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Calcium (Ca2+) is a universal second messenger essential for the growth and development of plants in normal and stress situations. In plants, the proteins, CBL (calcineurin B-like) and CIPK (CBL-interacting protein kinase), form one of the important Ca2+ decoding complexes to decipher Ca2+ signals elicited by environmental challenges. Multiple interactors distinguish CBL and CIPK protein family members to form a signaling network for regulated perception and transduction of environmental signals, e.g., signals generated under nutrient stress conditions. Conservation of equilibrium in response to varying soil nutrient status is an important aspect for plant vigor and yield. Signaling processes have been reported to observe nutrient fluctuations as a signal responsible for regulated nutrient transport adaptation. Recent studies have identified downstream targets of CBL–CIPK modules as ion channels or transporters and their association in signaling nutrient disposal including potassium, nitrate, ammonium, magnesium, zinc, boron, and iron. Ca2+–CBL–CIPK pathway modulates ion transporters/channels and hence maintains a homeostasis of several important plant nutrients in the cytosol and sub-cellular compartments. In this article, we summarize recent literature to discuss the role of the Ca2+–CBL–CIPK pathway in cellular osmoregulation and homeostasis on exposure to nutrient excess or deprived soils. This further establishes a link between taking up the nutrient in the roots and its distribution and homeostasis during the generation of signal for the development and survival of plants.

Sustained nutrient (fuel) excess, as occurs during obesity and diabetes, has been linked to increased inflammation, impaired mitochondrial homeostasis, lipotoxicity, and insulin resistance in skeletal muscle. Precisely how mitochondrial dysfunction is initiated and whether it contributes to insulin resistance in this tissue remains a poorly resolved issue. Herein, we examine the contribution that an increase in proinflammatory NFkB signalling makes towards regulation of mitochondrial bioenergetics, morphology, and dynamics and its impact upon insulin action in skeletal muscle cells subject to chronic fuel (glucose and palmitate) overloading. We show sustained nutrient excess of L6 myotubes promotes activation of the IKKβ-NFkB pathway (as judged by a six-fold increase in IL-6 mRNA expression; an NFkB target gene) and that this was associated with a marked reduction in mitochondrial respiratory capacity (>50%), a three-fold increase in mitochondrial fragmentation and 2.5-fold increase in mitophagy. Under these circumstances, we also noted a reduction in the mRNA and protein abundance of PGC1α and that of key mitochondrial components (SDHA, ANT-1, UCP3, and MFN2) as well as an increase in cellular ROS and impaired insulin action in myotubes. Strikingly, pharmacological or genetic repression of NFkB activity ameliorated disturbances in mitochondrial respiratory function/morphology, attenuated loss of SDHA, ANT-1, UCP3, and MFN2 and mitigated the increase in ROS and the associated reduction in myotube insulin sensitivity. Our findings indicate that sustained oversupply of metabolic fuel to skeletal muscle cells induces heightened NFkB signalling and that this serves as a critical driver for disturbances in mitochondrial function and morphology, redox status, and insulin signalling.

The Green New Deal requires a profound transformation of the agricultural sector, which will have to become more sustainable and ensure universal access to healthy food. Thus, it will be essential to introduce radical technological innovations. Nanotechnologies have the potential to produce a significant boost to the improvement of the food system. Within this context, in the next years, a strong challenge will need to be faced regarding developing new and more efficient uses of nutrients in agriculture, being the nutrient use efficiency (NUE) paramount in sustaining high crop productivity without depleting biodiversity, and altering both the natural and agricultural systems. Nutrients leaching causes environmental pollution and water eutrophication, while nutrient excess favors pest and weed widespread. Therefore, it will be mandatory to improve plant nutrition efficiency without affecting agricultural productivity and economic sustainability. A promising alternative consists of the introduction of the so-called nanomaterial enhanced fertilizers and plant growth stimulators. Such innovation includes nanotechnological solutions that can improve nutrient delivery for a more finely tuned, accurate, and saving-resources distribution of nutrients. This review provides a critical view of the latest advances in nanofertilizer research, mainly referring to nano-hydroxyapatite, silica nanoparticles, and chitosan-derived nanostructures.

