADP], [AMP], total adenylate pool (AP), and adenylate energy charge (AEC) in medulla oblongata (MB) and forebrain, midbrain, and diencephalon (FDMB)—were studied in the scorpionfish under acute hypoxia (0.9–1.2 mg O2·L−1, 90 min). A higher MDH activity level was observed in MB and FDMB, as compared to LDH (p < 0.05). At the same time, MB showed a higher adenylate content and increased AP (p < 0.05). AEC did not exceed ~ 0.7 (vs. the maximum of this index ~ 0.9–1.0) in the brain of the scorpionfish indicating adaptation of the tissue energy status to hypoxia. A rapid decrease in MDH activity (p < 0.05) was observed in MB under acute hypoxia. These changes were accompanied by insignificant LDH activation. A pronounced LDH activation (p < 0.05), a decrease in MDH activity, and the highest AP raise (p < 0.05) were observed in FDMB, suggesting activation of glycolysis and simultaneous decrease in the rate of ATP consumption. MB and FDMB demonstrated the ability to a relative retention of AEC during hypoxia. The unidirectional metabolic adaptation was based on the intensification of glycolysis, a decrease of ATP consumption, and a subsequent increase in adenylate concentration that allowed the scorpionfish brain structures to maintain the energy status under acute hypoxia. [ABSTRACT FROM AUTHOR]

A subunit of the Sec protein export system, SecD, was shown to be a potential MsrAB substrate as well as a group of lipo- and membrane proteins that are known virulence factors, such as Protein D (GlpQ), opacity-associated proteins, the OmpA porin, the HU toxin-repeat protein, the HMW adhesin and an IgA1 protease domain-containing protein. Keywords: Haemophilus influenzae; methionine sulfoxide reductase; oxidative damage; biochemical reconstitution; extracellular proteins EN Haemophilus influenzae methionine sulfoxide reductase oxidative damage biochemical reconstitution extracellular proteins N.PAG N.PAG 18 08/29/22 20220801 NES 220801 1. Our proteome analysis identified 29 putative MsrAB substrate proteins, including protein eP4, which is the first time that the targets for sulfoxide repair have been identified for an extracellular MsrAB methionine sulfoxide reductase. Only a handful of substrate proteins for Msr-type methionine sulfoxide reductases have been identified to date, and most of these proteins were substrates for cytoplasmic methionine sulfoxide reductases in I E. coli i and I H. pylori i , where the function of Msr proteins has been studied most extensively [[3]]. [Extracted from the article]

However, as discussed below, compared to the constitutive expression of AtNEET or H89C, the dynamics nature of the current experimental design allowed us to identify additional and/or new clues to AtNEET function in plants and revealed potential new links between AtNEET and different metabolic and acclimation networks in plants. While changes in AtNEET protein abundance in control (Col) plants were not significant throughout the experiment, the abundance of the AtNEET and H89C proteins was elevated at all time points (Figure 3B). Of particular importance to our understanding of NEET function in different biological systems are two studies, in which a mutated copy of NAF-1 or AtNEET with a high 2Fe-2S cluster stability (H114C of NAF-1, or H89C of AtNEET) was constitutively expressed in wild type cells to block NEET protein cluster transfer function [[9]]. Here we show for the first time that the protein expression of CIA1 and DRE2 is upregulated upon the inducible expression of AtNEET but not H89C, suggesting that augmenting the level of AtNEET results in the higher expression of some CIA proteins (Figure 5). Overall, there was a good overlap between changes in protein abundance identified by the current proteomics analysis conducted with inducible expression of AtNEET and H89C, and the previous study that used constitutive expression of these proteins (e.g., Figure 4 [[9]]). [Extracted from the article]

