Project acronym ARCHAIC ADAPT
Project Admixture accelerated adaptation: signals from modern, ancient and archaic DNA.
Researcher (PI) Emilia HUERTA-SANCHEZ
Host Institution (HI) THE PROVOST, FELLOWS, FOUNDATION SCHOLARS & THE OTHER MEMBERS OF BOARD OF THE COLLEGE OF THE HOLY & UNDIVIDED TRINITY OF QUEEN ELIZABETH NEAR DUBLIN
Country Ireland
Call Details Starting Grant (StG), LS8, ERC-2018-STG
Summary With the advent of new sequencing technologies, population geneticists now have access to more data than ever before. We have access to thousands of human genomes from a diverse set of populations around the globe, and, thanks to advances in DNA extraction and library preparation, we now are beginning to have access to ancient DNA sequence data. These data have greatly improved our knowledge of human history, human adaptation to different environments and human disease. Genome-wide studies have highlighted many genes or genomic loci that may play a role in adaptive or disease related phenotypes of biological importance.
With these collections of modern and ancient sequence data we want to answer a key evolutionary question: how do human adaptations arise? We strongly believe that the state-of-the-art methodologies for uncovering signatures of adaptation are blind to potential modes of adaptation because they are lacking two critical components – more complete integration of multiple population haplotype data (including archaic, ancient and modern samples), and an account of population interactions that facilitate adaptation.
Therefore I plan to develop new methods to detect shared selective events across populations by creating novel statistical summaries, and to detect admixture-facilitated adaptation which we believe is likely a common mode of natural selection. We will apply these tools to new datasets to characterize the interplay of natural selection, archaic and modern admixture in populations in the Americas and make a comparative analysis of modern and ancient European samples to understand the origin and changing profile of adaptive archaic alleles. As a result our work will reveal evolutionary processes that have played an important role in human evolution and disease.
Summary
With the advent of new sequencing technologies, population geneticists now have access to more data than ever before. We have access to thousands of human genomes from a diverse set of populations around the globe, and, thanks to advances in DNA extraction and library preparation, we now are beginning to have access to ancient DNA sequence data. These data have greatly improved our knowledge of human history, human adaptation to different environments and human disease. Genome-wide studies have highlighted many genes or genomic loci that may play a role in adaptive or disease related phenotypes of biological importance.
With these collections of modern and ancient sequence data we want to answer a key evolutionary question: how do human adaptations arise? We strongly believe that the state-of-the-art methodologies for uncovering signatures of adaptation are blind to potential modes of adaptation because they are lacking two critical components – more complete integration of multiple population haplotype data (including archaic, ancient and modern samples), and an account of population interactions that facilitate adaptation.
Therefore I plan to develop new methods to detect shared selective events across populations by creating novel statistical summaries, and to detect admixture-facilitated adaptation which we believe is likely a common mode of natural selection. We will apply these tools to new datasets to characterize the interplay of natural selection, archaic and modern admixture in populations in the Americas and make a comparative analysis of modern and ancient European samples to understand the origin and changing profile of adaptive archaic alleles. As a result our work will reveal evolutionary processes that have played an important role in human evolution and disease.
Max ERC Funding
1 500 000 €
Duration
Start date: 2020-12-01, End date: 2025-11-30
Project acronym CULTSONG
Project Culture as an evolutionary force: Does song learning accelerate speciation in a bat ring species?
Researcher (PI) Mirjam KNoeRNSCHILD
Host Institution (HI) MUSEUM FUR NATURKUNDE - LEIBNIZ-INSTITUT FUR EVOLUTIONS- UND BIODIVERSITATSFORSCHUNG AN DER HUMBOLDT-UNIVERSITAT ZU BERLIN
Country Germany
Call Details Starting Grant (StG), LS8, ERC-2018-STG
Summary Culture is highly relevant for human evolution but whether animal culture can be an evolutionary force that promotes speciation is an open and highly contested issue. While culturally induced song divergence can be correlated with increased speciation rates in songbirds, it is hard to resolve whether cultural differences are promoting speciation or vice versa. Studying ring species is a perfect solution for this problem since they illustrate divergence in space instead of time, thus allowing us to determine whether cultural differences are causes or consequences of speciation. A ring species originates from a population that expands around an uninhabitable barrier and gradually diverges until the terminal forms are reproductively isolated upon secondary contact. We will study whether culturally induced song divergence accelerates speciation in the bat Saccopteryx bilineata, the first known mammalian ring species. Cultural differences between S. bilineata populations are manifested in distinct and temporally stable song dialects which juvenile males learn from adults. First, we will study song divergence around the ring and the relative contribution of song dialects to reproductive isolation of the co-occurring terminal forms of the ring. Second, we will study potential genetic predispositions for learning specific song dialects and investigate neurogenetic mechanisms involved in mammalian song learning. Third, we will reconstruct the history, evolutionary patterns and processes of speciation in a ring using a genomic approach in S. bilineata and its sympatric sister species. This comparative approach will allow us to unravel factors involved in the rapid divergence of S. bilineata on a small spatial scale. In synthesis, we will be able to determine whether sexually selected, culturally transmitted traits can accelerate speciation and elucidate the role of culture as an evolutionary force.
