Project acronym ABEP
Project Asset Bubbles and Economic Policy
Researcher (PI) Jaume Ventura Fontanet
Host Institution (HI) Centre de Recerca en Economia Internacional (CREI)
Country Spain
Call Details Advanced Grant (AdG), SH1, ERC-2009-AdG
Summary Advanced capitalist economies experience large and persistent movements in asset prices that are difficult to justify with economic fundamentals. The internet bubble of the 1990s and the real state market bubble of the 2000s are two recent examples. The predominant view is that these bubbles are a market failure, and are caused by some form of individual irrationality on the part of market participants. This project is based instead on the view that market participants are individually rational, although this does not preclude sometimes collectively sub-optimal outcomes. Bubbles are thus not a source of market failure by themselves but instead arise as a result of a pre-existing market failure, namely, the existence of pockets of dynamically inefficient investments. Under some conditions, bubbles partly solve this problem, increasing market efficiency and welfare. It is also possible however that bubbles do not solve the underlying problem and, in addition, create negative side-effects. The main objective of this project is to develop this view of asset bubbles, and produce an empirically-relevant macroeconomic framework that allows us to address the following questions: (i) What is the relationship between bubbles and financial market frictions? Special emphasis is given to how the globalization of financial markets and the development of new financial products affect the size and effects of bubbles. (ii) What is the relationship between bubbles, economic growth and unemployment? The theory suggests the presence of virtuous and vicious cycles, as economic growth creates the conditions for bubbles to pop up, while bubbles create incentives for economic growth to happen. (iii) What is the optimal policy to manage bubbles? We need to develop the tools that allow policy makers to sustain those bubbles that have positive effects and burst those that have negative effects.
Summary
Advanced capitalist economies experience large and persistent movements in asset prices that are difficult to justify with economic fundamentals. The internet bubble of the 1990s and the real state market bubble of the 2000s are two recent examples. The predominant view is that these bubbles are a market failure, and are caused by some form of individual irrationality on the part of market participants. This project is based instead on the view that market participants are individually rational, although this does not preclude sometimes collectively sub-optimal outcomes. Bubbles are thus not a source of market failure by themselves but instead arise as a result of a pre-existing market failure, namely, the existence of pockets of dynamically inefficient investments. Under some conditions, bubbles partly solve this problem, increasing market efficiency and welfare. It is also possible however that bubbles do not solve the underlying problem and, in addition, create negative side-effects. The main objective of this project is to develop this view of asset bubbles, and produce an empirically-relevant macroeconomic framework that allows us to address the following questions: (i) What is the relationship between bubbles and financial market frictions? Special emphasis is given to how the globalization of financial markets and the development of new financial products affect the size and effects of bubbles. (ii) What is the relationship between bubbles, economic growth and unemployment? The theory suggests the presence of virtuous and vicious cycles, as economic growth creates the conditions for bubbles to pop up, while bubbles create incentives for economic growth to happen. (iii) What is the optimal policy to manage bubbles? We need to develop the tools that allow policy makers to sustain those bubbles that have positive effects and burst those that have negative effects.
Max ERC Funding
1 000 000 €
Duration
Start date: 2010-04-01, End date: 2015-03-31
Project acronym AFRISCREENWORLDS
Project African Screen Worlds: Decolonising Film and Screen Studies
Researcher (PI) Lindiwe Dovey
Host Institution (HI) SCHOOL OF ORIENTAL AND AFRICAN STUDIES ROYAL CHARTER
Country United Kingdom
Call Details Consolidator Grant (CoG), SH5, ERC-2018-COG
Summary A half century since it came into existence, the discipline of Film and Screen Studies remains mostly Eurocentric in its historical, theoretical and critical frameworks. Although “world cinema” and “transnational cinema” scholars have attempted to broaden its canon and frameworks, several major problems persist. Films and scholarship by Africans in particular, and by people of colour in general, are frequently marginalised if not altogether excluded. This prevents exciting exchanges that could help to re-envision Film and Screen Studies for the twenty-first century, in an era in which greater access to the technological means of making films, and circulating them on a range of screens, means that dynamic “screen worlds” are developing at a rapid rate. AFRISCREENWORLDS will study these “screen worlds” (in both their textual forms and industrial structures), with a focus on Africa, as a way of centring the most marginalised regional cinema. We will also elaborate comparative studies of global “screen worlds” – and, in particular, “screen worlds” in the Global South – exploring their similarities, differences, and parallel developments. We will respond to the exclusions of Film and Screen Studies not only in scholarly ways – through conferences and publications – but also in creative and activist ways – through drawing on cutting-edge creative research methodologies (such as audiovisual criticism and filmmaking) and through helping to decolonise Film and Screen Studies (through the production of ‘toolkits’ on how to make curricula, syllabi, and teaching more globally representative and inclusive). On a theoretical level, we will make an intervention through considering how the concept of “screen worlds” is better equipped than “world cinema” or “transnational cinema” to explore the complexities of audiovisual narratives, and their production and circulation in our contemporary moment, in diverse contexts throughout the globe.