Background: Sugarcane is the most important sugar crop, contributing > 80% of global sugar production. High sucrose content is a key target of sugarcane breeding, yet sucrose improvement in sugarcane remains extremely slow for decades. Molecular breeding has the potential to break through the genetic bottleneck of sucrose improvement. Dissecting the molecular mechanism(s) and identifying the key genetic elements controlling sucrose accumulation will accelerate sucrose improvement by molecular breeding. In our previous work, a proteomics dataset based on 12 independent samples from high- and low-sugar genotypes treated with ethephon or water was established. However, in that study, employing conventional analysis, only 25 proteins involved in sugar metabolism were identified. Results: In this work, the proteomics dataset used in our previous study was reanalyzed by three different statistical approaches, which include a logistic marginal regression, a penalized multiple logistic regression named Elastic net, as well as a Bayesian multiple logistic regression method named Stochastic search variable selection (SSVS) to identify more sugar metabolism-associated proteins. A total of 507 differentially abundant proteins (DAPs) were identified from this dataset, with 5 of them were validated by western blot. Among the DAPs, 49 proteins were found to participate in sugar metabolism-related processes including photosynthesis, carbon fixation as well as carbon, amino sugar, nucleotide sugar, starch and sucrose metabolism. Based on our studies, a putative network of key proteins regulating sucrose accumulation in sugarcane is proposed, with glucose-6-phosphate isomerase, 2-phospho-D-glycerate hydrolyase, malate dehydrogenase and phospho-glycerate kinase, as hub proteins. Conclusions: The sugar metabolism-related proteins identified in this work are potential candidates for sucrose improvement by molecular breeding. Further, this work provides an alternative solution for omics data processing. [ABSTRACT FROM AUTHOR]

O-linked β-N-acetylglucosamine (O-GlcNAc) modification is a ubiquitous, reversible, and highly dynamic post-translational modification, which takes charge of almost all biological processes examined. However, little information is available regarding the molecular regulation of O-GlcNAcylation in granulosa cell function and glucose metabolism. This study focused on the impact of disrupted O-GlcNAc cycling on the proliferation and apoptosis of bovine granulosa cells, and further aimed to determine how this influenced glucose metabolism. Pharmacological inhibition of OGT with benzyl-2-acetamido-2-deoxy-α-D-galactopyranoside (BADGP) led to decreased cellular O-GlcNAc levels, as well as OGT and OGA protein expressions, whereas increasing O-GlcNAc levels with the OGA inhibitor, O-(2-acetamido-2-deoxy- D -gluco-pyranosylidene) (PUGNAc), resulted in elevated OGA protein expression and decreased OGT protein expression in granulosa cells. Dysregulated O-GlcNAc cycling reduced cell viability, downregulated the proliferation-related genes of CDC42 and PCNA transcripts, upregulated the pro-apoptotic genes of BAX and CASPASE-3 mRNA and the ratio of BAX/BCL-2, and increased the apoptotic rate. Glycolytic enzyme activities of hexokinase and pyruvate kinase, metabolite contents of pyruvate and lactate, mitochondrial membrane potential, ATP levels, and intermediate metabolic enzyme activities of succinate dehydrogenase and malate dehydrogenase involved in the tricarboxylic acid cycle, were significantly impaired in response to altered O-GlcNAc levels. Moreover, inhibition of OGT significantly increased the expression level of thioredoxin-interacting protein (TXNIP), but repression of OGA had no effect. Collectively, our results suggest that perturbation of O-GlcNAc cycling has a profound effect on granulosa cell function and glucose metabolism. [ABSTRACT FROM AUTHOR]

In this study, for the first time, the coated tocosome by blend of chitosan, CS, and poly(N-isopropylacrylamide), PNIPAAm, was developed as the efficient and robust drug delivery system with improved drug encapsulation efficiency, extended stability, proper particle size and industrial upscaling for Sunitinib malate anti-cancer drug. Tocosome was synthesized by using Mozafari method as a scalable and robust method and without the need for organic solvents. The effects of tocosome composition and drug concentration on the stability, particle size of tocosome, zeta potential, encapsulation efficacy and loading of drug into it were investigated by Taguchi method, and optimum composition was selected for combining with the polymeric blend. Homopolymer of PNIPAAm was synthesized by two different polymerization methods, including free radical and reversible addition–fragmentation chain transfer (RAFT). Effects of molecular weight (MW) and chain length of the polymers on lower critical solution temperature (LCST) were examined. The developed nanocarrier in this research, CS-Raft-PNIPAAm-tocosome, indicated LCST value beyond 37°C (about 45°C) and this is suitable for hyperthermia and spatio-temporal release of drug particles. [Display omitted] [ABSTRACT FROM AUTHOR]

