Global determinants of freshwater and marine fish genetic diversity

Genetic diversity is estimated to be declining faster than species diversity under escalating threats, but its spatial distribution remains poorly documented at the global scale. Theory predicts that similar processes should foster congruent spatial patterns of genetic and species diversity, but empirical studies are scarce. Using a mined database of 50,588 georeferenced mitochondrial DNA barcode sequences (COI) for 3,815 marine and 1,611 freshwater fish species respectively, we examined the correlation between genetic diversity and species diversity and their global distributions in relation to climate and geography. Genetic diversity showed a clear spatial organisation, but a weak association with species diversity for both marine and freshwater species. We found a predominantly positive relationship between genetic diversity and sea surface temperature for marine species. Genetic diversity of freshwater species varied primarily across the regional basins and was negatively correlated with average river slope. The detection of genetic diversity patterns suggests that conservation measures should consider mismatching spatial signals across multiple facets of biodiversity

An integrated framework to identify wildlife populations under threat from climate change

Climate change is a major threat to global biodiversity that will produce a range of new selection pressures. Understanding species responses to climate change requires an interdisciplinary perspective, combining ecological, molecular and environmental approaches. We propose an applied integrated framework to identify populations under threat from climate change based on their extent of exposure, inherent sensitivity due to adaptive and neutral genetic variation and range shift potential. We consider intraspecific vulnerability and population-level responses, an important but often neglected conservation research priority. We demonstrate how this framework can be applied to vertebrates with limited dispersal abilities using empirical data for the bat Plecotus austriacus. We use ecological niche modelling and environmental dissimilarity analysis to locate areas at high risk of exposure to future changes. Combining outlier tests with genotype–environment association analysis, we identify potential climate-adaptive SNPs in our genomic data set and differences in the frequency of adaptive and neutral variation between populations. We assess landscape connectivity and show that changing environmental suitability may limit the future movement of individuals, thus affecting both the ability of populations to shift their distribution to climatically suitable areas and the probability of evolutionary rescue through the spread of adaptive genetic variation among populations. Therefore, a better understanding of movement ecology and landscape connectivity is needed for predicting population persistence under climate change. Our study highlights the importance of incorporating genomic data to determine sensitivity, adaptive potential and range shift potential, instead of relying solely on exposure to guide species vulnerability assessments and conservation planning

Identifying barriers to gene flow and hierarchical conservation units from seascape genomics : a modelling framework applied to a marine predator

The ongoing decline of large marine vertebrates must be urgently mitigated, particularly under increasing levels of climate change and other anthropogenic pressures. However, characterizing the connectivity among populations remains one of the greatest challenges for the effective conservation of an increasing number of endangered species. Achieving conservation targets requires an understanding of which seascape features influence dispersal and subsequent genetic structure. This is particularly challenging for adult-disperser species, and when distribution-wide sampling is difficult. Here, we developed a two-step modelling framework to investigate how seascape features drive the genetic connectivity of marine species without larval dispersal, to better guide the design of marine protected area networks and corridors. We applied this framework to the endangered grey reef shark, Carcharhinus amblyrhynchos, a reef-associated shark distributed across the tropical Indo-Pacific. In the first step, we developed a seascape genomic approach based on isolation-by-resistance models involving circuit theory applied to 515 shark samples, genotyped for 4991 nuclear single-nucleotide polymorphisms. We show that deep oceanic areas act as strong barriers to dispersal, while proximity to habitat facilitates dispersal. In the second step, we predicted the resulting genetic differentiation across the entire distribution range of the species, providing both local and global-scale conservation units for future management guidance. We found that grey reef shark populations are more fragmented than expected for such a mobile species, raising concerns about the resilience of isolated populations under high anthropogenic pressures. We recommend the use of this framework to identify barriers to gene flow and to help in the delineation of conservation units at different scales, together with its integration across multiple species when considering marine spatial planning.Peer reviewe

