ERC FUNDED PROJECTS

Dietary fibres are recognized for their health promoting properties; nevertheless, many of the physicochemical mechanisms behind these effects remain poorly understood. While it is understood that dietary fibres can associate with small molecules influencing, both positively or negatively their absorption, the molecular mechanism, by which these associations take place, have yet to be elucidated We propose a study of the binding in soluble dietary fibres at a molecular level to establish binding constants for various fibres and nutritionally relevant ligands. The interactions between fibres and target compounds may be quite weak, but still have a major impact on the bioavailability. To gain insight to the binding mechanisms at a level of detail that has not earlier been achieved, we will apply novel combinations of analytical techniques (MS, NMR, EPR) and both natural as well as synthetic probes to elucidate the associations in these complexes from macromolecular to atomic level. Glucans, xyloglucans and galactomannans will serve as model soluble fibres, representative of real food systems, allowing us to determine their binding constants with nutritionally relevant micronutrients, such as monosaccharides, bile acids, and metals. Furthermore, we will examine supramolecular interactions between fibre strands to evaluate possible contribution of several fibre strands to the micronutrient associations. At the atomic level, we will use complementary spectroscopies to identify the functional groups and atoms involved in the bonds between fibres and the ligands. The proposal describes a unique approach to quantify binding of small molecules by dietary fibres, which can be translated to polysaccharide interactions with ligands in a broad range of biological systems and disciplines. The findings from this study may further allow us to predictably utilize fibres in functional foods, which can have far-reaching consequences in human nutrition, and thereby also public health.

1 500 000 €

Start date: 2016-04-01, End date: 2021-03-31

Forests, of which globally 70% are managed, play a particularly important role in the global carbon cycle. Recently, forest management became a top priority on the agenda of the political negotiations to mitigate climate change because forest plantations may remove atmospheric CO2 and if used for energy production, the wood is a substitute for fossil fuel. However, this political imperative is at present running well ahead of the science required to deliver it. Despite the key implications of forest management on: 1) the carbon-energy-water balance, and 2) production, recreation and environmental protection, there are no integrated studies of its effects on the Earth s climate. The overall goal of DOFOCO is to quantify and understand the role of forest management in mitigating climate change. Specifically, I want to challenge the current focus on the carbon cycle and replace it with a total climate impact approach. Hence, the whole forest management spectrum ranging from short rotation coppice to old-growth forests will be analyzed for its effects on the water, energy and carbon cycles. Climate response of forest will be quantified by means of albedo, evapotranspiration, greenhouse gas sources and sinks and their resulting climate feedback mechanisms. The anticipated new quantitative results will be used to lay the foundations for a portfolio of management strategies which will sustain wood production while minimizing climate change impacts. DOFOCO is interdisciplinary and ground breaking because it brings together state-of-the art data and models from applied life and Earth system sciences; it will deliver the first quantitative insights into how forest management strategies can be linked to climate change mitigation.

1 296 125 €

Start date: 2010-02-01, End date: 2015-10-31

The aim of this project is to understand the causal factors contributing to the cognitive decline during senescence and to develop sensitive and standardized behaviour tests for early detection in order to increase the welfare of affected species. With the rapidly ageing population of Europe, related research is a priority in the European Union. We will focus both on characterising the ageing phenotype and the underlying biological processes in dogs as a well-established natural animal model. We develop a reliable and valid test battery applying innovative multidisciplinary methods (e.g. eye-tracking, motion path analysis, identification of behaviour using inertial sensors, EEG, fMRI, candidate gene, and epigenetics) in both longitudinal and cross-sectional studies. We expect to reveal specific environmental risk factors which hasten ageing and also protective factors which may postpone it. We aim to provide objective criteria (behavioural, physiological and genetic biomarkers) to assess and predict the ageing trajectory for specific individual dogs. This would help veterinarians to recognise the symptoms early, and initiate necessary counter actions. This approach establishes the framework for answering the broad question that how we can extend the healthy life of ageing dogs which indirectly also contributes to the welfare of the owner and decreases veterinary expenses. The detailed description of the ageing phenotype may also facilitate the use of dogs as a natural model for human senescence, including the development and application of pharmaceutical interventions. We expect that our approach offers the scientific foundation to delay the onset of cognitive ageing in dog populations by 1-2 years, and also increase the proportion of dogs that enjoy healthy ageing.

1 202 500 €

Start date: 2016-06-01, End date: 2021-05-31

Plants are continuously exposed to a wide variety of pathogenic attackers that cause major crop losses to agriculture worldwide. Unlike vertebrates that use specialized immune cells to detect non-self, each individual plant cell is thought to be capable of launching an effective immune response. Plant immune responses are largely orchestrated by the immune hormone, salicylic acid (SA), which accumulates upon infection and establishes both local and broad-spectrum systemic immunity. SA induces the reprogramming of thousands of genes to prioritize immune responses over normal cellular growth functions. Consequently, commercial SA mimics have been developed and applied as crop protection agents worldwide. Nonetheless, how SA reprograms the transcriptome remains poorly understood yet is critical for the design of improved crop protection strategies that avoid plant growth and yield penalties. SA-induced transcription reprogramming is largely mediated by NPR1, a master coactivator of gene expression. We recently reported that direct perception of SA by a Cullin3-RING ubiquitin ligase (CRL3) in the nucleus regulates the transcriptional activity of NPR1 by targeting it for degradation via the ubiquitin proteasome system (UPS). Our latest data suggest that ubiquitination by CRL3 and other ubiquitin chain modifying enzymes may be processive and establishes a transcriptional timer for NPR1 activity. This proposal aims to understand the flexibility and necessity of this transcriptional ubiquitin timer in meeting cellular demands for dynamic gene expression during SA-mediated plant immune responses. Moreover, we will uncover the full substrate ranges of SA-induced ubiquitin ligases and their post-translational regulation to precisely chart the intimate roles the UPS plays in coordinating plant immune gene expression. Importantly, these findings will provide novel chemical and genetic targets that can be harnessed in future crop improvement strategies.

1 499 960 €

Start date: 2016-03-01, End date: 2021-02-28