Carbon dioxide-fixing acetogenic bacteria (acetogens) utilizing the Wood-Ljungdahl Pathway (WLP) play an important role in CO 2 fixation in the biosphere and in the development of biological processes – alone or in cocultures, under both autotrophic and mixotrophic conditions – for production of chemicals and fuels. To date, limited work has been reported in experimentally validating and quantifying reaction fluxes of their core metabolic pathways. Here, the core metabolic model of the acetogen Clostridium ljungdahlii was interrogated using 13C-metabolic flux analysis (13C-MFA), which required the development of a new defined culture medium. Autotrophic, heterotrophic, and mixotrophic growth in defined medium was possible by adding 1 mM methionine to replace yeast extract. Our 13C-MFA found an incomplete TCA cycle and inactive core pathways/reactions, notably those of the oxidative pentose phosphate pathway, Entner-Doudoroff pathway, and malate dehydrogenase. 13C-MFA during mixotrophic growth using the parallel tracers [1–13C]fructose, [1,2–13C]fructose, [1,2,3–13C]fructose, and [U–13C]asparagine found that externally supplied CO 2 contributed the majority of carbon consumed. All internally-produced CO 2 from the catabolism of asparagine and fructose was consumed by the WLP. While glycolysis of fructose was active, it was not a major contributor to overall production of ATP, NADH, and acetyl-CoA. Gluconeogenic reactions were active despite the availability of organic carbon. Asparagine was catabolized equally via conversion to threonine and subsequent cleavage to produce acetaldehyde and glycine, and via deamination to fumarate and then the anaplerotic conversion of malate to pyruvate. Both pathways for asparagine catabolism produced acetyl-CoA, either directly via pyruvate or indirectly via the WLP. Cofactor stoichiometry based on our data predicted an essentially zero flux through the ferredoxin-dependent transhydrogenase (Nfn) reaction. Instead, nearly all of NADPH generated from the hydrogenase reaction was consumed by the WLP. Reduced ferredoxin produced by the hydrogenase reaction and glycolysis was mostly used for ATP generation via the RNF/ATPase system, with the remainder consumed by the WLP. NADH produced by RNF/ATPase was entirely consumed via the WLP. [Display omitted] • Methionine supplementation enables growth of Clostridium ljungdahlii on defined medium. • 13C Metabolic flux analysis validates core metabolism and quantifies pathway fluxes. • During mixotrophic growth 47% of consumed carbon comes from autotrophic metabolism. • Asparagine catabolism feeds the Wood-Ljungdahl pathway via degradation to glycine. [ABSTRACT FROM AUTHOR]

There is a paucity of detailed data related to the effect of senescence on the mitochondrial antioxidant capacity and redox state of senescent human cells. Activities of TCA cycle enzymes, respiratory chain complexes, hydrogen peroxide (H2O2), superoxide anions (SA), lipid peroxides (LPO), protein carbonyl content (PCC), thioredoxin reductase 2 (TrxR2), superoxide dismutase 2 (SOD2), glutathione peroxidase 1 (GPx1), glutathione reductase (GR), reduced glutathione (GSH), and oxidized glutathione (GSSG), along with levels of nicotinamide cofactors and ATP content were measured in young and senescent human foreskin fibroblasts. Primary and senescent cultures were biochemically identified by monitoring the augmented cellular activities of key glycolytic enzymes including phosphofructokinase, lactate dehydrogenase, and glycogen phosphorylase, and accumulation of H2O2, SA, LPO, PCC, and GSSG. Citrate synthase, aconitase, a-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, isocitrate dehydrogenase, and complex I-III, IIIII, and IV activities were significantly diminished in P25 and P35 cells compared to P5 cells. This was accompanied by significant accumulation of mitochondrial H2O2, SA, LPO, and PCC, along with increased transcriptional and enzymatic activities of TrxR2, SOD2, GPx1, and GR. Notably, the GSH/GSSG ratio was significantly reduced whereas NAD+/NADH and NADP+/NADPH ratios were significantly elevated. Metabolic exhaustion was also evident in senescent cells underscored by the severely diminished ATP/ADP ratio. Profound oxidative stress may contribute, at least in part, to senescence pointing at a potential protective role of antioxidants in aging-associated disease. [ABSTRACT FROM AUTHOR]