S6K1 has emerged as a critical signaling component in the development of insulin resistance through phosphorylation and inhibition of IRS-1 function. This effect can be triggered directly by nutrients such as amino acids or by insulin through a homeostatic negative-feedback loop. However, the role of S6K1 in mediating IRS-1 phosphorylation in a physiological setting of nutrient overload is unresolved. Here we show that S6K1 directly phosphorylates IRS-1 Ser-1101 in vitro in the C-terminal domain of the protein and that mutation of this site largely blocks the ability of amino acids to suppress IRS-1 tyrosine and Akt phosphorylation. Consistent with this finding, phosphorylation of IRS-1 Ser-1101 is increased in the liver of obese db/db and wild-type, but not S6K1⁻/⁻, mice maintained on a high-fat diet and is blocked by siRNA knockdown of S6K1 protein. Finally, infusion of amino acids in humans leads to the concomitant activation of S6K1, phosphorylation of IRS-1 Ser-1101, a reduction in IRS-1 function, and insulin resistance in skeletal muscle. These findings indicate that nutrient- and hormonal-dependent activation of S6K1 causes insulin resistance in mice and humans, in part, by mediating IRS-1 Ser-1101 phosphorylation.

Obesity shares with most chronic diseases the presence of an inflammatory component, which accounts for the development of metabolic disease and other associated health alterations. This inflammatory state is reflected in increased circulating levels of pro-inflammatory proteins, and it occurs not only in adults but also in adolescents and children. The chronic inflammatory response has its origin in the links existing between the adipose tissue and the immune system. Obesity, like other states of malnutrition, is known to impair the immune function, altering leucocyte counts as well as cell-mediated immune responses. In addition, evidence has arisen that an altered immune function contributes to the pathogenesis of obesity. This review attempts to briefly comment on the various plausible explanations that have been proposed for the phenomenon: (1) the obesity-associated increase in the production of leptin (pro-inflammatory) and the reduction in adiponectin (anti-inflammatory) seem to affect the activation of immune cells; (2) NEFA can induce inflammation through various mechanisms (such as modulation of adipokine production or activation of Toll-like receptors); (3) nutrient excess and adipocyte expansion trigger endoplasmic reticulum stress; and (4) hypoxia occurring in hypertrophied adipose tissue stimulates the expression of inflammatory genes and activates immune cells. Interestingly, data suggest a greater impact of visceral adipose tissue and central obesity, rather than total body fat, on the inflammatory process. In summary, there is a positive feedback loop between local inflammation in adipose tissue and altered immune response in obesity, both contributing to the development of related metabolic complications.

Following the publication of the landmark trial of Clark et al. in 1996 that appeared to show that Se could reduce the risk of cancer, awareness of the importance of Se to human health has markedly increased. As a result, there is now much more aggressive marketing of Se supplements and functional foods, even in situations where additional consumption of Se is inappropriate. The present review addresses how Se gets into the food chain, the wide variability in Se content of foods and the very different levels of intake between countries and regions. Though it is clear that there are adverse consequences for health of both deficient and excessive intake, health effects at intermediate levels of intake are less certain. Thus it is difficult to define optimal intake which depends on a large number of factors, such as which functions of Se are most relevant to a particular disease state, which species of Se is most prominent in the Se source, which health condition is being considered, the adequacy or otherwise of intake of other nutrients, the presence of additional stressors, and lastly whether the ability to make selenoproteins may be compromised. These complexities need to be understood, particularly by policy makers, in order to make informed judgments. Potential solutions for increasing Se intake, where required, include agronomic biofortification and genetic biofortification or, for individuals, increased intake of naturally Se-rich foods, functional foods or supplements. The difficulties of balancing the risks and benefits in relation to Se intake are highlighted.

Regions with intensive agriculture often encounter environmental problems caused by nutrient excess of agro-food-waste systems that have become increasingly linear over previous decades. In this study, nitrogen (N), phosphorus (P), potassium (K) and carbon (C) flows in the whole agro-food-waste system of district Cleves in Germany were quantified simultaneously using substance flow analysis. Moreover, nutrient use inefficiency hotspots were identified to establish options to improve nutrient self-sufficiency as a first step towards nutrient circularity. Data on mass flows and nutrient contents was acquired for the year 2016 from stakeholders, statistical databases, literature and modelling. Organic C was included for flows with potential as organic fertilizer. Results show that animal production drives the nutrient flows in the export-oriented district, with feed import, manure application and losses from housing and manure storage accounting for 40, 45 and 60% of all N, P and K flows, respectively. In particular agriculture is responsible for N losses, with 150 kg N lost ha −1 agricultural land. Crop production surplus and with that soil accumulation of P and K are 515 t and 4100 t respectively. Stoichiometry of N:P:K:C in the different organic materials does not allow direct application and meeting crop requirements without exceeding demand of especially P. Processing of biomass is therefore required. Based on mass, especially manure holds potential for processing into bio-based fertilizers. To improve nutrient cycling and soil C conservation, being an important element for a sustainable agricultural sector, local balances between crop and animal production need to be considered.

