Averting biodiversity collapse in tropical forest protected areas

The rapid disruption of tropical forests probably imperils global biodiversity more than any other contemporary phenomenon¹⁻³. With deforestation advancing quickly, protected areas are increasingly becoming final refuges for threatened species and natural ecosystem processes. However, many protected areas in the tropics are themselves vulnerable to human encroachment and other environmental stresses⁴⁻⁹. As pressures mount, it is vital to know whether existing reserves can sustain their biodiversity. A critical constraint in addressing this question has been that data describing a broad array of biodiversity groups have been unavailable for a sufficiently large and representative sample of reserves. Here we present a uniquely comprehensive data set on changes over the past 20 to 30 years in 31 functional groups of species and 21 potential drivers of environmental change, for 60 protected areas stratified across the world’s major tropical regions. Our analysis reveals great variation in reserve ‘health’: about half of all reserves have been effective or performed passably, but the rest are experiencing an erosion of biodiversity that is often alarmingly widespread taxonomically and functionally. Habitat disruption, hunting and forest-product exploitation were the strongest predictors of declining reserve health. Crucially, environmental changes immediately outside reserves seemed nearly as important as those inside in determining their ecological fate, with changes inside reserves strongly mirroring those occurring around them. These findings suggest that tropical protected areas are often intimately linked ecologically to their surrounding habitats, and that a failure to stem broad-scale loss and degradation of such habitats could sharply increase the likelihood of serious biodiversity declines.Keywords: Ecology, Environmental scienc

Nitrogen deposition effects on ecosystem services and interactions with other pollutants and climate change

Ecosystem services are defined as the ecological and socio-economic value of goods and services provided by natural and semi-natural ecosystems. Ecosystem services are being impacted by many human induced stresses, one of them being nitrogen (N) deposition and its interactions with other pollutants and climate change. It is concluded that N directly or indirectly affects a wide range of provisioning, regulating, supporting and cultural ecosystem services, many of which are interrelated. When considering the effects of N on ecosystem services, it is important to distinguish between different types of ecosystems/species and the protection against N impacts should include other aspects related to N, in addition to biodiversity. The Working Group considered the following priorities of ecosystem services in relation to N: biodiversity; air quality/atmosphere; ecosystem changes; NO3 leaching; climate regulation and cultural issues. These are the services for which the best evidence is available in the literature. There is a conflicting interest between greenhouse gas ecosystem services and biodiversity protection; up to some point of increasing N inputs, net greenhouse gas uptake is improved, while biodiversity is already adversely affected

PPM1D mutations are oncogenic drivers of de novo diffuse midline glioma formation

Abstract The role of PPM1D mutations in de novo gliomagenesis has not been systematically explored. Here we analyze whole genome sequences of 170 pediatric high-grade gliomas and find that truncating mutations in PPM1D that increase the stability of its phosphatase are clonal driver events in 11% of Diffuse Midline Gliomas (DMGs) and are enriched in primary pontine tumors. Through the development of DMG mouse models, we show that PPM1D mutations potentiate gliomagenesis and that PPM1D phosphatase activity is required for in vivo oncogenesis. Finally, we apply integrative phosphoproteomic and functional genomics assays and find that oncogenic effects of PPM1D truncation converge on regulators of cell cycle, DNA damage response, and p53 pathways, revealing therapeutic vulnerabilities including MDM2 inhibition