To investigate the effects of aluminum stress on root exudates of Helianthus tuberosus and the alleviating effect of exogenous salicylic acid(SA), we used aluminum-tolerant Nanjing H. tuberosus and aluminum-sensitive Ziyang H. tuberosus as experimental materials and set aluminum concentration of 500 μmol·L-1 by soil culture method, and analyzed the effects of different concentrations(10, 100, 1 000 μmol·L-1)of SA on the organic acids and amino acids in root exudates of H. tuberosus and related metabolic enzymes in root tips under aluminum stress. The results were as follows:(1)Concentrations of citric acid, oxalic acid and malic acid in the root exudates of H. tuberosus increased under single Al stress, and the increase was greater in Nanjing H. tuberosus than in Ziyang H. tuberosus; The activities of citrate synthase and malate dehydrogenase increased under single Al stress; The proline content increased significantly, and the concentration of total amino acids decreased significantly.(2)The concentrations of citric acid, oxalic acid and malic acid secreted by the root system ofNanjing H. tuberosus were increased to different degrees after the addition of exogenous SA, but the oxalic acid secreted by the root system of Ziyang H. tuberosus was significantly reduced after treatment with high concentration(1 000 μmol·L-1)of SA, and there was no significant change in malic acid concentration under all concentrations of SA treatment; The citrate synthase activity appeared to be enhanced to different degrees, but it had little effect on malate dehydrogenase activity in the root tips of Nanjing H. tuberosus, and malate dehydrogenase activity in the root tips of Ziyang H. tuberosus was significantly reduced after treatment with high concentration(1 000 μmol·L-1)of SA; The proline content decreased significantly, from terms of changes in total amino acid concentration, the maximum alleviating effect was obtained at high concentration(1 000 μmol·L-1)SA for Nanjing H. tuberosus and at low concentration(10 μmol·L-1)SA for Ziyang H. tuberosus. Therefore, H. tuberosus responds to aluminum toxicity by secreting organic acids, and exogenous SA can promote the rate of organic acid metabolism in the root system of H. tuberosus to secrete more organic acids to alleviate aluminum stress, and this alleviation effect is better in Nanjing H. tuberosus, which is relatively strong in aluminum tolerance. [ABSTRACT FROM AUTHOR]

In the current study, lipid-polymer hybrid nanoparticles (LPHNPs) fabricated with lipoid-90H and chitosan, sunitinib malate (SM), an anticancer drug was loaded using lecithin as a stabilizer by employing emulsion solvent evaporation technique. Four formulations (SLPN1–SLPN4) were developed by varying the concentration of chitosan polymer. Based on particle characterization, SLPN4 was optimized with size (439 ± 5.8 nm), PDI (0.269), ZP (+34 ± 5.3 mV), and EE (83.03 ± 4.9%). Further, the optimized formulation was characterized by FTIR, DSC, XRD, SEM, and in vitro release studies. In-vitro release of the drug from SPN4 was found to be 84.11 ± 2.54% as compared with pure drug SM 24.13 ± 2.67%; in 48 h, release kinetics followed the Korsmeyer–Peppas model with Fickian release mechanism. The SLPN4 exhibited a potent cytotoxicity against MCF-7 breast cancer, as evident by caspase 3, 9, and p53 activities. According to the findings, SM-loaded LPHNPs might be a promising therapy option for breast cancer. [ABSTRACT FROM AUTHOR]