Summary
Culture is highly relevant for human evolution but whether animal culture can be an evolutionary force that promotes speciation is an open and highly contested issue. While culturally induced song divergence can be correlated with increased speciation rates in songbirds, it is hard to resolve whether cultural differences are promoting speciation or vice versa. Studying ring species is a perfect solution for this problem since they illustrate divergence in space instead of time, thus allowing us to determine whether cultural differences are causes or consequences of speciation. A ring species originates from a population that expands around an uninhabitable barrier and gradually diverges until the terminal forms are reproductively isolated upon secondary contact. We will study whether culturally induced song divergence accelerates speciation in the bat Saccopteryx bilineata, the first known mammalian ring species. Cultural differences between S. bilineata populations are manifested in distinct and temporally stable song dialects which juvenile males learn from adults. First, we will study song divergence around the ring and the relative contribution of song dialects to reproductive isolation of the co-occurring terminal forms of the ring. Second, we will study potential genetic predispositions for learning specific song dialects and investigate neurogenetic mechanisms involved in mammalian song learning. Third, we will reconstruct the history, evolutionary patterns and processes of speciation in a ring using a genomic approach in S. bilineata and its sympatric sister species. This comparative approach will allow us to unravel factors involved in the rapid divergence of S. bilineata on a small spatial scale. In synthesis, we will be able to determine whether sexually selected, culturally transmitted traits can accelerate speciation and elucidate the role of culture as an evolutionary force.
Max ERC Funding
1 492 911 €
Duration
Start date: 2019-05-01, End date: 2024-04-30
Project acronym evolSingleCellGRN
Project Constraint, Adaptation, and Heterogeneity: Genomic and single-cell approaches to understanding the evolution of developmental gene regulatory networks
Researcher (PI) David GARFIELD
Host Institution (HI) HUMBOLDT-UNIVERSITAET ZU BERLIN
Country Germany
Call Details Starting Grant (StG), LS3, ERC-2018-STG
Summary Cell types in development arise from precise patterns of gene expression driven by differential usage of DNA regulatory elements. Mutations affecting these elements, or proteins binding them, are major contributors to disease and underlie the evolution of new morphologies. To better understand these elements and how they evolve, I introduce a set of single-cell RNA and ATAC-Seq sequencing technologies that: A) Identify tissue-specific regulatory elements and expression profiles by interrogating individual cells, B) Allow for a precise read-out of developmental responses to mutation and perturbation, including cell-fate re-specification, C) Lead to the development of a regulatory-information based concept of homology that will be used to understand developmental evolution. The research makes use of sea urchins. The well-annotated sea urchin regulatory network, a detailed understanding of inductive interactions in early development, and an active body of evolutionary research justify this choice. Using single-cell ATAC-Seq and a new method for resolving single-cell, nascent transcripts, I will build a detailed atlas of sea urchin development and use this atlas to understand how regulatory landscapes change during specification and how they evolve between closely related species. I will also investigate, at single-cell resolution, how larval skeletal cells are regenerated following the loss of a cell lineage that mirrors euechinoid evolution. To better understand the origins of cell types in sea urchins, I will characterize embryos of the cnidarian Nematostella, using shared regulatory sites to define cell types which I will compare to urchins and my previous work in Drosophila. The work will generate single-cell methods for non-traditional model systems and help to resolve the processes by which, and the paths along which, development evolves.
