Coral responses to a repeat bleaching event in Mayotte in 2010

Background High sea surface temperatures resulted in widespread coral bleaching and mortality in Mayotte Island (northern Mozambique channel, Indian Ocean: 12.1°S, 45.1°E) in April–June 2010. Methods Twenty three representative coral genera were sampled quantitatively for size class distributions during the peak of the bleaching event to measure its impact. Results Fifty two percent of coral area was impacted, comprising 19.3% pale, 10.7% bleached, 4.8% partially dead and 17.5% recently dead. Acropora, the dominant genus, was the second most susceptible to bleaching (22%, pale and bleached) and mortality (32%, partially dead and dead), only exceeded by Pocillopora (32% and 47%, respectively). The majority of genera showed intermediate responses, and the least response was shown by Acanthastrea and Leptastrea (6% pale and bleached). A linear increase in bleaching susceptibility was found from small colonies (80 cm, 33% unaffected), across all genera surveyed. Maximum mortality in 2010 was estimated at 32% of coral area or biomass, compared to half that (16%), by colony abundance. Discussion Mayotte reefs have displayed a high level of resilience to bleaching events in 1983, 1998 and the 2010 event reported here, and experienced a further bleaching event in 2016. However, prospects for continued resilience are uncertain as multiple threats are increasing: the rate of warming experienced (0.1 °C per decade) is some two to three times less than projected warming in coming decades, the interval between severe bleaching events has declined from 16 to 6 years, and evidence of chronic mortality from local human impacts is increasing. The study produced four recommendations for reducing bias when monitoring and assessing coral bleaching: coral colony size should be measured, unaffected colonies should be included in counts, quadrats or belt transects should be used and weighting coefficients in the calculation of indices should be used with caution

Status of Coral Reef Fish Communities within the Mombasa Marine Protected Area, Kenya, more than aDecade after Establishment

The abundance, trophic composition and diversity of fish were investigated in the Mombasa Marine Protected Area (MPA) on the Kenya coast over a period of four years (2004-2007) sixteen years after its establishment to determine its effectiveness. Fish monitoring data collected using belt transects revealed significant differences in fish abundance, distribution and composition between the MPA’s no-take area and a partially-protected area with controlled exploitation. Although seasonal variation was apparent in the trophic composition, annual differences over the four year study period were not significant. Results indicated that differences in fish composition within the MPA were due to a greater abundance of haemulids (nocturnal carnivores) and acanthurids (herbivores) in the no-take area than in the partially-protected area. Fish diversity also varied between the no-take area and the partially-protected area with a higher Shannon-Wiener diversity index associated with the no-take area. Dominance was higher in the partially-protected area than in the no-take area and was also higher during the southeast (SE) monsoon season. These results support the claim of greater effectiveness of the fully protected no-take area, compared to the partially-protected area in sustaining the rich fish community found in previous studies

Expert perspectives on global biodiversity loss and its drivers and impacts on people

Despite substantial progress in understanding global biodiversity loss, major taxonomic and geographic knowledge gaps remain. Decision makers often rely on expert judgement to fill knowledge gaps, but are rarely able to engage with sufficiently large and diverse groups of specialists. To improve understanding of the perspectives of thousands of biodiversity experts worldwide, we conducted a survey and asked experts to focus on the taxa and freshwater, terrestrial, or marine ecosystem with which they are most familiar. We found several points of overwhelming consensus (for instance, multiple drivers of biodiversity loss interact synergistically) and important demographic and geographic differences in specialists’ perspectives and estimates. Experts from groups that are underrepresented in biodiversity science, including women and those from the Global South, recommended different priorities for conservation solutions, with less emphasis on acquiring new protected areas, and provided higher estimates of biodiversity loss and its impacts. This may in part be because they disproportionately study the most highly threatened taxa and habitats