Background: Five hundred 8-d old male broilers Cobb500 were randomly allotted into 10 treatments in factorial arrangement with 5 Cu levels (0, 4, 8, 12, and 16 mg/kg), and 2 sources (Cu proteinate, CuPro and Cu sulphate, CuSO4.5H2O) for a 10-d-experiment. Results: Feed conversion ratio (FCR) was better (P < 0.05) in CuPro fed chicks compared with CuSO4.5H2O group. Average daily feed intake (ADFI) decreased linearly (P < 0.05) as dietary Cu increased. A quadratic response (P < 0.05) to Cu levels was found for FCR, being optimized at 9.87 and 8.84 mg Cu/kg in CuPro and CuSO4.5H2O diets, respectively. Copper supplementation linearly increased liver Cu content (P < 0.05) and tended to linearly increase (P = 0.07) phosphorus (P) and copper in tibia. Manganese and zinc were higher (P < 0.05) in tibia of CuPro fed birds. Broilers fed CuPro exhibited lower liver iron (P < 0.05) content, lower activities of Cu, Zn superoxide dismutase (CuZnSOD) in breast muscle and liver, and glutathione peroxidase in liver. Glutathione peroxidase reduced linearly (P < 0.05) with CuPro levels and increased linearly (P < 0.05) with CuSO4.5H2O levels and were lower (P < 0.05) in all CuPro levels in breast muscle. Breast muscle malondialdehyde concentration tended to be higher (P = 0.08) in broilers fed CuSO4.5H2O. Copper levels linearly increased (P < 0.05) metallothionein (MT) and malate dehydrogenase (MDH) expression in liver, and six-transmembrane epithelial antigen of the prostate-1 (STEAP-1) in the intestine. Copper elicited a quadratic response (P < 0.050) in AKT-1 and mammalian target of rapamycin (mTOR) in breast muscle, CuZnSOD in liver and antioxidant 1 copper chaperone (ATOX 1) in intestine. Broilers fed CuPro exhibited higher mRNA expression of mTOR in muscle breast and lower CuZnSOD in liver and ATOX 1 in intestine. Interaction (P < 0.05) between levels and sources was found in mRNA expression for GSK-3β, MT, and CuZnSOD in breast muscle, FAS and LPL in liver and MT and CTR1 in intestine. Conclusions: CuPro showed beneficial effects on feed conversion and bone mineralization. Organic and inorganic Cu requirements are 9.87 and 8.84 mg Cu/kg, respectively. [ABSTRACT FROM AUTHOR]

The study of the mechanisms of adaptogenic action of furostanol glycosides (FG) on plant cells was carried out in vitro and a comparison was made of the effects of hypothermia and hyperosmotic stress on a suspension cell culture of Medicago sativa L. It has been shown that the cell population of M. sativa in vitro possesses functional specificities that determine different sensitivity to the action of these abiotic stressors, which was expressed in different levels of cell viability: high (85%) under hypothermia and low (25%) under hyperosmotic action. Hypothermia stimulated the rate of generation of superoxide anion (), and it was accompanied by a high constitutive activity of antioxidant enzymes (guaiacol-peroxidase, ascorbate peroxidase and glutathione peroxidase), the level of which reflects the compensatory potential of cells. Preservation of a high level of cell viability under the action of hypothermia, despite a 40% increase in the rate of generation of , indicates that the formed reactive oxygen species did not cause damage to lipid structures and macromolecules in cells. Exogenous treatment with FG with this type of stress effect promoted an increase in the activity of antioxidant enzymes but did not have a noticeable effect on the initially high level of cell viability. In conditions of hyperosmotic stress, preliminary exposure to FG led to a threefold increase in cell survival (from 25 to 73%) and a 30% increase in the activity of soluble peroxidase in comparison with its level under the influence of only a stressor. Exposure to FG also caused an increase in activity antioxidant enzymes, a decrease in the level of lipid peroxidation and an increase in the activity of enzymes of the malate dehydrogenase (MDH) complex. However, in contrast to hypothermia, the observed changes caused a significant increase in the viability of M. sativa cells in vitro. An increase in the formation of osmolytes in the reactions NAD/NAD·H-MDH was indicated by the increased concentration of osmotic (mannitol), which causes the initial degree of cell plasmolysis, in comparison with the control. The article discusses specificities of M. sativa cell culture influencing the specificity of its stress-resistance, possible mechanisms of cell protection in vitro in hypothermia and hyperosmotic stress and the role of FG in these processes. [ABSTRACT FROM AUTHOR]