Summary
Cell types in development arise from precise patterns of gene expression driven by differential usage of DNA regulatory elements. Mutations affecting these elements, or proteins binding them, are major contributors to disease and underlie the evolution of new morphologies. To better understand these elements and how they evolve, I introduce a set of single-cell RNA and ATAC-Seq sequencing technologies that: A) Identify tissue-specific regulatory elements and expression profiles by interrogating individual cells, B) Allow for a precise read-out of developmental responses to mutation and perturbation, including cell-fate re-specification, C) Lead to the development of a regulatory-information based concept of homology that will be used to understand developmental evolution. The research makes use of sea urchins. The well-annotated sea urchin regulatory network, a detailed understanding of inductive interactions in early development, and an active body of evolutionary research justify this choice. Using single-cell ATAC-Seq and a new method for resolving single-cell, nascent transcripts, I will build a detailed atlas of sea urchin development and use this atlas to understand how regulatory landscapes change during specification and how they evolve between closely related species. I will also investigate, at single-cell resolution, how larval skeletal cells are regenerated following the loss of a cell lineage that mirrors euechinoid evolution. To better understand the origins of cell types in sea urchins, I will characterize embryos of the cnidarian Nematostella, using shared regulatory sites to define cell types which I will compare to urchins and my previous work in Drosophila. The work will generate single-cell methods for non-traditional model systems and help to resolve the processes by which, and the paths along which, development evolves.
Max ERC Funding
1 499 900 €
Duration
Start date: 2019-02-01, End date: 2024-01-31
Project acronym LoCoMacro
Project Local Control of Macroscopic Properties in Isolated Many-body Quantum Systems
Researcher (PI) Maurizio FAGOTTI
Host Institution (HI) CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS
Country France
Call Details Starting Grant (StG), PE2, ERC-2018-STG
Summary Studies of many-body quantum systems in the last century have been mainly focussed on equilibrium properties; the systems of interest were typically coupled to an environment, which brings about relaxation after short times. The situation changed with the advent of experiments on clouds of ultra-cold, trapped atoms. These are by design almost
isolated, and allow for investigations into nonequilibrium dynamics before the onset of dissipative processes. The characterization of such dynamics is now a main frontier of theoretical physics. One of the most exciting phenomena observed was the emergence of a new kind of relaxation, not caused by dissipation. The system acts as its own bath
and at late times it is as if the state were prepared at a different temperature, or, especially in low-dimensional systems, in some exotic state of matter. Recently, some progress has been made in extending this picture to inhomogeneous systems. In particular, an exceptional phenomenon was pointed out: a localized perturbation can have global effects on the stationary properties of the observables. LoCoMacro is born of this observation and has the ultimate aim of finding novel ways to control the macroscopic properties of a nonequilibrium state by acting on a small part of the system. We address the fundamental questions of relaxation and emergence of nonequilibrium steady states in the presence of inhomogeneities; we study the effects of localized perturbations on the key elements of the dynamics, as the conservation
laws. In integrable models we use the most advanced analytic techniques to obtain exact results, e.g., for correlation functions and entanglement measures. More generally, we rely on state-of-the-art numerical simulations. For the defining characteristics of the models studied, LoCoMacro creates a bridge between two fascinating topics: thermalization in homogeneous systems and many-body localization in disordered ones.
Summary
Studies of many-body quantum systems in the last century have been mainly focussed on equilibrium properties; the systems of interest were typically coupled to an environment, which brings about relaxation after short times. The situation changed with the advent of experiments on clouds of ultra-cold, trapped atoms. These are by design almost
isolated, and allow for investigations into nonequilibrium dynamics before the onset of dissipative processes. The characterization of such dynamics is now a main frontier of theoretical physics. One of the most exciting phenomena observed was the emergence of a new kind of relaxation, not caused by dissipation. The system acts as its own bath
and at late times it is as if the state were prepared at a different temperature, or, especially in low-dimensional systems, in some exotic state of matter. Recently, some progress has been made in extending this picture to inhomogeneous systems. In particular, an exceptional phenomenon was pointed out: a localized perturbation can have global effects on the stationary properties of the observables. LoCoMacro is born of this observation and has the ultimate aim of finding novel ways to control the macroscopic properties of a nonequilibrium state by acting on a small part of the system. We address the fundamental questions of relaxation and emergence of nonequilibrium steady states in the presence of inhomogeneities; we study the effects of localized perturbations on the key elements of the dynamics, as the conservation
laws. In integrable models we use the most advanced analytic techniques to obtain exact results, e.g., for correlation functions and entanglement measures. More generally, we rely on state-of-the-art numerical simulations. For the defining characteristics of the models studied, LoCoMacro creates a bridge between two fascinating topics: thermalization in homogeneous systems and many-body localization in disordered ones.