Summary
A half century since it came into existence, the discipline of Film and Screen Studies remains mostly Eurocentric in its historical, theoretical and critical frameworks. Although “world cinema” and “transnational cinema” scholars have attempted to broaden its canon and frameworks, several major problems persist. Films and scholarship by Africans in particular, and by people of colour in general, are frequently marginalised if not altogether excluded. This prevents exciting exchanges that could help to re-envision Film and Screen Studies for the twenty-first century, in an era in which greater access to the technological means of making films, and circulating them on a range of screens, means that dynamic “screen worlds” are developing at a rapid rate. AFRISCREENWORLDS will study these “screen worlds” (in both their textual forms and industrial structures), with a focus on Africa, as a way of centring the most marginalised regional cinema. We will also elaborate comparative studies of global “screen worlds” – and, in particular, “screen worlds” in the Global South – exploring their similarities, differences, and parallel developments. We will respond to the exclusions of Film and Screen Studies not only in scholarly ways – through conferences and publications – but also in creative and activist ways – through drawing on cutting-edge creative research methodologies (such as audiovisual criticism and filmmaking) and through helping to decolonise Film and Screen Studies (through the production of ‘toolkits’ on how to make curricula, syllabi, and teaching more globally representative and inclusive). On a theoretical level, we will make an intervention through considering how the concept of “screen worlds” is better equipped than “world cinema” or “transnational cinema” to explore the complexities of audiovisual narratives, and their production and circulation in our contemporary moment, in diverse contexts throughout the globe.
Max ERC Funding
1 985 578 €
Duration
Start date: 2019-06-01, End date: 2024-05-31
Project acronym BrainNanoFlow
Project Nanoscale dynamics in the extracellular space of the brain in vivo
Researcher (PI) Juan Alberto VARELA
Host Institution (HI) THE UNIVERSITY COURT OF THE UNIVERSITY OF ST ANDREWS
Country United Kingdom
Call Details Starting Grant (StG), LS5, ERC-2018-STG
Summary Aggregates of proteins such as amyloid-beta and alpha-synuclein circulate the extracellular space of the brain (ECS) and are thought to be key players in the development of neurodegenerative diseases. The clearance of these aggregates (among other toxic metabolites) is a fundamental physiological feature of the brain which is poorly understood due to the lack of techniques to study the nanoscale organisation of the ECS. Exciting advances in this field have recently shown that clearance is enhanced during sleep due to a major volume change in the ECS, facilitating the flow of the interstitial fluid. However, this process has only been characterised at a low spatial resolution while the physiological changes occur at the nanoscale. The recently proposed “glymphatic” pathway still remains controversial, as there are no techniques capable of distinguishing between diffusion and bulk flow in the ECS of living animals. Understanding these processes at a higher spatial resolution requires the development of single-molecule imaging techniques that can study the brain in living animals. Taking advantage of the strategies I have recently developed to target single-molecules in the brain in vivo with nanoparticles, we will do “nanoscopy” in living animals. Our proposal will test the glymphatic pathway at the spatial scale in which events happen, and explore how sleep and wake cycles alter the ECS and the diffusion of receptors in neuronal plasma membrane. Overall, BrainNanoFlow aims to understand how nanoscale changes in the ECS facilitate clearance of protein aggregates. We will also provide new insights to the pathological consequences of impaired clearance, focusing on the interactions between these aggregates and their putative receptors. Being able to perform single-molecule studies in vivo in the brain will be a major breakthrough in neurobiology, making possible the study of physiological and pathological processes that cannot be studied in simpler brain preparations.
Summary
Aggregates of proteins such as amyloid-beta and alpha-synuclein circulate the extracellular space of the brain (ECS) and are thought to be key players in the development of neurodegenerative diseases. The clearance of these aggregates (among other toxic metabolites) is a fundamental physiological feature of the brain which is poorly understood due to the lack of techniques to study the nanoscale organisation of the ECS. Exciting advances in this field have recently shown that clearance is enhanced during sleep due to a major volume change in the ECS, facilitating the flow of the interstitial fluid. However, this process has only been characterised at a low spatial resolution while the physiological changes occur at the nanoscale. The recently proposed “glymphatic” pathway still remains controversial, as there are no techniques capable of distinguishing between diffusion and bulk flow in the ECS of living animals. Understanding these processes at a higher spatial resolution requires the development of single-molecule imaging techniques that can study the brain in living animals. Taking advantage of the strategies I have recently developed to target single-molecules in the brain in vivo with nanoparticles, we will do “nanoscopy” in living animals. Our proposal will test the glymphatic pathway at the spatial scale in which events happen, and explore how sleep and wake cycles alter the ECS and the diffusion of receptors in neuronal plasma membrane. Overall, BrainNanoFlow aims to understand how nanoscale changes in the ECS facilitate clearance of protein aggregates. We will also provide new insights to the pathological consequences of impaired clearance, focusing on the interactions between these aggregates and their putative receptors. Being able to perform single-molecule studies in vivo in the brain will be a major breakthrough in neurobiology, making possible the study of physiological and pathological processes that cannot be studied in simpler brain preparations.
Max ERC Funding
1 552 948 €
Duration
Start date: 2018-12-01, End date: 2023-11-30
Project acronym BRAINPOWER
Project Brain energy supply and the consequences of its failure
Researcher (PI) David Ian Attwell
Host Institution (HI) University College London
Country United Kingdom
Call Details Advanced Grant (AdG), LS5, ERC-2009-AdG
Summary Energy, supplied in the form of oxygen and glucose in the blood, is essential for the brain s cognitive power. Failure of the energy supply to the nervous system underlies the mental and physical disability occurring in a wide range of economically important neurological disorders, such as stroke, spinal cord injury and cerebral palsy. Using a combination of two-photon imaging, electrophysiological, molecular and transgenic approaches, I will investigate the control of brain energy supply at the vascular level, and at the level of individual neurons and glial cells, and study the deleterious consequences for the neurons, glia and vasculature of a failure of brain energy supply. The work will focus on the following fundamental issues: A. Vascular control of the brain energy supply (1) How important is control of energy supply at the capillary level, by pericytes? (2) Which synapses control blood flow (and thus generate functional imaging signals) in the cortex? B. Neuronal and glial control of brain energy supply (3) How is grey matter neuronal activity powered? (4) How is the white matter supplied with energy? C. The pathological consequences of a loss of brain energy supply (5) How does a fall of energy supply cause neurotoxic glutamate release? (6) How similar are events in the grey and white matter in energy deprivation conditions? (7) How does a transient loss of energy supply affect blood flow regulation? (8) How does brain energy use change after a period without energy supply? Together this work will significantly advance our understanding of how the energy supply to neurons and glia is regulated in normal conditions, and how the loss of the energy supply causes disorders which consume more than 5% of the costs of European health services (5% of ~1000 billion euro/year).
