ERC FUNDED PROJECTS

This project addresses a key issue in fundamental research - one that has challenged ecologists ever since Darwin s time that is why some species are common, and others rare, and why, despite marked turnover at the level of individual species abundances, the structure of a community is generally conserved through time. Its aim is to examine the temporal dynamics of species abundance distributions (SADs), and to assess the capacity of these distributions to withstand change (resistance) and to recover from change (resilience). These are topical and important questions given the increasing impact that humans are having on the natural world. There are three components to the research. First, we will model SADs and predict responses to a range of events including climate change and the arrival of invasive species. A range of modeling approaches (including neutral, niche and statistical) will be adopted; by incorporating temporal turnover in hitherto static models we will advance the field. Second, we will test predictions concerning the resistance and resilience of SADs by a comparative analysis of existing data sets (that encompass communities in terrestrial, freshwater and marine environments for ecosystems extending from the poles to the tropics) and through a new field experiment that quantifies temporal turnover across a community (unicellular organisms to vertebrates) in relation to factors both natural (dispersal limitation) and anthropogenic (human disturbance) thought to shape SADs. In the final part of the project we will apply these new insights into the temporal dynamics of SADs to two important conservation challenges. These are 1) the conservation of biodiversity in a heavily utilized European landscape (Fife, Scotland) and 2) the conservation of biodiversity in Mamirauá and Amaña reserves in Amazonian flooded forest. Taken together this research will not only shed new light on the structure of ecological communities but will also aid conservation.

1 812 782 €

Start date: 2010-08-01, End date: 2016-01-31

CDREG develops the major new Earth system science research hypothesis that tectonic-related variations in Earth’s atmospheric CO2 concentration ([CO2]a) drive negative ecological feedbacks on terrestrial silicate weathering rates that stabilise further [CO2]a change and regulate climate. This paradigm-changing hypothesis integrates ecological and abiotic controls on silicate weathering to understand how terrestrial ecosystems have shaped past Earth system dynamics. The proposed ecological feedbacks are mechanistically linked to the extent and activities of forested ecosystems and their symbiotic fungal partners as the primary engines of biological weathering. CDREG’s core hypothesis establishes an exciting cross-disciplinary Research Programme that offers novel opportunities for major breakthroughs implemented through four linked hypothesis-driven work packages (WPs) employing experimental, geochemical and numerical modelling approaches. WP1 quantitatively characterises [CO2]a-driven tree/grass-fungal mineral weathering by coupling metabolic profiling with advanced nanometre scale surface metrological techniques for investigating hyphal-mineral interactions. WP2 quantifies the role [CO2]a-drought interactions on savanna tree mortality and C4 grass survivorship, plus symbiotic fungal-driven mineral weathering. WP3 exploits the past 8 Ma of marine sediment archives to investigate the links between forest to savanna transition, terrestrial weathering, fire, and climate in Africa. WP4 integrates findings from WP1-3 into a new Earth system modelling framework to rigorously investigate the biogeochemical feedbacks of [CO2]a-regulated ecological weathering on [CO2]a via marine carbonate deposition and organic C burial. The ultimate goal is to provide a new synthesis in which the role of [CO2]a in regulating the ecological weathering engine across scales from root-associated microorganisms to terrestrial ecosystems is mechanistically understood and assessed.

2 271 980 €

Start date: 2013-06-01, End date: 2018-05-31

Cooperation poses a problem to evolutionary theory because it can be exploited by selfish individuals. Evolutionary biologists have developed a detailed theoretical overview of possible solutions to the problem of cooperation. In contrast to our theoretical understanding of potential solutions, however,, we have been relatively unsuccessful at applying theory to understand observations of cooperative behaviour nature. We present a novel and interdisciplinary programme of research to address this problem by empirically testing assumptions and predictions of several leading explanations for cooperation. We will develop theory to make explicit testable predictions for specific systems. We will exploit the advantage offered by different study systems: experiments with bacteria, comparative studies on cooperative breeding vertebrates, and experiments on humans. In addition to addressing specific hypotheses, we will show how evolutionary theory links and differentiates explanations for cooperation across various taxa and levels of biological organization.