Max ERC Funding
1 499 716 €
Duration
Start date: 2019-01-01, End date: 2023-12-31
Project acronym mitoUPR
Project Cellular modulation by the mitochondrial unfolded protein response
Researcher (PI) Christian MueNCH
Host Institution (HI) JOHANN WOLFGANG GOETHE-UNIVERSITATFRANKFURT AM MAIN
Country Germany
Call Details Starting Grant (StG), LS3, ERC-2018-STG
Summary Mitochondrial function is central for cellular metabolism and energy balance. However, many diseases, including cancer and neurodegenerative diseases, affect mitochondrial function and proteostasis. Upon mitochondrial protein misfolding, mitochondria activate the mitochondrial unfolded protein response (UPRmt) to restore proteostasis, a poorly characterized pathway in mammalian cells. Notably, the effects of the UPRmt on its direct environment – mitochondria – and on cytosolic homeostasis remain unknown. Strikingly, non-cell autonomous signaling of metabolism and folding state has been described in recent years, particularly in worms. However, the possible role of UPRmt in such processes is undescribed.
Using newly available tools to acutely induce the UPRmt in mammalian cells, combined with cutting-edge quantitative mass spectrometry, microscopy, next generation sequencing, and gene editing approaches, we propose to address these important open questions by studying the influence UPRmt exerts on the environments of i) mitochondria (including to study the composition and regulation of RNA granules), ii) cytosol (adjustments of translation, metabolism, and proliferation) and iii) neighboring cells (modification by non-cell autonomous signaling). Additionally, we aim to develop an iPSC-based UPRmt model.
On cellular and organismal level, there ought to be mechanisms to signal changes in metabolism and proteostasis to increase robustness in neighboring environments. Studying these effects will be crucial for a better understanding of human disease and carries severe implications: i) the possibility of therapeutic treatment by modulating neighboring compartments or cells and ii) the possibility that diseases inducing the UPRmt could have unknown paracrine and endocrine effects on the organism. This proposal holds the potential to uncover a novel layer of regulation of cellular stress with an extensive influence on our understanding of the UPRmt and disease.
Summary
Mitochondrial function is central for cellular metabolism and energy balance. However, many diseases, including cancer and neurodegenerative diseases, affect mitochondrial function and proteostasis. Upon mitochondrial protein misfolding, mitochondria activate the mitochondrial unfolded protein response (UPRmt) to restore proteostasis, a poorly characterized pathway in mammalian cells. Notably, the effects of the UPRmt on its direct environment – mitochondria – and on cytosolic homeostasis remain unknown. Strikingly, non-cell autonomous signaling of metabolism and folding state has been described in recent years, particularly in worms. However, the possible role of UPRmt in such processes is undescribed.
Using newly available tools to acutely induce the UPRmt in mammalian cells, combined with cutting-edge quantitative mass spectrometry, microscopy, next generation sequencing, and gene editing approaches, we propose to address these important open questions by studying the influence UPRmt exerts on the environments of i) mitochondria (including to study the composition and regulation of RNA granules), ii) cytosol (adjustments of translation, metabolism, and proliferation) and iii) neighboring cells (modification by non-cell autonomous signaling). Additionally, we aim to develop an iPSC-based UPRmt model.
On cellular and organismal level, there ought to be mechanisms to signal changes in metabolism and proteostasis to increase robustness in neighboring environments. Studying these effects will be crucial for a better understanding of human disease and carries severe implications: i) the possibility of therapeutic treatment by modulating neighboring compartments or cells and ii) the possibility that diseases inducing the UPRmt could have unknown paracrine and endocrine effects on the organism. This proposal holds the potential to uncover a novel layer of regulation of cellular stress with an extensive influence on our understanding of the UPRmt and disease.
Max ERC Funding
1 437 500 €
Duration
Start date: 2019-02-01, End date: 2024-01-31
Project acronym MORPHEUS
Project Deciphering Bacteria-induced Morphogenesis and Protection in marine Eukaryotes
Researcher (PI) Christine BEEMELMANNS
Host Institution (HI) LEIBNIZ-INSTITUT FUR NATURSTOFF-FORSCHUNG UND INFEKTIONSBIOLOGIE EV HANS-KNOLL-ISTITUT
Country Germany
Call Details Starting Grant (StG), LS9, ERC-2018-STG
Summary Symbiotic bacteria play critical roles in animal evolution, development and metabolism. The molecular and cellular mechanisms underlying these fundamental interactions, however, are largely unknown.