Summary
Energy, supplied in the form of oxygen and glucose in the blood, is essential for the brain s cognitive power. Failure of the energy supply to the nervous system underlies the mental and physical disability occurring in a wide range of economically important neurological disorders, such as stroke, spinal cord injury and cerebral palsy. Using a combination of two-photon imaging, electrophysiological, molecular and transgenic approaches, I will investigate the control of brain energy supply at the vascular level, and at the level of individual neurons and glial cells, and study the deleterious consequences for the neurons, glia and vasculature of a failure of brain energy supply. The work will focus on the following fundamental issues: A. Vascular control of the brain energy supply (1) How important is control of energy supply at the capillary level, by pericytes? (2) Which synapses control blood flow (and thus generate functional imaging signals) in the cortex? B. Neuronal and glial control of brain energy supply (3) How is grey matter neuronal activity powered? (4) How is the white matter supplied with energy? C. The pathological consequences of a loss of brain energy supply (5) How does a fall of energy supply cause neurotoxic glutamate release? (6) How similar are events in the grey and white matter in energy deprivation conditions? (7) How does a transient loss of energy supply affect blood flow regulation? (8) How does brain energy use change after a period without energy supply? Together this work will significantly advance our understanding of how the energy supply to neurons and glia is regulated in normal conditions, and how the loss of the energy supply causes disorders which consume more than 5% of the costs of European health services (5% of ~1000 billion euro/year).
Max ERC Funding
2 499 947 €
Duration
Start date: 2010-04-01, End date: 2016-03-31
Project acronym CEAD
Project Contextualizing Evidence for Action on Diabetes in low-resource Settings: A mixed-methods case study in Quito and Esmeraldas, Ecuador.
Researcher (PI) Lucy Anne Parker
Host Institution (HI) UNIVERSIDAD MIGUEL HERNANDEZ DE ELCHE
Country Spain
Call Details Starting Grant (StG), SH3, ERC-2018-STG
Summary The relentless rise in diabetes is one of the greatest global health emergencies of the 21st century. The increase is most pronounced in low and middle income countries where today three quarters of people with diabetes live and over 80% of the deaths attributed to non-communicable diseases occur. In light of the wealth of knowledge already available about how to tackle the problem, most major international organizations call for the adoption healthy public policies and initiatives to strengthening health systems. However, implementation of recommended action remains limited in many settings. Most evidence comes from high-income settings and may generate recommendations that cannot be successfully implemented in other settings without careful consideration and contextualization. I propose here that this “know-do” gap can be reduced by revealing the barriers to implementing evidence-based recommendations, engaging local stakeholders in developing context-led innovations and developing a tool-kit for contextualizing and implementing diabetes recommendations in low-resource settings. I plan the research in two carefully selected settings in Ecuador, with mixed-methods combining quantitative epidemiological research and qualitative methodology to generate the rich and varied knowledge that is required to trigger policy action and/or changes in care models. Furthermore, I will engage patients, community members, health workers and decision makers in the process of knowledge generation, interpretation and use. The overarching objective is hence, to explore the process by which global recommendations can be translated into context-specific, evidence-informed action for diabetes prevention in low-resource settings. The findings will support the global endeavour to bridge the global “know-do” gap, one of the most important public health challenges this century and a great opportunity for strengthening health systems and achieving health equity.
Summary
The relentless rise in diabetes is one of the greatest global health emergencies of the 21st century. The increase is most pronounced in low and middle income countries where today three quarters of people with diabetes live and over 80% of the deaths attributed to non-communicable diseases occur. In light of the wealth of knowledge already available about how to tackle the problem, most major international organizations call for the adoption healthy public policies and initiatives to strengthening health systems. However, implementation of recommended action remains limited in many settings. Most evidence comes from high-income settings and may generate recommendations that cannot be successfully implemented in other settings without careful consideration and contextualization. I propose here that this “know-do” gap can be reduced by revealing the barriers to implementing evidence-based recommendations, engaging local stakeholders in developing context-led innovations and developing a tool-kit for contextualizing and implementing diabetes recommendations in low-resource settings. I plan the research in two carefully selected settings in Ecuador, with mixed-methods combining quantitative epidemiological research and qualitative methodology to generate the rich and varied knowledge that is required to trigger policy action and/or changes in care models. Furthermore, I will engage patients, community members, health workers and decision makers in the process of knowledge generation, interpretation and use. The overarching objective is hence, to explore the process by which global recommendations can be translated into context-specific, evidence-informed action for diabetes prevention in low-resource settings. The findings will support the global endeavour to bridge the global “know-do” gap, one of the most important public health challenges this century and a great opportunity for strengthening health systems and achieving health equity.