Cell size varies greatly among different types of cells, but the range in size that a specific cell type can reach is limited. A long-standing question in biology is how cells control their size. Escherichia coli adjusts size and growth rate according to the availability of nutrients so that it grows larger and faster in nutrient-rich media than in nutrient-poor media. Here, we describe how, using classical genetics, we have isolated a remarkably small E. coli mutant that has undergone a 70% reduction in cell volume with respect to wild type. This mutant lacks FabH, an enzyme involved in fatty acid biosynthesis that previously was thought to be essential for the viability of E. coli . We demonstrate that although FabH is not essential in wild-type E. coli , it is essential in cells that are defective in the production of the small-molecule and global regulator ppGpp. Furthermore, we have found that the loss of FabH causes a reduction in the rate of envelope growth and renders cells unable to regulate cell size properly in response to nutrient excess. Therefore we propose a model in which fatty acid biosynthesis plays a central role in regulating the size of E. coli cells in response to nutrient availability.

We know a great deal about the cellular response to starvation via AMPK, but less is known about the reaction to nutrient excess. Insulin resistance may be an appropriate response to nutrient excess, but the cellular sensors that link these parameters remain poorly defined. In the present study we provide evidence that mitochondrial superoxide production is a common feature of many different models of insulin resistance in adipocytes, myotubes, and mice. In particular, insulin resistance was rapidly reversible upon exposure to agents that act as mitochondrial uncouplers, ETC inhibitors, or mitochondrial superoxide dismutase (MnSOD) mimetics. Similar effects were observed with overexpression of mitochondrial MnSOD. Furthermore, acute induction of mitochondrial superoxide production using the complex III antagonist antimycin A caused rapid attenuation of insulin action independently of changes in the canonical PI3K/Akt pathway. These results were validated in vivo in that MnSOD transgenic mice were partially protected against HFD induced insulin resistance and MnSOD+/- mice were glucose intolerant on a standard chow diet. These data place mitochondrial superoxide at the nexus between intracellular metabolism and the control of insulin action potentially defining this as a metabolic sensor of energy excess.

Background Cultivated flax ( Linum usitatissimum L.) is widely used for production of textile, food, chemical and pharmaceutical products. However, various stresses decrease flax production. Search for genes, which are involved in stress response, is necessary for breeding of adaptive cultivars. Imbalanced concentration of nutrient elements in soil decrease flax yields and also results in heritable changes in some flax lines. The appearance of Linum Insertion Sequence 1 (LIS-1) is the most studied modification. However, LIS-1 function is still unclear. Results High-throughput sequencing of transcriptome of flax plants grown under normal (N), phosphate deficient (P), and nutrient excess (NPK) conditions was carried out using Illumina platform. The assembly of transcriptome was performed, and a total of 34924, 33797, and 33698 unique transcripts for N, P, and NPK sequencing libraries were identified, respectively. We have not revealed any LIS-1 derived mRNA in our sequencing data. The analysis of high-throughput sequencing data allowed us to identify genes with potentially differential expression under imbalanced nutrition. For further investigation with qPCR, 15 genes were chosen and their expression levels were evaluated in the extended sampling of 31 flax plants. Significant expression alterations were revealed for genes encoding WRKY and JAZ protein families under P and NPK conditions. Moreover, the alterations of WRKY family genes differed depending on LIS-1 presence in flax plant genome. Besides, we revealed slight and LIS-1 independent mRNA level changes of KRP2 and ING1 genes, which are adjacent to LIS-1, under nutrition stress. Conclusions Differentially expressed genes were identified in flax plants, which were grown under phosphate deficiency and excess nutrition, on the basis of high-throughput sequencing and qPCR data. We showed that WRKY and JAS gene families participate in flax response to imbalanced nutrient content in soil. Besides, we have not identified any mRNA, which could be derived from LIS-1, in our transcriptome sequencing data. Expression of LIS-1 flanking genes, ING1 and KRP2 , was suggested not to be nutrient stress-induced. Obtained results provide new insights into edaphic stress response in flax and the role of LIS-1 in these process.