Maximizing regional biodiversity requires a mosaic of protection levels

Protected areas are the flagship management tools to secure biodiversity from anthropogenic impacts. However, the extent to which adjacent areas with distinct protection levels host different species numbers and compositions remains uncertain. Here, using reef fishes, European alpine plants, and North American birds, we show that the composition of species in adjacent Strictly Protected, Restricted, and Non-Protected areas is highly dissimilar, whereas the number of species is similar, after controlling for environmental conditions, sample size, and rarity. We find that between 12% and 15% of species are only recorded in Non-Protected areas, suggesting that a non-negligible part of regional biodiversity occurs where human activities are less regulated. For imperiled species, the proportion only recorded in Strictly Protected areas reaches 58% for fishes, 11% for birds, and 7% for plants, highlighting the fundamental and unique role of protected areas and their environmental conditions in biodiversity conservation

Reviewing the ecosystem services, societal goods, and benefits of marine protected areas

Marine protected areas (MPAs) are globally important environmental management tools that provide protection from the effects of human exploitation and activities, supporting the conservation of marine biological diversity, habitats, ecosystems and the processes they host, as well as resources in a broad sense. Consequently, they are also expected to manage and enhance marine ecosystem services and material, non-material, consumptive and non-consumptive goods, and benefits for humans. There is however certain confusion on what constitutes an ecosystem service, and it is not always easy to distinguish between them and societal benefits. The main nuance is that an ecosystem service is the aptitude an ecosystem has or develops naturally or as consequence of a management action, and that manifests through its own properties (productivity, diversity, stability, quality of its key parameters, etc.), while a societal benefit is the economic or other profitability (emotional, educational, scientific, etc.) that humans obtain from said service or quality. In this work, 268 publications, together with our own experiences in the different investigations carried out in the MPAs that are part of the BiodivERsA3-2015-21 RESERVEBENEFIT European project, have been selected, reviewed and discussed to analyze the knowledge status of the expected ecosystem services of MPAs and the societal benefits derived from them, sometimes providing information on their evidence, when they exist. We define and classify the effects of protection, ecosystem services and societal benefits and elaborate a conceptual model of the cause-effect relationships between them

Biologically representative and well-connected marine reserves enhance biodiversity persistence in conservation planning

Current methods in conservation planning for promoting the persistence of biodiversity typically focus on either representing species geographic distributions or maintaining connectivity between reserves, but rarely both, and take a focal species, rather than a multispecies, approach. Here, we link prioritization methods with population models to explore the impact of integrating both representation and connectivity into conservation planning for species persistence. Using data on 288 Mediterranean fish species with varying conservation requirements, we show that: (1) considering both representation and connectivity objectives provides the best strategy for enhanced biodiversity persistence and (2) connectivity objectives were fundamental to enhancing persistence of small-ranged species, which are most in need of conservation, while the representation objective benefited only wide-ranging species. Our approach provides a more comprehensive appraisal of planning applications than approaches focusing on either representation or connectivity, and will hopefully contribute to build more effective reserve networks for the persistence of biodiversity

The Scaffolding Function of LSD1 Controls DNA Methylation in Mouse ESCs

Lysine-specific histone demethylase 1 (LSD1), which demethylates mono- or di- methylated histone H3 on lysine 4 (H3K4me1/2), is essential for early embryogenesis and development. Here we show that LSD1 is dispensable for mouse embryonic stem cell (ESC) self-renewal but is required for mouse ESC growth and differentiation. Reintroduction of a catalytically-impaired LSD1 (LSD1MUT) recovers the proliferation capability of mouse ESCs, yet the enzymatic activity of LSD1 is essential to ensure proper differentiation. Indeed, increased H3K4me1 in Lsd1 knockout (KO) mouse ESCs does not lead to major changes in global gene expression programs related to stemness. However, ablation of LSD1 but not LSD1MUT results in decreased DNMT1 and UHRF1 proteins coupled to global hypomethylation. We show that both LSD1 and LSD1MUT control protein stability of UHRF1 and DNMT1 through interaction with HDAC1 and the ubiquitin-specific peptidase 7 (USP7), consequently, facilitating the deacetylation and deubiquitination of DNMT1 and UHRF1. Our studies elucidate a mechanism by which LSD1 controls DNA methylation in mouse ESCs, independently of its lysine demethylase activity