To fill this major knowledge gap, I will establish the bacteria-Hydractinia symbiosis as a new model system to fully characterize key cross-kingdom signalling molecules and response mechanisms. The results of my ERC proposal (MORPHEUS) will lead to ground-breaking insights into molecular drivers of eukaryotic morphogenesis, illuminate the evolutionary history of developmental signals for animals – including humans – and provide new chemical scaffolds with intrinsic biological activities that are urgently needed for drug discovery.
The marine colonial hydroid Hydractinia belongs to an early branching metazoan lineage, dating back more than 500 million years. The organism reproduces through a larval stage, which upon perception of yet unidentified bacterial morphogenic signals, produced within marine bacterial biofilms, undergoes transformation into the mature organism. In the absence of the bacterial signals, the larva fails to settle and eventually dies. This fundamental process is the basis of this proposal. Capitalizing from my recent pioneering work, I will address the following pressing research questions: Which bacterial signals ensure larval recruitment and metamorphosis? How are bacterial signalling molecules perceived? How is the system protected against alien species? I will apply an innovative combination of state-of-the-art methodologies developed within the fields of natural product and synthetic organic chemistry, microbiology and molecular biology to pursue an in-depth biochemical analysis of this paradigmatic system. Results of MORPHEUS will be transformative for many scientific branches across biological and chemical disciplines, and directly impact the development of sustainable anti-biofouling and drug discovery strategies.
Summary
Symbiotic bacteria play critical roles in animal evolution, development and metabolism. The molecular and cellular mechanisms underlying these fundamental interactions, however, are largely unknown.
To fill this major knowledge gap, I will establish the bacteria-Hydractinia symbiosis as a new model system to fully characterize key cross-kingdom signalling molecules and response mechanisms. The results of my ERC proposal (MORPHEUS) will lead to ground-breaking insights into molecular drivers of eukaryotic morphogenesis, illuminate the evolutionary history of developmental signals for animals – including humans – and provide new chemical scaffolds with intrinsic biological activities that are urgently needed for drug discovery.
The marine colonial hydroid Hydractinia belongs to an early branching metazoan lineage, dating back more than 500 million years. The organism reproduces through a larval stage, which upon perception of yet unidentified bacterial morphogenic signals, produced within marine bacterial biofilms, undergoes transformation into the mature organism. In the absence of the bacterial signals, the larva fails to settle and eventually dies. This fundamental process is the basis of this proposal. Capitalizing from my recent pioneering work, I will address the following pressing research questions: Which bacterial signals ensure larval recruitment and metamorphosis? How are bacterial signalling molecules perceived? How is the system protected against alien species? I will apply an innovative combination of state-of-the-art methodologies developed within the fields of natural product and synthetic organic chemistry, microbiology and molecular biology to pursue an in-depth biochemical analysis of this paradigmatic system. Results of MORPHEUS will be transformative for many scientific branches across biological and chemical disciplines, and directly impact the development of sustainable anti-biofouling and drug discovery strategies.
Max ERC Funding
1 498 750 €
Duration
Start date: 2019-02-01, End date: 2024-01-31
Project acronym Neuro-UTR
Project Mechanism and functional impact of ultra-long 3’ UTRs in the Drosophila nervous system
Researcher (PI) Valerie HILGERS
Host Institution (HI) MAX-PLANCK-GESELLSCHAFT ZUR FORDERUNG DER WISSENSCHAFTEN EV
Country Germany
Call Details Starting Grant (StG), LS3, ERC-2018-STG
Summary Neurons employ cell-specific gene regulatory mechanisms. One particularly striking process is the recently discovered, drastic lengthening of the 3’ untranslated region (3’ UTR) of hundreds of genes, which occurs in neurons from flies to humans. The function of the resulting ultra-long 3’ UTRs is unknown. RNA deregulation plays a central role in neurological diseases; to understand underlying causes, it is essential to study regulatory processes and define the function of these novel 3’ UTRs.
In Drosophila, the neuronal RNA-binding protein ELAV is the main effector of nervous system specific 3’ UTR extension. ELAV’s association with the promoter region of its target genes is required for synthesis of alternative, ultra-long 3’ UTRs. The mechanistic framework of this novel and exciting link between transcription initiation and alternative 3’ end processing is not understood yet.