Max ERC Funding
1 475 334 €
Duration
Start date: 2019-01-01, End date: 2023-12-31
Project acronym ChaperoneRegulome
Project ChaperoneRegulome: Understanding cell-type-specificity of chaperone regulation
Researcher (PI) Ritwick SAWARKAR
Host Institution (HI) THE CHANCELLOR MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE
Country United Kingdom
Call Details Consolidator Grant (CoG), LS3, ERC-2018-COG
Summary Protein misfolding causes devastating health conditions such as neurodegeneration. Although the disease-causing protein is widely expressed, its misfolding occurs only in certain cell-types such as neurons. What governs the susceptibility of some tissues to misfolding is a fundamental question with biomedical relevance.
Molecular chaperones help cellular proteins fold into their native conformation. Despite the generality of their function, chaperones are differentially expressed across various tissues. Moreover exposure to misfolding stress changes chaperone expression in a cell-type-dependent manner. Thus cell-type-specific regulation of chaperones is a major determinant of susceptibility to misfolding. The molecular mechanisms governing chaperone levels in different cell-types are not understood, forming the basis of this proposal. We will take a multidisciplinary approach to address two key questions: (1) How are chaperone levels co-ordinated with tissue-specific demands on protein folding? (2) How do different cell-types regulate chaperone genes when exposed to the same misfolding stress?
Cellular chaperone levels and their response to misfolding stress are both driven by transcriptional changes and influenced by chromatin. The proposed work will bring the conceptual, technological and computational advances of chromatin/ transcription field to understand chaperone biology and misfolding diseases. Using in vivo mouse model and in vitro differentiation model, we will investigate molecular mechanisms that control chaperone levels in relevant tissues. Our work will provide insights into functional specialization of chaperones driven by tissue-specific folding demands. We will develop a novel and ambitious approach to assess protein-folding capacity in single cells moving the chaperone field beyond state-of-the-art. Thus by implementing genetic, computational and biochemical approaches, we aim to understand cell-type-specificity of chaperone regulation.
Summary
Protein misfolding causes devastating health conditions such as neurodegeneration. Although the disease-causing protein is widely expressed, its misfolding occurs only in certain cell-types such as neurons. What governs the susceptibility of some tissues to misfolding is a fundamental question with biomedical relevance.
Molecular chaperones help cellular proteins fold into their native conformation. Despite the generality of their function, chaperones are differentially expressed across various tissues. Moreover exposure to misfolding stress changes chaperone expression in a cell-type-dependent manner. Thus cell-type-specific regulation of chaperones is a major determinant of susceptibility to misfolding. The molecular mechanisms governing chaperone levels in different cell-types are not understood, forming the basis of this proposal. We will take a multidisciplinary approach to address two key questions: (1) How are chaperone levels co-ordinated with tissue-specific demands on protein folding? (2) How do different cell-types regulate chaperone genes when exposed to the same misfolding stress?
Cellular chaperone levels and their response to misfolding stress are both driven by transcriptional changes and influenced by chromatin. The proposed work will bring the conceptual, technological and computational advances of chromatin/ transcription field to understand chaperone biology and misfolding diseases. Using in vivo mouse model and in vitro differentiation model, we will investigate molecular mechanisms that control chaperone levels in relevant tissues. Our work will provide insights into functional specialization of chaperones driven by tissue-specific folding demands. We will develop a novel and ambitious approach to assess protein-folding capacity in single cells moving the chaperone field beyond state-of-the-art. Thus by implementing genetic, computational and biochemical approaches, we aim to understand cell-type-specificity of chaperone regulation.