Rhizobium sp. RM solubilized tri-calcium phosphate (TCP: 324–463 µg ml−1) and rock phosphate (RP: 36–46.58 µg ml−1) in the presence of common rhizospheric sugars-glucose, arabinose, xylose and their combinations. Fructose, though did not support RP solubilization individually, surprisingly solubilized significantly higher phosphate when combined with aldoses. The highest TCP (644 µg ml−1) and RP (75 µg ml−1) solubilization was achieved in fructose + glucose combination. Presence of gluconate, malate and oxalate in culture supernatant indicated functioning of periplasmic glucose oxidation, the non-phosphorylative arabinose dehydrogenase pathway and the tricarboxylate (TCA) cycle, respectively. Aldoses, when present together, were co-utilized (monoauxic growth) however, when added with fructose, prevented the uptake of fructose yielding a typical diauxic growth. This presented an unusual sequential utilization of aldoses over a ketose (fructose) in strain RM. The prevention of fructose uptake by aldoses was investigated through real-time expression of key genes coding fructose transport proteins and initial enzymes of sugar metabolism. Fructose was actively transported via fructose-specific ABC transporters as suggested by upregulation of frcB and frcC only in fructose and fructose growth phases of fructose + aldose combinations. The probable route of initial fructose metabolism involved either fructokinase and/or xylose isomerase, as confirmed by enzyme activities. The upregulation of hfq and hprK genes only in aldose phase of fructose + aldose combinations suggested their possible involvement in governing the preferential utilization. The novel aspects of this study are enhanced organic acid mediated P solubilization in fructose + aldose combinations and a rare hierarchy of aldoses over fructose which is possibly regulated at the level of fructose transport and fructokinase. Key points: • Sugars when provided in different dual combinations, supported enhanced P solubilization from complex phosphate sources like TCP and RP in Rhizobium sp. RM. • Transcriptional status of genes in cells of RM when grown in different individual sugars and their combinations suggested that fructose might be a less preferred carbon source and hence was utilized after aldoses with the possible regulation by Hfq and HPrK. • First study to present a unique phenomenon of sequential utilization of aldoses (glucose, arabinose and xylose) over fructose in a concentration-independent manner in Rhizobium sp. RM. and to present the effect of dual combinations of sugars on organic acid mediated P solubilization trait of rhizobia. [ABSTRACT FROM AUTHOR]

Malate dehydrogenase (MDH) is widely present in nature and regulates plant growth and development, as well as playing essential roles, especially in abiotic stress responses. Nevertheless, there is no comprehensive knowledge to date on MDH family members in rice. In this study, a total of 12 MDH members in rice were identified through genome-wide analysis and divided into three groups on the basis of their phylogenetic relationship and protein-conserved motifs. Evolutionary analysis showed that MDH proteins from rice, maize and wheat shared a close phylogenetic relationship, and the MDH family was conserved in the long-term process of domestication. We identified two segmental duplication events involving four genes, which could be the major force driving the expansion of the OsMDH family. The expression profile, cis-regulatory elements and qRT-PCR results of these genes revealed that a few OsMDH showed high tissue specificity, almost all of which had stress response elements in the promoter region, and ten MDH members were significantly induced by salt stress. Through gene-based association analysis, we found a significant correlation between salt tolerance at the seedling stage and the genetic variation of OsMDH8.1 and OsMDH12.1. Additionally, we found that the polymorphism in the promoter region of OsMDH8.1 might be related to the salt tolerance of rice. This study aimed to provide valuable information on the functional study of the rice MDH gene family related to salt stress response and revealed that OsMDH8.1 might be an important gene for the cultivar improvement of salt tolerance in rice. [ABSTRACT FROM AUTHOR]