We hypothesise that mRNAs carrying ultra-long 3’ UTRs create an important communication avenue between transcription regulation and synaptic function. In this proposal, we will study the regulation of ELAV-mediated 3’ UTR extension in a Drosophila model. First, we will provide mechanistic insight into the co-transcriptional processes that give rise to ultra-long 3’ UTRs. Employing genomics, proteomics and biochemistry, we will study the recruitment of ELAV at gene promoters and to nascent mRNA. Second, we will follow the journey of extended mRNAs from their site of synthesis to their destination using imaging, proteomics, and functional genetics. Finally, based on our unpublished results that 3’ UTR plasticity impacts neuronal function, we will analyse the role of ultra-long 3’ UTRs in memory, aging and disease.
Our study will integrate the molecular mechanisms that govern biogenesis and function of ultra-long 3’ UTRs, from nucleus to synapse, in an animal model. The results of this research will create a major impact on our understanding of neuronal gene regulation in health and disease.
Summary
Neurons employ cell-specific gene regulatory mechanisms. One particularly striking process is the recently discovered, drastic lengthening of the 3’ untranslated region (3’ UTR) of hundreds of genes, which occurs in neurons from flies to humans. The function of the resulting ultra-long 3’ UTRs is unknown. RNA deregulation plays a central role in neurological diseases; to understand underlying causes, it is essential to study regulatory processes and define the function of these novel 3’ UTRs.
In Drosophila, the neuronal RNA-binding protein ELAV is the main effector of nervous system specific 3’ UTR extension. ELAV’s association with the promoter region of its target genes is required for synthesis of alternative, ultra-long 3’ UTRs. The mechanistic framework of this novel and exciting link between transcription initiation and alternative 3’ end processing is not understood yet.
We hypothesise that mRNAs carrying ultra-long 3’ UTRs create an important communication avenue between transcription regulation and synaptic function. In this proposal, we will study the regulation of ELAV-mediated 3’ UTR extension in a Drosophila model. First, we will provide mechanistic insight into the co-transcriptional processes that give rise to ultra-long 3’ UTRs. Employing genomics, proteomics and biochemistry, we will study the recruitment of ELAV at gene promoters and to nascent mRNA. Second, we will follow the journey of extended mRNAs from their site of synthesis to their destination using imaging, proteomics, and functional genetics. Finally, based on our unpublished results that 3’ UTR plasticity impacts neuronal function, we will analyse the role of ultra-long 3’ UTRs in memory, aging and disease.
Our study will integrate the molecular mechanisms that govern biogenesis and function of ultra-long 3’ UTRs, from nucleus to synapse, in an animal model. The results of this research will create a major impact on our understanding of neuronal gene regulation in health and disease.
Max ERC Funding
1 497 500 €
Duration
Start date: 2019-01-01, End date: 2023-12-31
Project acronym PartonicNucleus
Project Understanding the Quark and Gluon Structure of the Nucleus
Researcher (PI) Raphael DUPRE
Host Institution (HI) CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS
Country France
Call Details Starting Grant (StG), PE2, ERC-2018-STG
Summary The representation of the nucleus as an aggregate of protons and neutrons has been quite successful to describe nuclear properties in the past. However, it is now the time to understand the nuclear structure in terms of quarks and gluons (i.e. the partons). We have known for more than 30 years that the quark distribution deviates by up to 20% from the standard model of nuclear physics. With time, most explanations of this phenomenon have come to fail and this major nuclear effect remains today a mystery, but clearly tells us that a description of the nucleus in which protons and neutrons are not affected by their surrounding medium is incomplete. I propose here to use several recent developments in detection technologies and in hadron physics theory to perform new experiments that will unravel the deeper structure of the atomic nucleus. The first measurement will give the 3D tomography of the nucleus in terms of quarks and gluons. Second, I lay out a strategy to measure transverse momentum dependent parton distribution functions in cold nuclear matter and show how
it can help understand the gluon saturation scale, i.e. the onset of non linear behavior in the nuclear gluon structure. Third, I propose to measure reactions, in which we detect nuclear remnants, to link the nucleon and quark dynamics of the nucleus together. The proposed measurements necessitate the development of a dedicated nuclear low energy recoil tracker (ALERT), that I propose to develop and build in the IPN Orsay laboratory at the Paris-Saclay University (France). This detector will be used at the recently upgraded electron accelerator of Jefferson Lab (USA). This facility offers a unique setup with the most intense multi-GeV electron beam in the world. Together, these three unique measurements form a comprehensive program to decisively advance our understanding of the nuclear structure in terms of quarks and gluons.
