Project acronym AlgoFinance
Project Algorithmic Finance: Inquiring into the Reshaping of Financial Markets
Researcher (PI) Christian BORCH
Host Institution (HI) COPENHAGEN BUSINESS SCHOOL
Call Details Consolidator Grant (CoG), SH3, ERC-2016-COG
Summary Present-day financial markets are turning algorithmic, as market orders are increasingly being executed by fully automated computer algorithms, without any direct human intervention. Although algorithmic finance seems to fundamentally reshape the central dynamics in financial markets, and even though it prompts core sociological questions, it has not yet received any systematic attention. In a pioneering contribution to economic sociology and social studies of finance, ALGOFINANCE aims to understand how and with what consequences the turn to algorithms is changing financial markets. The overall concept and central contributions of ALGOFINANCE are the following: (1) on an intra-firm level, the project examines how the shift to algorithmic finance reshapes the ways in which trading firms operate, and does so by systematically and empirically investigating the reconfiguration of organizational structures and employee subjectivity; (2) on an inter-algorithmic level, it offers a ground-breaking methodology (agent-based modelling informed by qualitative data) to grasp how trading algorithms interact with one another in a fully digital space; and (3) on the level of market sociality, it proposes a novel theorization of how intra-firm and inter-algorithmic dynamics can be conceived of as introducing a particular form of sociality that is characteristic to algorithmic finance: a form of sociality-as-association heuristically analyzed as imitation. None of these three levels have received systematic attention in the state-of-the-art literature. Addressing them will significantly advance the understanding of present-day algorithmic finance in economic sociology. By contributing novel empirical, methodological, and theoretical understandings of the functioning and consequences of algorithms, ALGOFINANCE will pave the way for other research into digital sociology and the broader algorithmization of society.
Summary
Present-day financial markets are turning algorithmic, as market orders are increasingly being executed by fully automated computer algorithms, without any direct human intervention. Although algorithmic finance seems to fundamentally reshape the central dynamics in financial markets, and even though it prompts core sociological questions, it has not yet received any systematic attention. In a pioneering contribution to economic sociology and social studies of finance, ALGOFINANCE aims to understand how and with what consequences the turn to algorithms is changing financial markets. The overall concept and central contributions of ALGOFINANCE are the following: (1) on an intra-firm level, the project examines how the shift to algorithmic finance reshapes the ways in which trading firms operate, and does so by systematically and empirically investigating the reconfiguration of organizational structures and employee subjectivity; (2) on an inter-algorithmic level, it offers a ground-breaking methodology (agent-based modelling informed by qualitative data) to grasp how trading algorithms interact with one another in a fully digital space; and (3) on the level of market sociality, it proposes a novel theorization of how intra-firm and inter-algorithmic dynamics can be conceived of as introducing a particular form of sociality that is characteristic to algorithmic finance: a form of sociality-as-association heuristically analyzed as imitation. None of these three levels have received systematic attention in the state-of-the-art literature. Addressing them will significantly advance the understanding of present-day algorithmic finance in economic sociology. By contributing novel empirical, methodological, and theoretical understandings of the functioning and consequences of algorithms, ALGOFINANCE will pave the way for other research into digital sociology and the broader algorithmization of society.
Max ERC Funding
1 590 036 €
Duration
Start date: 2017-05-01, End date: 2021-04-30
Project acronym CHROMATINREPLICATION
Project How to Replicate Chromatin - Maturation, Timing Control and Stress-Induced Aberrations
Researcher (PI) Anja Groth
Host Institution (HI) KOBENHAVNS UNIVERSITET
Call Details Starting Grant (StG), LS1, ERC-2011-StG_20101109
Summary Inheritance of DNA sequence and its proper organization into chromatin is fundamental for eukaryotic life. The challenge of propagating genetic and epigenetic information is met in S phase and entails genome-wide disruption and restoration of chromatin coupled to faithful copying of DNA. How specific chromatin structures are restored on new DNA and transmitted through mitotic cell division remains a fundamental question in biology central to understand cell fate and identity.
Chromatin restoration on new DNA involves a complex set of events including nucleosome assembly and remodelling, restoration of marks on DNA and histones, deposition of histone variants and establishment of higher order chromosomal structures including sister-chromatid cohesion. To dissect these fundamental processes and their coordination in time and space with DNA replication, we have developed a novel technology termed nascent chromatin capture (NCC) that provides unique possibility for biochemical and proteomic analysis of chromatin replication in human cells. I propose to apply this innovative cutting-edge technique for a comprehensive characterization of chromatin restoration during DNA replication and to reveal how replication timing and genotoxic stress impact on final chromatin state. This highly topical project brings together the fields of chromatin biology, DNA replication, epigenetics and genome stability and we expect to make groundbreaking discoveries that will improve our understanding of human development, somatic cell reprogramming and complex diseases like cancer.
The proposed research will 1) identify and characterize novel mechanisms in chromatin restoration and 2) address molecularly how replication timing and genotoxic insults influence chromatin maturation and final chromatin state.
Summary
Inheritance of DNA sequence and its proper organization into chromatin is fundamental for eukaryotic life. The challenge of propagating genetic and epigenetic information is met in S phase and entails genome-wide disruption and restoration of chromatin coupled to faithful copying of DNA. How specific chromatin structures are restored on new DNA and transmitted through mitotic cell division remains a fundamental question in biology central to understand cell fate and identity.
Chromatin restoration on new DNA involves a complex set of events including nucleosome assembly and remodelling, restoration of marks on DNA and histones, deposition of histone variants and establishment of higher order chromosomal structures including sister-chromatid cohesion. To dissect these fundamental processes and their coordination in time and space with DNA replication, we have developed a novel technology termed nascent chromatin capture (NCC) that provides unique possibility for biochemical and proteomic analysis of chromatin replication in human cells. I propose to apply this innovative cutting-edge technique for a comprehensive characterization of chromatin restoration during DNA replication and to reveal how replication timing and genotoxic stress impact on final chromatin state. This highly topical project brings together the fields of chromatin biology, DNA replication, epigenetics and genome stability and we expect to make groundbreaking discoveries that will improve our understanding of human development, somatic cell reprogramming and complex diseases like cancer.
The proposed research will 1) identify and characterize novel mechanisms in chromatin restoration and 2) address molecularly how replication timing and genotoxic insults influence chromatin maturation and final chromatin state.
Max ERC Funding
1 692 737 €
Duration
Start date: 2011-11-01, End date: 2017-04-30
Project acronym CRIMTANG
Project Criminal Entanglements.A new ethnographic approach to transnational organised crime.
Researcher (PI) Henrik VIGH
Host Institution (HI) KOBENHAVNS UNIVERSITET
Call Details Consolidator Grant (CoG), SH3, ERC-2016-COG
Summary Linked to terrorism, moral breakdown, and societal decay, Transnational Organised Crime (TOC) has come to embody current global anxieties as a figure of fear and cause of disquiet. Yet despite its central position on the social and political radar, our knowledge of it remains limited and fragmentary. Quantitative analyses may have identified the scale of the problem, but its underlying socio-cultural logic and practices remain under-researched and largely obscure. TOC is on the rise, and we need better insights into how it develops and expands, who engages in it and why, and how it is linked to and embedded in social networks that straddle countries and contexts.
CRIMTANG proposes a unique approach to the study of the social infrastructure of contemporary TOC. It develops a research strategy that is ethnographic and transnational in design and so attuned to the human flows and formations of TOC. The project comprises a trans-disciplinary research team of anthropologists, criminologists and political scientists, and builds on their prior experience of the people, regions and languages under study. It explores the illegal and overlapping flows of migrants and drugs from North-West Africa into Europe, following a key trafficking trajectory stretching from Tangiers to Barcelona, Paris and beyond.
