ERC FUNDED PROJECTS

"This project will develop the use of relict, extraterrestrial minerals in Archean to Cenozoic slowly formed sediments as tracers of events in the solar system and cosmos, and to decipher the possible relation between such events and evolution of life and environmental change on Earth. There has been consensus that it would not be possible to reconstruct variations in the flux of different types of meteorites to Earth through the ages. Meteorite falls are rare and meteorites weather and decay rapidly on the Earth surface. However, the last years we have developed the first realistic approach to circumvent these problems. Almost all meteorite types contain a small fraction of spinel minerals that survives weathering and can be recovered from large samples of condensed sediments of any age. Inside the spinels we can locate by synchrotron-light X-ray tomography 1-30 micron sized inclusions of most of the other minerals that made up the original meteorite. With cutting-edge frontier microanalyses such as Ne-21 (solar wind, galactic rays), oxygen isotopes (meteorite group and type) and cosmic ray tracks (supernova densities) we will be able to unravel from the geological record fundamental new information about the solar system at specific times through the past 3.8 Gyr. Variations in flux and types of meteorites may reflect solar-system and galaxy gravity disturbances as well as the sequence of disruptions of the parent bodies for meteorite types known and not yet known. Cosmic-ray tracks in spinels may identify the galactic year (230 Myr) in the geological record. For the first time it will be possible to systematically relate major global biotic and tectonic events, changes in sea-level, climate and asteroid and comet impacts to what happened in the larger astronomical realm. In essence, the project is a robust approach to establish a pioneer ""astrostratigraphy"" for Earth's geological record, complementing existing bio-, chemo-, and magnetostratigraphies."

1 950 000 €

Start date: 2012-04-01, End date: 2017-03-31

In the bone-enclosed CNS, increased vascular permeability may cause life-threatening tissue swelling, and/or ischemia and inflammation which compromise tissue repair after trauma or stroke. The brain vasculature possesses several unique features collectively named the blood-brain barrier (BBB) in which passive permeability is almost completely abolished and replaced by a complex of specific transport mechanisms. The BBB is necessary to uphold the specific milieu necessary for neuronal function. Whereas breakdown of the BBB is part of many CNS diseases, including stroke, neuroinflammation, trauma and neurodegenerative disorders, its molecular mechanisms and consequences are unclear and debated. Conversely, the intact BBB is a huge obstacle for drug delivery to the brain. Research on the BBB therefore has two seemingly opposing aims: 1) to seal a damaged BBB and protect the brain from toxic blood products, and 2) to open the BBB “on demand” for drug delivery. A major problem in the BBB field has been the lack of in vivo animal models for molecular and functional studies. So far, available in vitro models are not recapitulating the in vivo BBB. Our recent work on mouse models lacking pericytes, a BBB-associated cell type, demonstrates a specific role for pericytes in the development and regulation of the mammalian BBB. These animal models are the first ones showing a general and significant BBB impairment in adulthood, and as such they provide a unique opportunity to address molecular mechanisms of BBB disruption in disease and in drug transport across the BBB. Importantly, the new models and tools that we have developed allow us to search for relevant druggable mechanisms and molecular targets in the BBB. The long-term goals of this proposal are to develop molecular strategies and tools to open and close the BBB “on demand” for drug delivery to the CNS, and to explore the importance and mechanisms of BBB dysfunction in neurodegenerative diseases and stroke.

2 499 427 €

Start date: 2012-08-01, End date: 2017-07-31

The enormous quantities of frozen carbon in the Arctic, held in shallow soils and sediments, act as “capacitors” of the global carbon system. Thawing permafrost (PF) and collapsing methane hydrates are top candidates to cause a net transfer of carbon from land/ocean to the atmosphere this century, yet uncertainties abound. Our program targets the East Siberian Arctic Ocean (ESAO), the World’s largest shelf sea, as it holds 80% of coastal PF, 80% of subsea PF and 75% of shallow hydrates. Our initial findings (e.g., Science, 2010; Nature, 2012; PNAS; 2013; Nature Geoscience, 2013, 2014) are challenging earlier notions by showing complexities in terrestrial PF-Carbon remobilization and extensive venting of methane from subsea PF/hydrates. The objective of the CC-Top Program is to transform descriptive and data-lean pictures into quantitative understanding of the CC system, to pin down the present and predict future releases from these “Sleeping Giants” of the global carbon system. The CC-Top program combines unique Arctic field capacities with powerful molecular-isotopic characterization of PF-carbon/methane to break through on: The “awakening” of terrestrial PF-C pools: CC-Top will employ great pan-arctic rivers as natural integrators and by probing the δ13C/Δ14C and molecular fingerprints, apportion release fluxes of different PF-C pools. The ESAO subsea cryosphere/methane: CC-Top will use recent spatially-extensive observations, deep sediment cores and gap-filling expeditions to (i) estimate distribution of subsea PF and hydrates; (ii) establish thermal state (thawing rate) of subsea PF-C; (iii) apportion sources of releasing methane btw subsea-PF, shallow hydrates vs seepage from the deep petroleum megapool using source-diagnostic triple-isotope fingerprinting. Arctic Ocean slope hydrates: CC-Top will investigate sites (discovered by us 2008-2014) of collapsed hydrates venting methane, to characterize geospatial distribution and causes of destabilization.

2 499 756 €

Start date: 2016-11-01, End date: 2021-10-31

Eco-immunology targets one of the great challenges in biology and medicine - how the immune system has evolved to optimize protection and minimize immunopathology (incl. autoimmune) costs. A primary target of my proposal is to study low-virulent pathogens causing mild infections, which for long have been considered harmless. Recent research suggests that this notion is false and that seemingly harmless pathogens entail delayed (‘hidden’) fitness costs. However, the mechanisms mediating these costs are still unknown. I will experimentally test if accelerated telomere degradation is a causative mechanism through which small immune costs can accumulate and be translated into senescence and reduced Darwinian fitness. Another key target is immune costs, which may be ‘hidden’ because of sexually antagonistic effects, and I will study how this may affect immune gene variation, immune costs and Darwinian fitness. These aspects are central for advancing our understanding of the evolution of disease resistance and immune function, incl. immune over-reactions (autoimmunity). My project exploits a comprehensive 32-year study of great reed warblers to analyze selection patterns in the wild (Fig. 1a), and uses established captive songbird set-ups to conduct carefully designed experiments. The exceptional quality of the long-term data set, together with cutting-edge techniques to measure and manipulate parasite infection, telomere length, oxidative stress and immune gene diversity, provides exciting opportunities to conduct research that previously was unfeasible, pushing the rapidly growing field of eco-immunology (Fig. 1b) to new frontiers. The work integrates theory and methods of evolutionary ecology, immunology and molecular biology, and has broad significance including for e.g. epidemiology and ageing research. I envision my research to change how we look upon causes, consequences (and precautions) of mild infectious, autoimmune and degenerative diseases.

2 500 000 €

Start date: 2017-08-01, End date: 2022-07-31