1 200 000 €

Start date: 2009-10-01, End date: 2015-09-30

Understanding the process of spontaneous mutation is fundamental for understanding the genetic basis of quantitative variation, the threat posed by declining population size in conservation biology and the distribution of nucleotide variation in the genome. I will address these and other unanswered questions concerning the evolutionary impact of spontaneous mutation using the house mouse as a model system. With the first, highly replicated mutation accumulation (MA) experiment in any vertebrate, I will study the impact of mutation accumulation on fitness and other quantitative traits and on genomic variation. I will pay particular attention to the effects of mutations in the heterozygous state, since this is important for resolving two important questions: 1. The threat posed by deleterious mutation accumulation in humans, where natural selection has weakened in many populations, and in endangered species, where declining effective population size has made selection less effective, and 2. The extent by which new mutations sustain response to artificial selection. By characterizing many thousands of mutation events by genome sequencing of MA lines and wild mice, I will determine the molecular spectrum and the factors explaining mutation rate variation across the genome. I will exploit this new knowledge to address the long-unanswered question of the causes of correlations between nucleotide diversity and the recombination rate and the density of conserved genomic elements. I will develop new approaches, incorporating the simultaneous action of mutation, selection, drift and recombination, to determine the contributions of background selection and selective sweeps to variation in nucleotide diversity, and to quantify the contributions of coding and noncoding mutations to fitness variation. The project will lead to substantial advances in the understanding of the role of new mutations in explaining phenotypic and molecular diversity in mammals.

2 499 331 €

Start date: 2017-01-01, End date: 2021-12-31

Division of labour is fundamental to the evolution of life on earth, allowing genes to work together to form genomes, cells to build organisms, pathogens to escape immune attack, and eusocial insect societies to achieve ecological dominance. Consequently, if we want to understand how life on earth evolved, we need to understand why division of labour does or, just as importantly, does not evolve. There are two major outstanding problems for our understanding of division of labour: First, how can we explain why division of labour has evolved with some traits, in some species, but not others? Given the potential benefits of dividing labour, why does it not arise more frequently in cooperative species? Second, in cases where division of labour has evolved, how can we explain the form that it takes? Why do factors such as the degree of specialisation, or mechanism used to produce different phenotypes, vary across species? I will combine my social evolution expertise with novel synthetic and genomic approaches to address these problems. I will explain the distribution and form of division of labour in the natural world, with an interdisciplinary research programme, divided into four work packages: (1) I will provide the first experimental test of the fundamental assumption that division of labour provides an efficiency benefit, by synthetically manipulating bacteria. (2) I will test how selection has acted for and against the evolution of division of labour in natural populations of bacteria, using novel genomic analysis techniques. (3) I will determine why division of labour evolved in some species, but not others, with an across species study on insects, and experimental evolution of bacteria. (4) I will establish a new field of research on why different species use different mechanisms to divide labour: genetic differences, environmental cues, or random assignment of roles. I will develop theory to explain this variation, and test this theory experimentally.

2 491 766 €

Start date: 2020-01-01, End date: 2024-12-31

The current pace of change is such that many organisms face ever more rapid and severe fluctuations in their physical and biotic environments. A major challenge for ecologists and evolutionary biologists is in understanding how this will influence individuals, populations and ecosystems, and over what time scale such effects will occur. There is now great interest in so called 'maternal effects', which can generate rapid phenotypic responses, with both positive and negative fitness consequences in an ecological timeframe. In this project, I propose to examine a hitherto unconsidered route whereby the state of the mother alters the DNA that her offspring inherit, with profound effects on offspring reproductive performance and potential lifespan. This route is the effect of maternal state on telomeres, the DNA sequences that cap chromosomes ends; changes in the length and loss rate of telomeres could affect the longevity and reproductive output of individuals, their offspring and even grand-offspring. We still know very little about what telomere loss measurable at the cellular level actually means for organismal level performance, how it is influenced by environmental factors and intergenerational maternal effects, and how telomere dynamics relate to Darwinian fitness parameters. We lack experimental studies that track telomere loss within individuals subjected to varying environmental circumstances and relate this to organismal level outcomes for parents and offspring. I plan to address this gap in our understanding in a novel and innovative experimental programme that tests the idea that the effects of environmental stressors on senescence rates and lifespan are linked to accelerated telomere loss and that, through this route, can affect more than one generation.

