Ectomycorrhizal fungi integrate nitrogen mobilisation and mineral weathering in boreal forest soil.

Tree growth in boreal forests is driven by ectomycorrhizal fungal mobilisation of organic nitrogen and mineral nutrients in soils with discrete organic and mineral horizons. However, there are no studies of how ectomycorrhizal mineral weathering and organic nitrogen mobilisation processes are integrated across the soil profile. We studied effects of organic matter (OM) availability on ectomycorrhizal functioning by altering the proportions of natural organic and mineral soil in reconstructed podzol profiles containing Pinus sylvestris plants, using 13 CO2 pulse labelling, patterns of naturally occurring stable isotopes (26 Mg and 15 N) and high-throughput DNA sequencing of fungal amplicons. Reduction in OM resulted in nitrogen limitation of plant growth and decreased allocation of photosynthetically derived carbon and mycelial growth in mineral horizons. Fractionation patterns of 26 Mg indicated that magnesium mobilisation and uptake occurred primarily in the deeper mineral horizon and was driven by carbon allocation to ectomycorrhizal mycelium. In this horizon, relative abundance of ectomycorrhizal fungi, carbon allocation and base cation mobilisation all increased with increased OM availability. Allocation of carbon through ectomycorrhizal fungi integrates organic nitrogen mobilisation and mineral weathering across soil horizons, improving the efficiency of plant nutrient acquisition. Our findings have fundamental implications for sustainable forest management and belowground carbon sequestration.

Multiple enzymatic approaches to hydrolysis of fungal ß-glucans by the soil bacterium Chitinophaga pinensis.

The genome of the soil Bacteroidota Chitinophaga pinensis encodes a large number of glycoside hydrolases (GHs) with noteworthy features and potentially novel functions. Several are predicted to be active on polysaccharide components of fungal and oomycete cell walls, such as chitin, ß-1,3-glucan and ß-1,6-glucan. While several fungal ß-1,6-glucanase enzymes are known, relatively few bacterial examples have been characterised to date. We have previously demonstrated that C. pinensis shows strong growth using ß-1,6-glucan as the sole carbon source, with the efficient release of oligosaccharides from the polymer. We here characterise the capacity of the C. pinensis secretome to hydrolyse the ß-1,6-glucan pustulan and describe three distinct enzymes encoded by its genome, all of which show different levels of ß-1,6-glucanase activity and which are classified into different GH families. Our data show that C. pinensis has multiple tools to deconstruct pustulan, allowing the species' broad utility of this substrate, with potential implications for bacterial biocontrol of pathogens via cell wall disruption. Oligosaccharides derived from fungal ß-1,6-glucans are valuable in biomedical research and drug synthesis, and these enzymes could be useful tools for releasing such molecules from microbial biomass, an underexploited source of complex carbohydrates.

Elimination of fibrin polymer formation or crosslinking, but not fibrinogen deficiency, is protective against diet-induced obesity and associated pathologies.

BACKGROUND: Obesity predisposes individuals to metabolic syndrome, which increases the risk of cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD), and type 2 diabetes. A pathological manifestation of obesity is the activation of the coagulation system. In turn, extravascular fibrin(ogen) deposits accumulate in adipose tissues and liver. These deposits promote adiposity and downstream sequelae by driving pro-inflammatory macrophage function through binding the leukocyte integrin receptor αM ß2 . OBJECTIVES: An unresolved question is whether conversion of soluble fibrinogen to a crosslinked fibrin matrix is required to exacerbate obesity-driven diseases. METHODS: Here, fibrinogen-deficient/depleted mice (Fib- or treated with siRNA against fibrinogen [siFga]), mice expressing fibrinogen that cannot polymerize to fibrin (FibAEK ), and mice deficient in the fibrin crosslinking transglutaminase factor XIII (FXIII-) were challenged with a high-fat diet (HFD) and compared to mice expressing a mutant form of fibrinogen lacking the αM ß2 -binding domain (Fib𝛾390-396A ). RESULTS AND CONCLUSIONS: Consistent with prior studies, Fib𝛾390-396A mice were significantly protected from increased adiposity, NAFLD, hypercholesterolemia, and diabetes while Fib- and siFga-treated mice gained as much weight and developed obesity-associated pathologies identical to wildtype mice. FibAEK and FXIII- mice displayed an intermediate phenotype with partial protection from some obesity-associated pathologies. Results here indicate that fibrin(ogen) lacking αM ß2 binding function offers substantial protection from obesity and associated disease that is partially recapitulated by preventing fibrin polymer formation or crosslinking of the wildtype molecule, but not by reduction or complete elimination of fibrinogen. Finally, these findings support the concept that fibrin polymerization and crosslinking are required for the full implementation of fibrin-driven inflammation in obesity.

Assessing the impact of alcohol consumption on the genetic contribution to mean corpuscular volume.

The relationship between the genetic loci that influence mean corpuscular volume (MCV) and those associated with excess alcohol drinking is unknown. We used white British participants from the UK Biobank (n = 362 595) to assess the association between alcohol consumption and MCV, and whether this was modulated by genetic factors. Multivariable regression was applied to identify predictors of MCV. GWAS, with and without stratification for alcohol consumption, determined how genetic variants influence MCV. SNPs in ADH1B, ADH1C and ALDH1B were used to construct a genetic score to test the assumption that acetaldehyde formation is an important determinant of MCV. Additional investigations using Mendelian randomization and phenome-wide association analysis were conducted. Increasing alcohol consumption by 40 g/week resulted in a 0.30% [95% confidence interval CI: 0.30-0.31%] increase in MCV (P < 1.0 × 10-320). Unstratified (irrespective of alcohol intake) GWAS identified 212 loci associated with MCV, of which 108 were novel. There was no heterogeneity of allelic effects by drinking status. No association was found between MCV and the genetic score generated from alcohol metabolizing genes. Mendelian randomization demonstrated a causal effect for alcohol on MCV. Seventy-one SNP-outcome pairs reached statistical significance in phenome-wide association analysis, with evidence of shared genetic architecture for MCV and thyroid dysfunction, and mineral metabolism disorders. MCV increases linearly with alcohol intake in a causal manner. Many genetic loci influence MCV, with new loci identified in this analysis that provide novel biological insights. However, there was no interaction between alcohol consumption and the allelic variants associated with MCV.