Summary
The representation of the nucleus as an aggregate of protons and neutrons has been quite successful to describe nuclear properties in the past. However, it is now the time to understand the nuclear structure in terms of quarks and gluons (i.e. the partons). We have known for more than 30 years that the quark distribution deviates by up to 20% from the standard model of nuclear physics. With time, most explanations of this phenomenon have come to fail and this major nuclear effect remains today a mystery, but clearly tells us that a description of the nucleus in which protons and neutrons are not affected by their surrounding medium is incomplete. I propose here to use several recent developments in detection technologies and in hadron physics theory to perform new experiments that will unravel the deeper structure of the atomic nucleus. The first measurement will give the 3D tomography of the nucleus in terms of quarks and gluons. Second, I lay out a strategy to measure transverse momentum dependent parton distribution functions in cold nuclear matter and show how
it can help understand the gluon saturation scale, i.e. the onset of non linear behavior in the nuclear gluon structure. Third, I propose to measure reactions, in which we detect nuclear remnants, to link the nucleon and quark dynamics of the nucleus together. The proposed measurements necessitate the development of a dedicated nuclear low energy recoil tracker (ALERT), that I propose to develop and build in the IPN Orsay laboratory at the Paris-Saclay University (France). This detector will be used at the recently upgraded electron accelerator of Jefferson Lab (USA). This facility offers a unique setup with the most intense multi-GeV electron beam in the world. Together, these three unique measurements form a comprehensive program to decisively advance our understanding of the nuclear structure in terms of quarks and gluons.
Max ERC Funding
1 405 881 €
Duration
Start date: 2018-10-01, End date: 2023-09-30
Project acronym PRiSM
Project Programming Sensory regulation of Metabolism
Researcher (PI) Sophie Marie Francine STECULORUM
Host Institution (HI) MAX-PLANCK-GESELLSCHAFT ZUR FORDERUNG DER WISSENSCHAFTEN EV
Country Germany
Call Details Starting Grant (StG), LS4, ERC-2018-STG
Summary Sensory perception has recently emerged as a master regulator of integrative physiology and behavior, including feeding, by controlling fundamental and pleiotropic regulatory processes of energy and glucose homeostasis. Further, sensory perception is altered in obesity and type 2 diabetes, and childhood obesity correlates with early sensory deficit. Along this line, the discovery of the developmental origins of health and diseases revealed that metabolic diseases have recognized roots in the very early stages of life and can be predisposed to by changes in the perinatal hormonal and nutritional environments, such as occur in cases of maternal obesity and unhealthy diet. In this context, an accumulating body of evidence suggests that maternal health and nutrition could negatively impinge on the development of sensory perception, and subsequently, on the lifelong regulation of sensory-dependent control of metabolic, physiological, and behavioral regulatory processes. This innovative research program consists of four autonomous but complementary projects aimed at (1) deciphering the exact central regulatory processes mediating sensory control of feeding behavior and glucose homeostasis, (2) uncovering the influence of maternal health and nutrition on lifelong sensory regulation of metabolism, and (3) & (4) investigating two independent, yet synergistic, mechanisms that could mediate developmental programming of sensory metabolic regulation. This research program will employ a technology framework of physiological, behavioral, and developmental analyses in mice in concert with state-of-the-art systems neuroscience approaches, including optogenetics, chemogenetics, and in vivo calcium imaging. Collectively, the overarching goals of this research program are to provide new insights into the precise regulatory processes of sensory metabolic regulation and to shed light on critical basic mechanisms underlying the developmental programming of metabolic diseases.
