The whiff of decay: Linking volatile production and extracellular enzymes to outcomes of fungal interactions at different temperatures

The terrestrial carbon cycle is largely driven by photosynthetic plants and decomposer organisms that process biomass to CO2. In forest ecosystems, the decomposers are predominantly wood decay fungi, and the response of community structure and activity to increasing global temperatures is likely critical to forest biogeochemical processes. Metabolic products can drive community structure and substrate utilisation, and the role of volatile organic compounds (VOCs), as well as extracellular enzymes, are of particular interest. Pair-wise interactions of a community of basidiomycetes were made under 3 different microclimate conditions that mimic fluctuations in local climate conditions, and the outcome of interactions was assessed in terms of: (1) which fungus won the confrontation or whether it was a draw (deadlock); (2) the production of volatile organic compounds (VOCs) and enzyme activities; and (3) the rate of decomposition. While substrate utilisation and exploitation in terms of decomposition was not affected, community response to changing temperature was underpinned by altered outcomes of interactions and changes to territory occupation, which were reflected by changes in VOC production and extracellular enzyme activity. This study underlines the importance of understanding the impact of community structure on carbon cycling in forest ecosystems under a changing climate

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice