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Development and performance evaluation of macropore intelligent plugging hydrogels
Fully-connected microwave photonic multi-beamformer with fast beam-steering for broadband wireless communication
Adaptive competitive balance regulation in professional sports leagues via graph attention networks and proximal policy optimization
Gradient-distributed metal-halide dynamic memristors for adaptive and robust voiceprint recognition
Assessing the potential for biogeochemical deterioration of building materials by green algae in temperate climate via an integrated metabolomic approach
Abstract Biodeterioration of building materials by aerophytic green algae is increasingly recognized as a significant factor affecting the aesthetic value and durability of brick and plaster façades, yet the biochemical mechanisms underlying this process remain poorly understood. This study investigates the metabolomic profiles of five algal taxa: Chloroidium saccharophilum PNK010, Klebsormidium nitens PNK013, Bracteacoccus minor PNK015, Diplosphaera chodatii PNK021, and Stichococcus bacillaris PNK040 growing on brick and plaster for a year under laboratory and environmental conditions. Untargeted UHPLC–MS/MS metabolomics, with metabolic pathway and chemical-class enrichment analyses, were used to characterize substrate- and condition-associated metabolic signatures and to detect metabolites potentially involved in material deterioration. The research demonstrated strain-specific and substrate-driven metabolic differentiation. Plaster exhibited higher metabolic heterogeneity and stress-related pathways, whereas brick showed more conserved, growth-associated metabolic profiles. Across taxa, low-molecular-weight organic acids, including citric/isocitric, acetic, and oxalic, were recurrently detected, suggesting their potential involvement in acidification- and metal-complexation-related processes at the algal–mineral interface. Enrichment of flavin nucleotides, carboxylic acids, fatty acyls, and aromatic secondary metabolites further supports the involvement of redox activity, stress adaptation, and biofilm persistence. These findings allow a provisional ranking of the algae based on their potential for geochemical biodeterioration, as follows: PNK010 > PNK040> PNK015 > PNK021> PNK013.
Paleorecords inform the limits of Indo-Pacific coral reef survival under accelerating sea-level rise
A pilot study on aging-related effects on step performance: The role of muscle quality, size, and strength
All-2D vertical metal-semiconductor field-effect transistor with sub-10 nm channel and contact lengths
Indices of trophic and competitive relationships in a planktonic meta-network of carp ponds
Conformational cycling of the Wntless transporter drives trafficking and secretion of Wnt morphogens
Abstract Wnt proteins are lipid-modified morphogens fundamental in development and disease. During Wnt biogenesis, the G-protein-coupled receptor (GPCR)-like transporter Wntless (WLS) escorts lipidated Wnts from the endoplasmic reticulum to the plasma membrane, then transfers them to extracellular carriers, forming active and soluble morphogen-carrier complexes. To dissect the mechanisms involved, we solve cryo-EM structures of Wnt-bound WLS and unliganded WLS, and perform structure-guided functional experiments. Wnts engage WLS via three conserved hairpins, which are all required for Wnt trafficking to the cell surface and carrier-mediated secretion. Wnt release from cells is driven by dramatic conformational changes in the WLS transmembrane domain, reminiscent of GPCR activation, together with WLS extracellular rearrangements. Unexpectedly, we find that Wnt5a bound to WLS forms dimers, with implications for Wnt signaling. These findings define the mechanism of WLS conformational cycling that governs the intracellular transport and extracellular release of Wnt morphogens, essential steps in the Wnt pathway.
Co-occurrence of uranium, fluoride and nitrate in Sahelian groundwater of Agadez (Niger) drives population health risks
Molecular mechanisms of transhydrogenase activity and allosteric regulation in eukaryotic type II PHGDH Ser33
Abstract L-serine is a critical structural constituent of proteins and membrane phospholipids, playing major roles in cell signaling, metabolism and development. L-Serine is synthesized through a conserved de novo pathway starting from the glycolytic intermediate 3-phosphoglycerate (PGA), being oxidized by 3-phosphoglycerate dehydrogenase (PHGDH) into 3-phosphohydroxypyruvate (PHP). In certain organisms, PHGDH operates as a transhydrogenase using α-ketoglutarate rather than NAD + as the final electron acceptor and producing both PHP and D-2-hydroxyglutarate (2HG). We provide high-resolution X-ray crystal structures of the transhydrogenase Ser33 from Saccharomyces cerevisiae , in complex with the cofactor NADH, and with PGA, PHP, 2HG and the negative allosteric regulator L-serine. Combining extensive alanine scanning mutagenesis, enzyme activity assays and kinetics, molecular dynamics simulations, biophysical methods, and phylogenetic analysis, we establish the molecular basis of substrate recognition, transhydrogenase activity, and allosteric inhibition mechanisms, including the role of an N-terminal extension in the regulation of eukaryotic Type II PHGDHs.