In so doing, CRIMTANG sheds new light on the actual empirical processes in operation at different points along this trafficking route, whilst simultaneously developing new theoretical and methodological apparatuses for apprehending TOC that can be exported and applied in other regions and contexts. It reimagines the idea of social entanglement and proposes new transnational and collective fieldwork strategies. Finally, it will advance and consolidate the European research environment on TOC by creating a research hub for transnational ethnographic criminology at the University of Copenhagen.
Summary
Linked to terrorism, moral breakdown, and societal decay, Transnational Organised Crime (TOC) has come to embody current global anxieties as a figure of fear and cause of disquiet. Yet despite its central position on the social and political radar, our knowledge of it remains limited and fragmentary. Quantitative analyses may have identified the scale of the problem, but its underlying socio-cultural logic and practices remain under-researched and largely obscure. TOC is on the rise, and we need better insights into how it develops and expands, who engages in it and why, and how it is linked to and embedded in social networks that straddle countries and contexts.
CRIMTANG proposes a unique approach to the study of the social infrastructure of contemporary TOC. It develops a research strategy that is ethnographic and transnational in design and so attuned to the human flows and formations of TOC. The project comprises a trans-disciplinary research team of anthropologists, criminologists and political scientists, and builds on their prior experience of the people, regions and languages under study. It explores the illegal and overlapping flows of migrants and drugs from North-West Africa into Europe, following a key trafficking trajectory stretching from Tangiers to Barcelona, Paris and beyond.
In so doing, CRIMTANG sheds new light on the actual empirical processes in operation at different points along this trafficking route, whilst simultaneously developing new theoretical and methodological apparatuses for apprehending TOC that can be exported and applied in other regions and contexts. It reimagines the idea of social entanglement and proposes new transnational and collective fieldwork strategies. Finally, it will advance and consolidate the European research environment on TOC by creating a research hub for transnational ethnographic criminology at the University of Copenhagen.
Max ERC Funding
1 999 909 €
Duration
Start date: 2018-02-01, End date: 2023-01-31
Project acronym DEVOMIND
Project How do infants mentalize? Bringing a neuroimaging approach to the puzzle of early mindreading.
Researcher (PI) Victoria SOUTHGATE
Host Institution (HI) KOBENHAVNS UNIVERSITET
Call Details Consolidator Grant (CoG), SH4, ERC-2016-COG
Summary Human social interaction and learning depends on making the right inferences about other people’s thoughts, a process commonly called mentalizing, or Theory of Mind, a cognitive achievement which several decades of research concluded was reached at around age 4. The last 10 years has radically changed this view, and innovative new paradigms suggest that even preverbal infants can think about others’ minds. This new developmental data has created arguably one of the biggest puzzles in the history of developmental science: How can infants be mentalizing when years of research have shown that a) pre-schoolers fail at mentalizing tasks and b) mentalizing depends on the development of cognitive control, language, and brain maturation? The key issue is whether behaviour that looks like infant mentalizing really is mentalizing, or might infants’ success belie alternative processes? The most powerful strategy for resolving this puzzle is to look to brain activity. By applying the same methods and paradigms across infancy and early childhood, DEVOMIND will investigate whether infants’ success on mentalizing tasks recruits the same network of brain regions, and neural processes, that we know are involved in success in older children and adults. In the second half of the project, we will use our neural indicators of mentalizing to test a completely novel hypothesis in which infants’ success is possible because they have a limited ability to distinguish self from other. Although novel, this hypothesis deserves to be tested because it has the potential to explain both infants’ success and preschoolers’ failures under a single, unified theory. By bringing a neuroimaging approach to the puzzle of early mentalizing, DEVOMIND will allow us to move beyond the current impasse, and to generate a new theory of Theory of Mind.