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Protein degradation, a major eukaryotic response to cellular signals, is subject to numerous layers of regulation. In yeast, the evolutionarily conserved GID E3 ligase mediates glucose-induced degradation of fructose-1,6-bisphosphatase (Fbp1), malate dehydrogenase (Mdh2), and other gluconeogenic enzymes. "GID" is a collection of E3 ligase complexes; a core scaffold, RING-type catalytic core, and a supramolecular assembly module together with interchangeable substrate receptors select targets for ubiquitylation. However, knowledge of additional cellular factors directly regulating GID-type E3s remains rudimentary. Here, we structurally and biochemically characterize Gid12 as a modulator of the GID E3 ligase complex. Our collection of cryo-EM reconstructions shows that Gid12 forms an extensive interface sealing the substrate receptor Gid4 onto the scaffold, and remodeling the degron binding site. Gid12 also sterically blocks a recruited Fbp1 or Mdh2 from the ubiquitylation active sites. Our analysis of the role of Gid12 establishes principles that may more generally underlie E3 ligase regulation. The GID E3 ligase regulates glucose-induced degradation in yeast, and key physiology. This study unveils E3 ligase regulation by reshaping the substrate binding site, blocking substrate access to ubiquitination active sites, and a Cage-like assembly. [ABSTRACT FROM AUTHOR]

Postharvest events enhance fruit palatability, fragrance and sweetness and reduce sourness. With passion fruit (Passiflora edulis) the underlying molecular events occurring during the postharvest period remain largely unknown. In this study we define how passion fruit flavor alters during the postharvest period using integrated transcriptome and metabolome analyses. Passion fruits were stored under three conditions: room temperature, low temperature, and room temperature with a pre-fumigation with 100 μM methyljasmonate (MeJA). During the postharvest period, organic acid content decreased but sugars and most volatiles increased. While both low temperature and MeJA treatment effectively delayed the aging process, MeJA better maintained fruit flavor. Transcriptomic and network modelling analyses targeted PeWRKY20 was a potential key regulator of the flavor of passion fruit. PeWRKY20 was shown to bind to the Malate Dehydrogenase 1 (PeMDH1) promoter to represses PeMDH1 expression. Transient assays in Nicotiana benthamiana leaves suggested that PeWRKY20 and PeMDH1 function oppositely to regulate the production of malic acid and volatiles, such as heptadecane, dimeththyl phthalate, and L-α-terpineol. Our work unravels a key regulatory hub in postharvest passion fruit development based on an association between malic acid and volatiles. [Display omitted] • Butyric acid metabolism and volatiles are tightly related during postharvest. • PeWRKY20 directly represses the expression of Malate Dehydrogenase 1 (PeMDH1). • PeWRKY20 is a potential key regulator of butyric acid and volatiles metabolism. • MeJA retards postharvest senescence and maintains passion fruit flavor. [ABSTRACT FROM AUTHOR]

Considering that the presence of cognitive and behavioral impairment is a prognostic factor in ALS and that genetic variability influences the patient's survival when administering novel treatments, TMEM106B should be considered as a susceptibility factor in ALS. Swim training partially reverses changes in LA metabolism in ALS murine skeletal muscle by influencing the glycolytic enzyme and malate dehydrogenase activities, thus improving skeletal muscle mass by adjusting the energy demands. The goal of this Special Issue is to report new research progress and reviews concerning amyotrophic lateral sclerosis (ALS). [Extracted from the article]