Max ERC Funding
1 992 500 €
Duration
Start date: 2020-01-01, End date: 2024-12-31
Project acronym CHROMOCOND
Project A molecular view of chromosome condensation
Researcher (PI) Frank Uhlmann
Host Institution (HI) CANCER RESEARCH UK LBG
Country United Kingdom
Call Details Advanced Grant (AdG), LS3, ERC-2009-AdG
Summary Eukaryotic cells inherit much of their genomic information in the form of chromosomes during cell division. Centimetre-long DNA molecules are packed into micrometer-sized chromosomes to enable this process. How DNA is organised within mitotic chromosomes is still largely unknown. A key structural protein component of mitotic chromosomes, implicated in their compaction, is the condensin complex. In this proposal, we aim to elucidate the molecular architecture of mitotic chromosomes, taking advantage of new genomic techniques and the relatively simple genome organisation of yeast model systems. We will place particular emphasis on elucidating the contribution of the condensin complex, and the cell cycle regulation of its activities, in promoting chromosome condensation. Our previous work has provided genome-wide maps of condensin binding to budding and fission yeast chromosomes. We will continue to decipher the molecular determinants for condensin binding. To investigate how condensin mediates DNA compaction, we propose to generate chromosome-wide DNA/DNA proximity maps. Our approach will be an extension of the chromosome conformation capture (3C) technique. High throughput sequencing of interaction points has provided a first glimpse of the interactions that govern chromosome condensation. The role that condensin plays in promoting these interactions will be investigated. The contribution of condensin s ATP-dependent activities, and cell cycle-dependent post-translational modifications, will be studied. This will be complemented by mathematical modelling of the condensation process. In addition to chromosome condensation, condensin is required for resolution of sister chromatids in anaphase. We will develop an assay to study the catenation status of sister chromatids and how condensin may contribute to their topological resolution.
Summary
Eukaryotic cells inherit much of their genomic information in the form of chromosomes during cell division. Centimetre-long DNA molecules are packed into micrometer-sized chromosomes to enable this process. How DNA is organised within mitotic chromosomes is still largely unknown. A key structural protein component of mitotic chromosomes, implicated in their compaction, is the condensin complex. In this proposal, we aim to elucidate the molecular architecture of mitotic chromosomes, taking advantage of new genomic techniques and the relatively simple genome organisation of yeast model systems. We will place particular emphasis on elucidating the contribution of the condensin complex, and the cell cycle regulation of its activities, in promoting chromosome condensation. Our previous work has provided genome-wide maps of condensin binding to budding and fission yeast chromosomes. We will continue to decipher the molecular determinants for condensin binding. To investigate how condensin mediates DNA compaction, we propose to generate chromosome-wide DNA/DNA proximity maps. Our approach will be an extension of the chromosome conformation capture (3C) technique. High throughput sequencing of interaction points has provided a first glimpse of the interactions that govern chromosome condensation. The role that condensin plays in promoting these interactions will be investigated. The contribution of condensin s ATP-dependent activities, and cell cycle-dependent post-translational modifications, will be studied. This will be complemented by mathematical modelling of the condensation process. In addition to chromosome condensation, condensin is required for resolution of sister chromatids in anaphase. We will develop an assay to study the catenation status of sister chromatids and how condensin may contribute to their topological resolution.
Max ERC Funding
2 076 126 €
Duration
Start date: 2010-04-01, End date: 2015-03-31
Project acronym CULTRWORLD
Project The evolution of cultural norms in real world settings
Researcher (PI) Ruth Helen Mace
Host Institution (HI) University College London
Country United Kingdom
Call Details Advanced Grant (AdG), SH4, ERC-2009-AdG
Summary An intense debate is raging within evolutionary anthropology as to whether the evolution of human behaviour is driven by selection pressure on the individual or on the group. Until recently there was consensus amongst evolutionary biologists and evolutionary anthropologists that natural selection caused behaviours to evolve that benefit the individual or close kin. However the idea that cultural behaviours that favour the group can evolve, even at the expense of individual well-being, is now being supported by some evolutionary anthropologists and economists. Models of cultural group selection rely on patterns of cultural transmission that maintain differences between cultural groups, because either decisions are based on what most others in the group do, or non-conformists are punished in some way. If such biased transmission occurs, then humans may be following a unique evolutionary trajectory towards extreme sociality; such models potentially explain behaviours such as altruism towards non-relatives or limiting your reproductive rate. However, relevant empirical evidence from real world populations, concerning behaviour that potentially influences reproductive success, is almost entirely lacking. The projects proposed here are designed to help fill that gap. In micro-evolutionary studies we will seek evidence for the patterns cultural transmission or social learning that enable cultural group selection to act, and ask how these processes depend on properties of the community, and thus how robust are they to the demographic and societal changes that accompany modernisation. These include studies of the spread of modern contraception through communities; and studies of punishment of selfish players in economic games. In macro-evolutionary studies, we will use phylogenetic cross-cultural comparative methods to show how different cultural traits change over the long term, and ask whether social or ecological variables are driving that cultural change.
Summary
An intense debate is raging within evolutionary anthropology as to whether the evolution of human behaviour is driven by selection pressure on the individual or on the group. Until recently there was consensus amongst evolutionary biologists and evolutionary anthropologists that natural selection caused behaviours to evolve that benefit the individual or close kin. However the idea that cultural behaviours that favour the group can evolve, even at the expense of individual well-being, is now being supported by some evolutionary anthropologists and economists. Models of cultural group selection rely on patterns of cultural transmission that maintain differences between cultural groups, because either decisions are based on what most others in the group do, or non-conformists are punished in some way. If such biased transmission occurs, then humans may be following a unique evolutionary trajectory towards extreme sociality; such models potentially explain behaviours such as altruism towards non-relatives or limiting your reproductive rate. However, relevant empirical evidence from real world populations, concerning behaviour that potentially influences reproductive success, is almost entirely lacking. The projects proposed here are designed to help fill that gap. In micro-evolutionary studies we will seek evidence for the patterns cultural transmission or social learning that enable cultural group selection to act, and ask how these processes depend on properties of the community, and thus how robust are they to the demographic and societal changes that accompany modernisation. These include studies of the spread of modern contraception through communities; and studies of punishment of selfish players in economic games. In macro-evolutionary studies, we will use phylogenetic cross-cultural comparative methods to show how different cultural traits change over the long term, and ask whether social or ecological variables are driving that cultural change.
Max ERC Funding
1 801 978 €
Duration
Start date: 2010-05-01, End date: 2016-04-30
Project acronym DARCGENS
Project Derived and Ancestral RNAs: Comparative Genomics and Evolution of ncRNAs
Researcher (PI) Christopher Paul Ponting
Host Institution (HI) THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Country United Kingdom
Call Details Advanced Grant (AdG), LS2, ERC-2009-AdG
Summary Much light has been shed on the number, mechanisms and functions of protein-coding genes in the human genome. In comparison, we know almost nothing about the origins and mechanisms of the functional dark matter , including sequence that is transcribed outside of protein-coding gene loci. This interdisciplinary proposal will capitalize on new theoretical and experimental opportunities to establish the extent by which long non-coding RNAs contribute to mammalian and fruit fly biology. Since 2001, the Ponting group has pioneered the comparative analysis of protein-coding genes across the amniotes and Drosophilids within many international genome sequencing consortia. This Advanced Grant will break new ground by applying these approaches to long intergenic non-coding RNA (lincRNA) genes from mammals to birds and to flies. The Grant will allow Ponting to free himself of the constraints normally associated with in silico analyses by analysing lincRNAs in vitro and in vivo. The integration of computational and experimental approaches for lincRNAs from across the metazoan tree provides a powerful new toolkit for elucidating the origins and biological roles of these enigmatic molecules. Catalogues of lincRNA loci will be built for human, mouse, fruit fly, zebrafinch, chicken and Aplysia by exploiting data from next-generation sequencing technologies. This will immediately provide a new perspective on how these loci arise, evolve and function, including whether their orthologues are apparent across diverse species. Using new evidence that lincRNA loci act in cis with neighbouring protein-coding loci, we will determine lincRNA mechanisms and will establish the consequences of lincRNA knock-down, knock-out and over-expression in mouse, chick and fruitfly.
Summary
Much light has been shed on the number, mechanisms and functions of protein-coding genes in the human genome. In comparison, we know almost nothing about the origins and mechanisms of the functional dark matter , including sequence that is transcribed outside of protein-coding gene loci. This interdisciplinary proposal will capitalize on new theoretical and experimental opportunities to establish the extent by which long non-coding RNAs contribute to mammalian and fruit fly biology. Since 2001, the Ponting group has pioneered the comparative analysis of protein-coding genes across the amniotes and Drosophilids within many international genome sequencing consortia. This Advanced Grant will break new ground by applying these approaches to long intergenic non-coding RNA (lincRNA) genes from mammals to birds and to flies. The Grant will allow Ponting to free himself of the constraints normally associated with in silico analyses by analysing lincRNAs in vitro and in vivo. The integration of computational and experimental approaches for lincRNAs from across the metazoan tree provides a powerful new toolkit for elucidating the origins and biological roles of these enigmatic molecules. Catalogues of lincRNA loci will be built for human, mouse, fruit fly, zebrafinch, chicken and Aplysia by exploiting data from next-generation sequencing technologies. This will immediately provide a new perspective on how these loci arise, evolve and function, including whether their orthologues are apparent across diverse species. Using new evidence that lincRNA loci act in cis with neighbouring protein-coding loci, we will determine lincRNA mechanisms and will establish the consequences of lincRNA knock-down, knock-out and over-expression in mouse, chick and fruitfly.
Max ERC Funding
2 400 000 €
Duration
Start date: 2010-05-01, End date: 2015-04-30
Project acronym DCFM
Project Default and Collateral in Financial Markets
Researcher (PI) Ioannis Vailakis
Host Institution (HI) THE UNIVERSITY OF EXETER
Country United Kingdom
Call Details Starting Grant (StG), SH1, ERC-2009-StG
Summary The main objective of this project is to research the economic implications of default and collateral in financial markets. It is motivated from the observation that much of the lending in modern economies is secured by some form of collateral and by the empirical fact that modern economies experience a substantial amount of default and bankruptcy. From a theoretical perspective, the research aims to explore new ways of modelling default and collateral and employ them to evaluate the impact of default and collateral on market outcomes. From a policy recommendation perspective, the research aims to develop models with testable implications that can be used by practitioners to discuss the consequences of a wide range of policies. In particular, to explore which kind of regulation procedures should be implemented in order to lower the risk of default and at the same time not to reduce too much risk-sharing. The agenda includes two research directions. The first research direction will focus on the implications of default and collateral in economies with bounded rational agents. Our aim is to understand how default and collateral affect market outcomes in environments where agents are allowed to have very divergent and therefore possibly incorrect beliefs about endogenous economic variables like future prices and delivery rates. The second research direction will focus on the implications of default and collateral in economies with an open ended horizon. Our aim is to investigate endogenous debt constraints that are compatible with equilibrium and simultaneously allow for as much risk sharing as possible.
Summary
The main objective of this project is to research the economic implications of default and collateral in financial markets. It is motivated from the observation that much of the lending in modern economies is secured by some form of collateral and by the empirical fact that modern economies experience a substantial amount of default and bankruptcy. From a theoretical perspective, the research aims to explore new ways of modelling default and collateral and employ them to evaluate the impact of default and collateral on market outcomes. From a policy recommendation perspective, the research aims to develop models with testable implications that can be used by practitioners to discuss the consequences of a wide range of policies. In particular, to explore which kind of regulation procedures should be implemented in order to lower the risk of default and at the same time not to reduce too much risk-sharing. The agenda includes two research directions. The first research direction will focus on the implications of default and collateral in economies with bounded rational agents. Our aim is to understand how default and collateral affect market outcomes in environments where agents are allowed to have very divergent and therefore possibly incorrect beliefs about endogenous economic variables like future prices and delivery rates. The second research direction will focus on the implications of default and collateral in economies with an open ended horizon. Our aim is to investigate endogenous debt constraints that are compatible with equilibrium and simultaneously allow for as much risk sharing as possible.
Max ERC Funding
156 538 €
Duration
Start date: 2010-06-01, End date: 2012-06-30