Summary
Human social interaction and learning depends on making the right inferences about other people’s thoughts, a process commonly called mentalizing, or Theory of Mind, a cognitive achievement which several decades of research concluded was reached at around age 4. The last 10 years has radically changed this view, and innovative new paradigms suggest that even preverbal infants can think about others’ minds. This new developmental data has created arguably one of the biggest puzzles in the history of developmental science: How can infants be mentalizing when years of research have shown that a) pre-schoolers fail at mentalizing tasks and b) mentalizing depends on the development of cognitive control, language, and brain maturation? The key issue is whether behaviour that looks like infant mentalizing really is mentalizing, or might infants’ success belie alternative processes? The most powerful strategy for resolving this puzzle is to look to brain activity. By applying the same methods and paradigms across infancy and early childhood, DEVOMIND will investigate whether infants’ success on mentalizing tasks recruits the same network of brain regions, and neural processes, that we know are involved in success in older children and adults. In the second half of the project, we will use our neural indicators of mentalizing to test a completely novel hypothesis in which infants’ success is possible because they have a limited ability to distinguish self from other. Although novel, this hypothesis deserves to be tested because it has the potential to explain both infants’ success and preschoolers’ failures under a single, unified theory. By bringing a neuroimaging approach to the puzzle of early mentalizing, DEVOMIND will allow us to move beyond the current impasse, and to generate a new theory of Theory of Mind.
Max ERC Funding
1 761 190 €
Duration
Start date: 2018-02-01, End date: 2023-01-31
Project acronym DPC_REPAIR
Project Mechanism of DNA-protein cross-link repair in S phase
Researcher (PI) Julien Philippe Carlos Duxin
Host Institution (HI) KOBENHAVNS UNIVERSITET
Call Details Starting Grant (StG), LS1, ERC-2016-STG
Summary DNA-protein cross-links (DPCs) are common DNA lesions caused by endogenous, environmental, and chemotherapeutic agents. Cells are susceptible to these lesions during S phase, as DPCs impede replication fork progression and are likely to induce genomic instability, a cause of cancer and aging. Despite its relevance to human health, the repair of DPCs is poorly understood. Research on DPC repair has mainly involved testing cellular responses to compounds such as formaldehyde, but these agents induce a wide variety of DNA lesions, and conflicting results have been reported. To overcome these obstacles, I have developed the first in vitro system that recapitulates replication-coupled DPC repair. In this system, a plasmid containing a site-specific DPC is replicated in Xenopus egg extracts. Using this approach, I demonstrated that DPC repair requires DNA replication. When a replication fork encounters a DPC, the DPC is degraded into a peptide-adduct, which allows replication bypass by translesion DNA synthesis. Importantly, these experiments identified a novel proteolytic pathway whose activity is regulated by replication.
This in vitro system now provides a powerful means to identify and characterize the different factors that participate in S phase DPC repair. I speculate that for DPC processing to occur, the protein-adduct must first be detected, then marked for degradation and ultimately degraded. Using a series of complementary strategies, which will take advantage of the in vitro system combined with proteome and genome wide approaches, I seek to uncover the different players that participate in each of these events. This project will enable a detailed mechanistic outlook of a complex multi-step reaction that has not been feasible to achieve using existing methodologies. It will also improve our understanding of how DPCs impact genomic stability and the consequences of not repairing these lesions for human health.
Summary
DNA-protein cross-links (DPCs) are common DNA lesions caused by endogenous, environmental, and chemotherapeutic agents. Cells are susceptible to these lesions during S phase, as DPCs impede replication fork progression and are likely to induce genomic instability, a cause of cancer and aging. Despite its relevance to human health, the repair of DPCs is poorly understood. Research on DPC repair has mainly involved testing cellular responses to compounds such as formaldehyde, but these agents induce a wide variety of DNA lesions, and conflicting results have been reported. To overcome these obstacles, I have developed the first in vitro system that recapitulates replication-coupled DPC repair. In this system, a plasmid containing a site-specific DPC is replicated in Xenopus egg extracts. Using this approach, I demonstrated that DPC repair requires DNA replication. When a replication fork encounters a DPC, the DPC is degraded into a peptide-adduct, which allows replication bypass by translesion DNA synthesis. Importantly, these experiments identified a novel proteolytic pathway whose activity is regulated by replication.
This in vitro system now provides a powerful means to identify and characterize the different factors that participate in S phase DPC repair. I speculate that for DPC processing to occur, the protein-adduct must first be detected, then marked for degradation and ultimately degraded. Using a series of complementary strategies, which will take advantage of the in vitro system combined with proteome and genome wide approaches, I seek to uncover the different players that participate in each of these events. This project will enable a detailed mechanistic outlook of a complex multi-step reaction that has not been feasible to achieve using existing methodologies. It will also improve our understanding of how DPCs impact genomic stability and the consequences of not repairing these lesions for human health.
Max ERC Funding
1 498 856 €
Duration
Start date: 2017-01-01, End date: 2021-12-31
Project acronym HISTONEMEMORY
Project New and Old Histones in Epigenetic Cell Memory
Researcher (PI) Anja Groth
Host Institution (HI) KOBENHAVNS UNIVERSITET
Call Details Consolidator Grant (CoG), LS1, ERC-2016-COG
Summary Cell type specific organization of DNA into chromatin is an important determinant of gene expression and cell identity. During cell division, epigenetic information in chromatin must be transmitted to daughter cells in order to maintain cell identity or commit to a developmental program. However, it remains unknown how epigenetic states are inherited during cell division. Elucidating molecular mechanisms underlying epigenetic cell memory thus represents a major challenge in biology critical to understand development and disease.
Chromatin undergoes genome-wide disruption during DNA replication and histone marks are diluted 2-fold due to new histone deposition. Yet, how this impacts on establishment and maintenance of gene expression programs is not known. I hypothesize that chromatin replication represents a critical window for epigenetic cell memory and cell fate decisions, and predict that three histone-based processes play critical roles in guarding cell identity: 1) new histone deposition to regulate nucleosome occupancy and transcription factor (TF) binding, 2) accurate transmission of old modified histones by dedicated recycling machinery, and 3) recruitment of regulatory proteins to new and old histones to direct epigenome maintenance. To dissect these events mechanistically and test causal roles in cell fate decisions, I propose a research program integrating explorative proteomics and histone chaperone structure-function analysis with stem cell biology and new cutting-edge genomic tools developed by my research group.
The proposed research will 1) identify novel mechanisms of histone chaperoning and deposition specific to new and old histones, 2) reveal how nucleosome assembly govern TF binding during DNA replication, and 3) address the significance of old histone recycling and new histone deposition for pluripotency and commitment. This will provide a major advance in understanding the molecular mechanisms that govern epigenetic cell memory.
Summary
Cell type specific organization of DNA into chromatin is an important determinant of gene expression and cell identity. During cell division, epigenetic information in chromatin must be transmitted to daughter cells in order to maintain cell identity or commit to a developmental program. However, it remains unknown how epigenetic states are inherited during cell division. Elucidating molecular mechanisms underlying epigenetic cell memory thus represents a major challenge in biology critical to understand development and disease.
Chromatin undergoes genome-wide disruption during DNA replication and histone marks are diluted 2-fold due to new histone deposition. Yet, how this impacts on establishment and maintenance of gene expression programs is not known. I hypothesize that chromatin replication represents a critical window for epigenetic cell memory and cell fate decisions, and predict that three histone-based processes play critical roles in guarding cell identity: 1) new histone deposition to regulate nucleosome occupancy and transcription factor (TF) binding, 2) accurate transmission of old modified histones by dedicated recycling machinery, and 3) recruitment of regulatory proteins to new and old histones to direct epigenome maintenance. To dissect these events mechanistically and test causal roles in cell fate decisions, I propose a research program integrating explorative proteomics and histone chaperone structure-function analysis with stem cell biology and new cutting-edge genomic tools developed by my research group.
The proposed research will 1) identify novel mechanisms of histone chaperoning and deposition specific to new and old histones, 2) reveal how nucleosome assembly govern TF binding during DNA replication, and 3) address the significance of old histone recycling and new histone deposition for pluripotency and commitment. This will provide a major advance in understanding the molecular mechanisms that govern epigenetic cell memory.
Max ERC Funding
1 999 750 €
Duration
Start date: 2017-05-01, End date: 2022-04-30
