Habitat patches providing south–north connectivity are under-protected in a fragmented landscape

As species’ ranges shift to track climate change, conservationists increasingly recognize the need to consider connectivity when designating protected areas (PAs). In fragmented landscapes, some habitat patches are more important than others in maintaining connectivity, and methods are needed for their identification. Here, using the Condatis methodology, we model range expansion through an adaptation of circuit theory. Specifically, we map ‘flow’ through 16 conservation priority habitat networks in England, quantifying how patches contribute to functional South–North connectivity. We also explore how much additional connectivity could be protected via a connectivity-led protection procedure. We find high-flow patches are often left out of existing PAs; across 12 of 16 habitat networks, connectivity protection falls short of area protection by 13.6% on average. We conclude that the legacy of past protection decisions has left habitat-specialist species vulnerable to climate change. This situation may be mirrored in many countries which have similar habitat protection principles. Addressing this requires specific planning tools that can account for the directions species may shift. Our connectivity-led reserve selection procedure efficiently identifies additional PAs that prioritize connectivity, protecting a median of 40.9% more connectivity in these landscapes with just a 10% increase in area

Evolution of substrate specificity in a recipient's enzyme following horizontal gene transfer

Despite the prominent role of horizontal gene transfer (HGT) in shaping bacterial metabolism, little is known about the impact of HGT on the evolution of enzyme function. Specifically, what is the influence of a recently acquired gene on the function of an existing gene? For example, certain members of the genus Corynebacterium have horizontally acquired a whole L-tryptophan biosynthetic operon, whereas in certain closely related actinobacteria, for example, Mycobacterium, the trpF gene is missing. In Mycobacterium, the function of the trpF gene is performed by a dual-substrate (βα)8 phosphoribosyl isomerase (priA gene) also involved in L-histidine (hisA gene) biosynthesis. We investigated the effect of a HGT-acquired TrpF enzyme upon PriA’s substrate specificity in Corynebacterium through comparative genomics and phylogenetic reconstructions. After comprehensive in vivo and enzyme kinetic analyses of selected PriA homologs, a novel (βα)8 isomerase subfamily with a specialized function in L-histidine biosynthesis, termed subHisA, was confirmed. X-ray crystallography was used to reveal active-site mutations in subHisA important for narrowing of substrate specificity, which when mutated to the naturally occurring amino acid in PriA led to gain of function. Moreover, in silico molecular dynamic analyses demonstrated that the narrowing of substrate specificity of subHisA is concomitant with loss of ancestral protein conformational states. Our results show the importance of HGT in shaping enzyme evolution and metabolism

Local-scale attributes determine the suitability of woodland creation sites for Diptera

New native woodlands are typically created in a small and isolated configuration, potentially reducing their value as a resource for biodiversity. The use of ecological networks for habitat restoration and creation could be beneficial for woodland biodiversity. This approach is conceptualised as local and landscape-scale conservation actions to increase the area, quality, amount and connectivity of habitat types. However, there is limited evidence about the value of secondary woodlands and the relative or combined effects of network variables for woodland insects.  Seventy-eight woodland sites created in the last 160 years across England and Scotland were sampled for hoverflies (Diptera: Syrphidae) and craneflies (Diptera: Tipuloidea), using two Malaise net traps placed in the centre of each woodland. The diversity of insects supported by created woodland patches was analysed using measures of dissimilarity, and the relative direct and indirect effects of ecological network variables on their abundance and species richness were assessed using structural equation models.  We found 27% of British woodland hoverfly species and 43% of British woodland cranefly species in the study sites, indicating that woodland insects are colonising created native woodlands, despite their fragmented nature. However, these species communities were highly variable across woodland patches.  Landscape-scale variables had no effect on woodland-associated hoverflies or craneflies relative to local-scale variables. Local-scale variables relating to habitat 34 quality (i.e. structural heterogeneity of trees and understory cover) had the strongest influence on abundance and species richness.  Synthesis and applications – To benefit woodland-associated Diptera, woodland creation and restoration should maintain a focus on habitat quality. This should include active management to facilitate a diverse tree and understorey vegetation structure. Many woodlands in the UK are privately owned and landowners should be encouraged to plant and actively manage their woodlands to increase structural heterogeneity and resources for woodland insects

Species mobility and landscape context determine the importance of local and landscape-level attributes

Conservation strategies to tackle habitat loss and fragmentation require actions at local (e.g. improving/expanding existing habitat patches) and landscape level (e.g. creating new habitat in the matrix). However, the relative importance of these actions for biodiversity is still poorly understood, leading to debate on how to prioritise conservation activities. Here, we assess the relative importance of local vs. landscape-level attributes in determining the use of woodlands by bats in fragmented landscapes; we also compare the role of habitat amount in the surrounding landscape per se vs. a combination of both habitat amount and configuration and explore whether the relative importance of these attributes varies with species mobility and landscape context. We conducted acoustic surveys in 102 woodland patches in the UK which form part of the WrEN project (www.wren-project.com), a large-scale natural experiment designed to study the effects of 160 years of woodland creation on biodiversity and inform landscape-scale conservation. We used multivariate analysis and a model-selection approach to assess the relative importance of local (e.g. vegetation structure) and landscape-level (e.g. amount/configuration of surrounding land types) attributes on bat occurrence and activity levels. Species mobility was an important trait determining the relative importance of local vs. landscape-level attributes for different bat species. Lower mobility species were most strongly influenced by local habitat quality; the landscape became increasingly important for higher mobility species. At the landscape-scale, a combination of habitat amount and configuration appeared more important than habitat amount alone for lower mobility species, whilst the opposite was observed for higher mobility species. Regardless of species mobility, landscape-level attributes appeared more important for bats in a more homogeneous and intensively farmed landscape. Conservation strategies involving habitat creation and restoration should take into account the mobility of target species and prioritise landscape-level actions in more homogeneous and intensively farmed landscapes where habitat loss and fragmentation have been more sever

Bird-community responses to habitat creation in a long-term, large-scale natural experiment

Ecosystem function and resilience are compromised when habitats become fragmented due to land-use change. This has led to national and international conservation strategies aimed at restoring habitat extent and improving functional connectivity (i.e. maintaining dispersal processes). However, biodiversity responses to landscape-scale habitat creation and the relative importance of spatial and temporal scales is poorly understood, and there is disagreement over which conservation strategies should be prioritised. Addressing these knowledge gaps has been challenging because (1) there can be a significant time lag between habitat creation and biodiversity responses, and (2) many taxa respond to landscape characteristics over large spatial scales. These conditions can be difficult to replicate in a controlled setting but can be simulated using ‘natural’ experiments. Here, we used 160 years of historic post-agricultural woodland creation as a natural experiment to evaluate biodiversity responses to landscape-scale habitat creation. Specifically, we disentangle the direct and indirect relationships between bird abundance and diversity, ecological continuity, patch characteristics and landscape structure, and quantify the relative importance of local and landscape scales. Results suggest that ecological continuity has an indirect effect on total bird species richness through its direct effects on stand structure. However, for functional groups most closely associated with woodland habitats, ecological continuity had little influence. This was probably because woodlands were rapidly colonised by woodland generalists in < 10 years (the minimum patch age), but were on average too young (median 50 years) to be colonised by woodland specialists. Local, patch characteristics were relatively more important than landscape characteristics. We conclude that biodiversity responses to habitat creation are dependent on local and landscape-scale factors that interact across time and space. We also suggest that knowledge gained from studies of habitat fragmentation/loss should be used to inform habitat creation with caution, since the two are not necessarily reciprocal.This article is protected by copyright. All rights reserve

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

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease