The Multi-allelic Genetic Architecture of a Variance-Heterogeneity Locus for Molybdenum Concentration in Leaves Acts as a Source of Unexplained Additive Genetic Variance

Funding: We acknowledge support from the US National Institutes of Health (http://www.nih.gov/) (grant 2R01GM078536 to DES), European Commission (http://ec.europa.eu/index_en.htm) (grant PCIG9-GA-2011-291798 to DES) and UK Biotechnology and Biological Sciences Research Council (http://www.bbsrc.ac.uk/) (grants BB/L000113/1 to DES). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewedPublisher PD

Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana

Sulphur (S) is an essential element for all living organisms. The uptake, assimilation and metabolism of S in plants are well studied. However, the regulation of S homeostasis remains largely unknown. Here, we report on the identification and characterisation of the more sulphur accumulation1 (msa1-1) mutant. The MSA1 protein is localized to the nucleus and is required for both S adenosylmethionine (SAM) production and DNA methylation. Loss of function of the nuclear localised MSA1 leads to a reduction in SAM in roots and a strong S-deficiency response even at ample S supply, causing an over- accumulation of sulphate, sulphite, cysteine and glutathione. Supplementation with SAM suppresses this high S phenotype. Furthermore, mutation of MSA1 affects genome-wide DNA methylation, including the methylation of S-deficiency responsive genes. Elevated S accumulation in msa1-1 requires the increased expression of the sulphate transporter genes SULTR1;1 and SULTR1;2 which are also differentially methylated in msa1-1. Our results suggest a novel function for MSA1 in the nucleus in regulating SAM biosynthesis and maintaining S homeostasis epigenetically via DNA methylation

Damage growth in fibre bundle models with localized load sharing and environmentally-assisted ageing

One of the most fundamental models for the complex behaviour of damage accumulation in earth materials is the fibre bundle model. One distinguishes between models with localized load sharing (LLS) and models with equal load sharing (ELS). While ELS models can be treated by mean field theory, the behaviour of LLS models is usually more complicated. Here, we consider a fibre bundle model with LLS where, in addition, we introduce a time scale by incorporating time dependent ageing of the fibres due to the accumulation of damage driven by the locally acting stress in a chemically active environment. If the accumulated damage exceeds a random threshold, the fibres fail. The non-trivial time dependence of the cumulative damage in the system can be attributed to different mechanisms that dominate at different time scales. We include this information into an analytical description of the damage accumulation process and show that the analytical description is in agreement with numerical results

Genome-wide association mapping identifies a new arsenate reductase enzyme critical for limiting arsenic accumulation in plants

Inorganic arsenic is a carcinogen, and its ingestion through foods such as rice presents a significant risk to human health. Plants chemically reduce arsenate to arsenite. Using genome-wide association (GWA) mapping of loci controlling natural variation in arsenic accumulation in Arabidopsis thaliana allowed us to identify the arsenate reductase required for this reduction, which we named High Arsenic Content 1 (HAC1). Complementation verified the identity of HAC1, and expression in Escherichia coli lacking a functional arsenate reductase confirmed the arsenate reductase activity of HAC1. The HAC1 protein accumulates in the epidermis, the outer cell layer of the root, and also in the pericycle cells surrounding the central vascular tissue. Plants lacking HAC1 lose their ability to efflux arsenite from roots, leading to both increased transport of arsenic into the central vascular tissue and on into the shoot. HAC1 therefore functions to reduce arsenate to arsenite in the outer cell layer of the root, facilitating efflux of arsenic as arsenite back into the soil to limit both its accumulation in the root and transport to the shoot. Arsenate reduction by HAC1 in the pericycle may play a role in limiting arsenic loading into the xylem. Loss of HAC1-encoded arsenic reduction leads to a significant increase in arsenic accumulation in shoots, causing an increased sensitivity to arsenate toxicity. We also confirmed the previous observation that the ACR2 arsenate reductase in A. thaliana plays no detectable role in arsenic metabolism. Furthermore, ACR2 does not interact epistatically with HAC1, since arsenic metabolism in the acr2 hac1 double mutant is disrupted in an identical manner to that described for the hac1 single mutant. Our identification of HAC1 and its associated natural variation provides an important new resource for the development of low arsenic-containing food such as rice

Variation in Molybdenum Content Across Broadly Distributed Populations of Arabidopsis thaliana Is Controlled by a Mitochondrial Molybdenum Transporter (MOT1)

Molybdenum (Mo) is an essential micronutrient for plants, serving as a cofactor for enzymes involved in nitrate assimilation, sulfite detoxification, abscisic acid biosynthesis, and purine degradation. Here we show that natural variation in shoot Mo content across 92 Arabidopsis thaliana accessions is controlled by variation in a mitochondrially localized transporter (Molybdenum Transporter 1 - MOT1) that belongs to the sulfate transporter superfamily. A deletion in the MOT1 promoter is strongly associated with low shoot Mo, occurring in seven of the accessions with the lowest shoot content of Mo. Consistent with the low Mo phenotype, MOT1 expression in low Mo accessions is reduced. Reciprocal grafting experiments demonstrate that the roots of Ler-0 are responsible for the low Mo accumulation in shoot, and GUS localization demonstrates that MOT1 is expressed strongly in the roots. MOT1 contains an N-terminal mitochondrial targeting sequence and expression of MOT1 tagged with GFP in protoplasts and transgenic plants, establishing the mitochondrial localization of this protein. Furthermore, expression of MOT1 specifically enhances Mo accumulation in yeast by 5-fold, consistent with MOT1 functioning as a molybdate transporter. This work provides the first molecular insight into the processes that regulate Mo accumulation in plants and shows that novel loci can be detected by association mapping

Daily magnesium fluxes regulate cellular timekeeping and energy balance

Circadian clocks are fundamental to the biology of most eukaryotes, coordinating behaviour and physiology to resonate with the environmental cycle of day and night through complex networks of clock-controlled genes1, 2, 3. A fundamental knowledge gap exists, however, between circadian gene expression cycles and the biochemical mechanisms that ultimately facilitate circadian regulation of cell biology4, 5. Here we report circadian rhythms in the intracellular concentration of magnesium ions, [Mg2+]i, which act as a cell-autonomous timekeeping component to determine key clock properties both in a human cell line and in a unicellular alga that diverged from each other more than 1 billion years ago6. Given the essential role of Mg2+ as a cofactor for ATP, a functional consequence of [Mg2+]i oscillations is dynamic regulation of cellular energy expenditure over the daily cycle. Mechanistically, we find that these rhythms provide bilateral feedback linking rhythmic metabolism to clock-controlled gene expression. The global regulation of nucleotide triphosphate turnover by intracellular Mg2+ availability has potential to impact upon many of the cell’s more than 600 MgATP-dependent enzymes7 and every cellular system where MgNTP hydrolysis becomes rate limiting. Indeed, we find that circadian control of translation by mTOR8 is regulated through [Mg2+]i oscillations. It will now be important to identify which additional biological processes are subject to this form of regulation in tissues of multicellular organisms such as plants and humans, in the context of health and disease

Time evolution of damage due to environmentally assisted aging in a fiber bundle model

Damage growth in composite materials is a complex process which is of interest in many fields of science and engineering. We consider this problem in a fiber bundle model where fibers undergo an aging process due to the accumulation of damage driven by the locally acting stress in a chemically active environment. By subjecting the bundle to a constant external load, fibers fail either when the load on them exceeds their individual intrinsic strength or when the accumulated internal damage exceeds a random threshold. We analyze the time evolution of the breaking process under low external loads where aging of fibers dominates. In the mean field limit, we show analytically that the aging system continuously accelerates in a way which can be characterized by an inverse power law of the event rate with a singularity that defines a failure time. The exponent is not universal; it depends on the details of the aging process. For localized load sharing, a more complex damage process emerges which is dominated by distinct spatial regions of the system with different degrees of stress concentration. Analytical calculations revealed that the final acceleration to global failure is preceded by a stationary accumulation of damage. When the disorder is strong, the accelerating phase has the same functional behavior as in the mean field limit. The analytical results are verified by computer simulations

Research On Recycling Of Hardened Mortar From Construction And Demolition Waste

Abstract The recycling issues related to the construction and demolition (C&amp;D) wastes in the sustainable development and the circular economy context represent a continuous challenge for researchers. This paper reveals the possibility to recycle the hardened mortar recovered from C&amp;D wastes. Thus, the recovered hardened mortar with grains size less than 16 mm was used in the concrete structure. The compression resistance of the final concrete was determined using a Heckert 3000 KN testing machine and the results showed a better compressive strength for the samples with C&amp;D waste content than the standard sample of about 1.19 times. This is a good premise for improving the researches related to C&amp;D waste usage in concrete production.</jats:p