2 113 818 €

Start date: 2011-04-01, End date: 2016-07-31

Understanding the origin and evolution of eukaryotes, their genomes and organelles, are among the most important and exciting challenges facing biology. However, determining ancient gene origins tests methods and data to their limits, and it is unrealistic to expect progress to be easy. A comparative cross-disciplinary approach involving sophisticated phylogenetics allied with mathematical understanding, offers the best hope of obtaining robust hypotheses for gene and genomic origins. It is also necessary to look beyond the narrow focus of a few model organisms, and to thoughtfully embrace a wider selection of eukaryotic diversity. Over the past few years, my lab has studied the genomes and mitochondrial homologues (mitosomes and hydrogenosomes) of parasitic protozoa that represent significant health hazards in both the developed and developing world. These microbial eukaryotes will provide the model systems for investigations which aim to deliver major progress in understanding the importance of lateral gene transfer for eukaryotic genome origins and flux, for understanding how parasites exploit their host cells, and for identifying the essential functions of organelles related to mitochondria, which now appear to be vital components of all eukaryotic cells.

1 998 703 €

Start date: 2011-03-01, End date: 2017-02-28

To make for better diagnostics and safer applications of genomics we need a better understanding of our genome and how it functions. Until recently we thought we knew: intergenic sequence must be largely “junk” and mutations that, for example, affect genes but not the protein (synonymous mutations) must be effectively neutral. This degenerate genome view accords with the nearly-neutral theory’s prediction that selection will be weaker when populations are small. But is this all there is to it? I shall investigate two new interrelated perspectives on genome evolution. First, I suggest that to mitigate errors, owing to our high error rates, our genome can be under stronger, not weaker, selection. Second, that errors might be a source of evolutionary novelty. Error mitigation, my team has shown, often involves selection on seemingly innocuous mutations such as synonymous changes. Remarkably, we discovered that selection to ensure error-proof splicing is possibly more prevalent on synonymous mutations when populations are small, making seemingly innocuous mutations stronger candidates for human diseases. I shall provide the first test of the new error-proofing perspective through comparative genomic analysis on synonymous site evolution. To investigate error as a source of novelty I shall consider whether expression piggy-backing (expression of a gene affecting its neighbors) forces rewiring of gene networks. Importantly, I shall translate our new understanding to enable better diagnostics and improved therapeutics. I shall develop a much-needed computer package to identify candidate disease-causing synonymous changes. In addition, knowing how synonymous sites modulate splicing will allow me to design better intronless transgenes. Transgenes must also be inserted in genomic regions immune to piggy-backing. I will examine transposable element related piggy-backing to characterize “safe” sites for therapeutic gene insertion and mammalian transgenesis more generally.

2 497 996 €

Start date: 2016-01-01, End date: 2020-12-31

The evolution of multicellularity allowed specialization of cells into functions that support rather than cause propagation. While yielding immense gain of function, the organisation of these somatic cells into tissues and organs required novel cell-cell signalling systems. We seek to identify the genetic changes that caused transitions to multicellularity and enabled cell specialization. We use genetically tractable Dictyostelia with multicellular structures that contain from 1 to 5 cell-types to address these fundamental questions. Dictyostelia evolved from unicellular Amoebozoa and are subdivided into 4 major groups, with most novel cell-types appearing in group 4. We found that gene expression patterns changed most frequently at the transition between groups 3 and 4, and that across groups ~10% of genes were alternatively spliced in the 5’UTR, indicative of promoter elaboration. Among known genes essential for multicellular development, those involved in intracellular signal processing were mostly conserved between Dictyostelia and unicellular Amoebozoa, while those encoding exposed and secreted proteins (ESPs) were unique to Dictyostelia or groups within Dictyostelia. Starting from a hypothesis that diversification of ESPs and gene regulatory mechanisms are major drivers of multicellular evolution, we will place unicellular relatives of Dictyostelia under selection to induce multicellularity, establish which genes are most changed in evolved populations and whether this involves ESP families that are also most changed in Dictyostelia. We will overexpress altered genes in unicellular forms to assess whether this induces multicellularity. We will retrace evolution of cell specialization by lineage analysis and phenotyping and seek correlations between cell-type innovation and alternative splice events and with emergence of novel signalling genes. Causality will be assessed by replacement of genes or promoters with ancestral forms in evolved species and vice versa

2 128 602 €

Start date: 2017-05-01, End date: 2022-04-30