The nuclear receptor PPARγ selectively inhibits Th17 differentiation in a T cell–intrinsic fashion and suppresses CNS autoimmunity

T helper cells secreting interleukin (IL)-17 (Th17 cells) play a crucial role in autoimmune diseases like multiple sclerosis (MS). Th17 differentiation, which is induced by a combination of transforming growth factor (TGF)-β/IL-6 or IL-21, requires expression of the transcription factor retinoic acid receptor–related orphan receptor γt (RORγt). We identify the nuclear receptor peroxisome proliferator–activated receptor γ (PPARγ) as a key negative regulator of human and mouse Th17 differentiation. PPARγ activation in CD4+ T cells selectively suppressed Th17 differentiation, but not differentiation into Th1, Th2, or regulatory T cells. Control of Th17 differentiation by PPARγ involved inhibition of TGF-β/IL-6–induced expression of RORγt in T cells. Pharmacologic activation of PPARγ prevented removal of the silencing mediator for retinoid and thyroid hormone receptors corepressor from the RORγt promoter in T cells, thus interfering with RORγt transcription. Both T cell–specific PPARγ knockout and endogenous ligand activation revealed the physiological role of PPARγ for continuous T cell–intrinsic control of Th17 differentiation and development of autoimmunity. Importantly, human CD4+ T cells from healthy controls and MS patients were strongly susceptible to PPARγ-mediated suppression of Th17 differentiation. In summary, we report a PPARγ-mediated T cell–intrinsic molecular mechanism that selectively controls Th17 differentiation in mice and in humans and that is amenable to pharmacologic modulation. We therefore propose that PPARγ represents a promising molecular target for specific immunointervention in Th17-mediated autoimmune diseases such as MS

SCORE2-Diabetes: 10-year cardiovascular risk estimation in type 2 diabetes in Europe

Aims: To develop and validate a recalibrated prediction model (SCORE2-Diabetes) to estimate the 10-year risk of cardiovascular disease (CVD) in individuals with type 2 diabetes in Europe. Methods and results: SCORE2-Diabetes was developed by extending SCORE2 algorithms using individual-participant data from four large-scale datasets comprising 229 460 participants (43 706 CVD events) with type 2 diabetes and without previous CVD. Sex-specific competing risk-adjusted models were used including conventional risk factors (i.e. age, smoking, systolic blood pressure, total, and HDL-cholesterol), as well as diabetes-related variables (i.e. age at diabetes diagnosis, glycated haemoglobin [HbA1c] and creatinine-based estimated glomerular filtration rate [eGFR]). Models were recalibrated to CVD incidence in four European risk regions. External validation included 217 036 further individuals (38 602 CVD events), and showed good discrimination, and improvement over SCORE2 (C-index change from 0.009 to 0.031). Regional calibration was satisfactory. SCORE2-Diabetes risk predictions varied several-fold, depending on individuals' levels of diabetes-related factors. For example, in the moderate-risk region, the estimated 10-year CVD risk was 11% for a 60-year-old man, non-smoker, with type 2 diabetes, average conventional risk factors, HbA1c of 50 mmol/mol, eGFR of 90 mL/min/1.73 m2, and age at diabetes diagnosis of 60 years. By contrast, the estimated risk was 17% in a similar man, with HbA1c of 70 mmol/mol, eGFR of 60 mL/min/1.73 m2, and age at diabetes diagnosis of 50 years. For a woman with the same characteristics, the risk was 8% and 13%, respectively. Conclusion: SCORE2-Diabetes, a new algorithm developed, calibrated, and validated to predict 10-year risk of CVD in individuals with type 2 diabetes, enhances identification of individuals at higher risk of developing CVD across Europe