Combating the effects of climatic change on forests by mitigation strategies

<p>Abstract</p> <p>Background</p> <p>Forests occur across diverse biomes, each of which shows a specific composition of plant communities associated with the particular climate regimes. Predicted future climate change will have impacts on the vulnerability and productivity of forests; in some regions higher temperatures will extend the growing season and thus improve forest productivity, while changed annual precipitation patterns may show disadvantageous effects in areas, where water availability is restricted. While adaptation of forests to predicted future climate scenarios has been intensively studied, less attention was paid to mitigation strategies such as the introduction of tree species well adapted to changing environmental conditions.</p> <p>Results</p> <p>We simulated the development of managed forest ecosystems in Germany for the time period between 2000 and 2100 under different forest management regimes and climate change scenarios. The management regimes reflect different rotation periods, harvesting intensities and species selection for reforestations. The climate change scenarios were taken from the IPCC's Special Report on Emission Scenarios (SRES). We used the scenarios A1B (rapid and successful economic development) and B1 (high level of environmental and social consciousness combined with a globally coherent approach to a more sustainable development). Our results indicate that the effects of different climate change scenarios on the future productivity and species composition of German forests are minor compared to the effects of forest management.</p> <p>Conclusions</p> <p>The inherent natural adaptive capacity of forest ecosystems to changing environmental conditions is limited by the long life time of trees. Planting of adapted species and forest management will reduce the impact of predicted future climate change on forests.</p

A disease-associated gene desert directs macrophage inflammation through ETS2

Increasing rates of autoimmune and inflammatory disease present a burgeoning threat to human health1. This is compounded by the limited efficacy of available treatments1 and high failure rates during drug development2, highlighting an urgent need to better understand disease mechanisms. Here we show how functional genomics could address this challenge. By investigating an intergenic haplotype on chr21q22—which has been independently linked to inflammatory bowel disease, ankylosing spondylitis, primary sclerosing cholangitis and Takayasu’s arteritis3–6—we identify that the causal gene, ETS2, is a central regulator of human inflammatory macrophages and delineate the shared disease mechanism that amplifies ETS2 expression. Genes regulated by ETS2 were prominently expressed in diseased tissues and more enriched for inflammatory bowel disease GWAS hits than most previously described pathways. Overexpressing ETS2 in resting macrophages reproduced the inflammatory state observed in chr21q22-associated diseases, with upregulation of multiple drug targets, including TNF and IL-23. Using a database of cellular signatures7, we identified drugs that might modulate this pathway and validated the potent anti-inflammatory activity of one class of small molecules in vitro and ex vivo. Together, this illustrates the power of functional genomics, applied directly in primary human cells, to identify immune-mediated disease mechanisms and potential therapeutic opportunities