Summary
Sensory perception has recently emerged as a master regulator of integrative physiology and behavior, including feeding, by controlling fundamental and pleiotropic regulatory processes of energy and glucose homeostasis. Further, sensory perception is altered in obesity and type 2 diabetes, and childhood obesity correlates with early sensory deficit. Along this line, the discovery of the developmental origins of health and diseases revealed that metabolic diseases have recognized roots in the very early stages of life and can be predisposed to by changes in the perinatal hormonal and nutritional environments, such as occur in cases of maternal obesity and unhealthy diet. In this context, an accumulating body of evidence suggests that maternal health and nutrition could negatively impinge on the development of sensory perception, and subsequently, on the lifelong regulation of sensory-dependent control of metabolic, physiological, and behavioral regulatory processes. This innovative research program consists of four autonomous but complementary projects aimed at (1) deciphering the exact central regulatory processes mediating sensory control of feeding behavior and glucose homeostasis, (2) uncovering the influence of maternal health and nutrition on lifelong sensory regulation of metabolism, and (3) & (4) investigating two independent, yet synergistic, mechanisms that could mediate developmental programming of sensory metabolic regulation. This research program will employ a technology framework of physiological, behavioral, and developmental analyses in mice in concert with state-of-the-art systems neuroscience approaches, including optogenetics, chemogenetics, and in vivo calcium imaging. Collectively, the overarching goals of this research program are to provide new insights into the precise regulatory processes of sensory metabolic regulation and to shed light on critical basic mechanisms underlying the developmental programming of metabolic diseases.
Max ERC Funding
1 500 000 €
Duration
Start date: 2019-06-01, End date: 2024-05-31
Project acronym QNets
Project Open Quantum Neural Networks: from Fundamental Concepts to Implementations with Atoms and Photons
Researcher (PI) Markus MUELLER
Host Institution (HI) FORSCHUNGSZENTRUM JULICH GMBH
Country Germany
Call Details Starting Grant (StG), PE2, ERC-2018-STG
Summary Reaching a fundamental understanding of quantum many-body systems and fully harnessing their computational power for information processing is one of today’s greatest scientific challenges. To date, unprecedented research efforts are underway to build quantum devices, which would outperform the most powerful classical computers. At the same time, neural networks are currently revolutionising the handling of large amounts of data, with enormous success in pattern and speech recognition, machine learning, the analysis of ‘big data’ and ‘deep learning’. Driven by the hope of combining massive parallel information processing in neural networks with quantum advantages like computational speedup, there have been various efforts to develop quantum neural networks – without satisfactory answers to date. The overarching goal of this theoretical research programme is to tackle this enormous challenge from a fresh perspective: we will establish and explore a conceptual framework for quantum neural networks and identify quantum optical physical building blocks, based on concepts in the domain of open many-body quantum systems. This ambitious aim will be achieved by interlinking a multitude of scientific areas ranging from atomic physics, quantum optics, quantum engineering and condensed matter physics to quantum information and computer science. This research will not only generate a genuine step change in our fundamental understanding of the ways nature allows for quantum information processing. It will also lay the foundation for quantum neuromorphic engineering of a new generation of quantum neural hardware in state-of-the-art and newly emerging experimental systems of ultra-cold atoms and trapped ions. With my interdisciplinary background in quantum information and quantum engineering, quantum optics and atomic physics, I am in a unique position to successfully realise this research. I will also strongly benefit from the vital scientific environment at Swansea University.
Summary
Reaching a fundamental understanding of quantum many-body systems and fully harnessing their computational power for information processing is one of today’s greatest scientific challenges. To date, unprecedented research efforts are underway to build quantum devices, which would outperform the most powerful classical computers. At the same time, neural networks are currently revolutionising the handling of large amounts of data, with enormous success in pattern and speech recognition, machine learning, the analysis of ‘big data’ and ‘deep learning’. Driven by the hope of combining massive parallel information processing in neural networks with quantum advantages like computational speedup, there have been various efforts to develop quantum neural networks – without satisfactory answers to date. The overarching goal of this theoretical research programme is to tackle this enormous challenge from a fresh perspective: we will establish and explore a conceptual framework for quantum neural networks and identify quantum optical physical building blocks, based on concepts in the domain of open many-body quantum systems. This ambitious aim will be achieved by interlinking a multitude of scientific areas ranging from atomic physics, quantum optics, quantum engineering and condensed matter physics to quantum information and computer science. This research will not only generate a genuine step change in our fundamental understanding of the ways nature allows for quantum information processing. It will also lay the foundation for quantum neuromorphic engineering of a new generation of quantum neural hardware in state-of-the-art and newly emerging experimental systems of ultra-cold atoms and trapped ions. With my interdisciplinary background in quantum information and quantum engineering, quantum optics and atomic physics, I am in a unique position to successfully realise this research. I will also strongly benefit from the vital scientific environment at Swansea University.
Max ERC Funding
1 486 439 €
Duration
Start date: 2019-10-01, End date: 2024-09-30