Achieving a nature- and people-positive future

Despite decades of increasing investment in conservation, we have not succeeded in “bending the curve” of biodiversity decline. Efforts to meet new targets and goals for the next three decades risk repeating this outcome due to three factors: neglect of increasing drivers of decline; unrealistic expectations and time frames of biodiversity recovery; and insufficient attention to justice within and between generations and across countries. Our Earth system justice approach identifies six sets of actions that when tackled simultaneously address these failings: (1) reduce and reverse direct and indirect drivers causing decline; (2) halt and reverse biodiversity loss; (3) restore and regenerate biodiversity to a safe state; (4) raise minimum wellbeing for all; (5) eliminate over-consumption and excesses associated with accumulation of capital; and (6) uphold and respect the rights and responsibilities of all communities, present and future. Current conservation campaigns primarily address actions 2 and 3, with urgent upscaling of actions 1, 4, 5, and 6 needed to help deliver the post-2020 global biodiversity framework

Diversity and Distribution of Symbiodinium Associated with Seven Common Coral Species in the Chagos Archipelago, Central Indian Ocean

The Chagos Archipelago designated as a no-take marine protected area in 2010, lying about 500 km south of the Maldives in the Indian Ocean, has a high conservation priority, particularly because of its fast recovery from the ocean-wide massive coral mortality following the 1998 coral bleaching event. The aims of this study were to examine Symbiodinium diversity and distribution associated with scleractinian corals in five atolls of the Chagos Archipelago, spread over 10,000 km 2. Symbiodinium clade diversity in 262 samples of seven common coral species, Acropora muricata, Isopora palifera, Pocillopora damicornis, P. verrucosa, P. eydouxi, Seriatopora hystrix, and Stylophora pistillata were determined using PCR-SSCP of the ribosomal internal transcribed spacer 1 (ITS1), PCR-DDGE of ITS2, and phylogenetic analyses. The results indicated that Symbiodinium in clade C were the dominant symbiont group in the seven coral species. Our analysis revealed types of Symbiodinium clade C specific to coral species. Types C1 and C3 (with C3z and C3i variants) were dominant in Acroporidae and C1 and C1c were the dominant types in Pocilloporidae. We also found 2 novel ITS2 types in S. hystrix and 1 novel ITS2 type of Symbiodinium in A. muricata. Some colonies of A. muricata and I. palifera were also associated with Symbiodinium A1. These results suggest that corals in the Chagos Archipelago host different assemblages of Symbiodinium types then their conspecifics from other locations in the Indian Ocean; and that future research will show whether these patterns in Symbiodinium genotypes may be due to local adaptation to specific conditions in the Chagos

Linking capacity development to GOOS monitoring networks to achieve sustained ocean observation

Developing enduring capacity to monitor ocean life requires investing in people and their institutions to build infrastructure, ownership, and long-term support networks. International initiatives can enhance access to scientific data, tools and methodologies, and develop local expertise to use them, but without ongoing engagement may fail to have lasting benefit. Linking capacity development and technology transfer to sustained ocean monitoring is a win-win proposition. Trained local experts will benefit from joining global communities of experts who are building the comprehensive Global Ocean Observing System (GOOS). This two-way exchange will benefit scientists and policy makers in developing and developed countries. The first step toward the GOOS is complete: identification of an initial set of biological Essential Ocean Variables (EOVs) that incorporate the Group on Earth Observations (GEO) Essential Biological Variables (EBVs), and link to the physical and biogeochemical EOVs. EOVs provide a globally consistent approach to monitoring where the costs of monitoring oceans can be shared and where capacity and expertise can be transferred globally. Integrating monitoring with existing international reporting and policy development connects ocean observations with agreements underlying many countries' commitments and obligations, including under SDG 14, thus catalyzing progress toward sustained use of the ocean. Combining scientific expertise with international capacity development initiatives can help meet the need of developing countries to engage in the agreed United Nations (UN) initiatives including new negotiations for the conservation and sustainable use of marine biological diversity of areas beyond national jurisdiction, and the needs of the global community to understand how the ocean is changing

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Abstract Background Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Funding GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file 32: Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.Peer reviewedPublisher PD

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Funding Information: GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file : Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services. Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe