Project acronym 2-HIT
Project Genetic interaction networks: From C. elegans to human disease
Researcher (PI) Ben Lehner
Host Institution (HI) FUNDACIO CENTRE DE REGULACIO GENOMICA
Call Details Starting Grant (StG), LS2, ERC-2007-StG
Summary Most hereditary diseases in humans are genetically complex, resulting from combinations of mutations in multiple genes. However synthetic interactions between genes are very difficult to identify in population studies because of a lack of statistical power and we fundamentally do not understand how mutations interact to produce phenotypes. C. elegans is a unique animal in which genetic interactions can be rapidly identified in vivo using RNA interference, and we recently used this system to construct the first genetic interaction network for any animal, focused on signal transduction genes. The first objective of this proposal is to extend this work and map a comprehensive genetic interaction network for this model metazoan. This project will provide the first insights into the global properties of animal genetic interaction networks, and a comprehensive view of the functional relationships between genes in an animal. The second objective of the proposal is to use C. elegans to develop and validate experimentally integrated gene networks that connect genes to phenotypes and predict genetic interactions on a genome-wide scale. The methods that we develop and validate in C. elegans will then be applied to predict phenotypes and interactions for human genes. The final objective is to dissect the molecular mechanisms underlying genetic interactions, and to understand how these interactions evolve. The combined aim of these three objectives is to generate a framework for understanding and predicting how mutations interact to produce phenotypes, including in human disease.
Summary
Most hereditary diseases in humans are genetically complex, resulting from combinations of mutations in multiple genes. However synthetic interactions between genes are very difficult to identify in population studies because of a lack of statistical power and we fundamentally do not understand how mutations interact to produce phenotypes. C. elegans is a unique animal in which genetic interactions can be rapidly identified in vivo using RNA interference, and we recently used this system to construct the first genetic interaction network for any animal, focused on signal transduction genes. The first objective of this proposal is to extend this work and map a comprehensive genetic interaction network for this model metazoan. This project will provide the first insights into the global properties of animal genetic interaction networks, and a comprehensive view of the functional relationships between genes in an animal. The second objective of the proposal is to use C. elegans to develop and validate experimentally integrated gene networks that connect genes to phenotypes and predict genetic interactions on a genome-wide scale. The methods that we develop and validate in C. elegans will then be applied to predict phenotypes and interactions for human genes. The final objective is to dissect the molecular mechanisms underlying genetic interactions, and to understand how these interactions evolve. The combined aim of these three objectives is to generate a framework for understanding and predicting how mutations interact to produce phenotypes, including in human disease.
Max ERC Funding
1 100 000 €
Duration
Start date: 2008-09-01, End date: 2014-04-30
Project acronym 4DVIDEO
Project 4DVideo: 4D spatio-temporal modeling of real-world events from video streams
Researcher (PI) Marc Pollefeys
Host Institution (HI) EIDGENOESSISCHE TECHNISCHE HOCHSCHULE ZUERICH
Call Details Starting Grant (StG), PE5, ERC-2007-StG
Summary The focus of this project is the development of algorithms that allow one to capture and analyse dynamic events taking place in the real world. For this, we intend to develop smart camera networks that can perform a multitude of observation tasks, ranging from surveillance and tracking to high-fidelity, immersive reconstructions of important dynamic events (i.e. 4D videos). There are many fundamental questions in computer vision associated with these problems. Can the geometric, topologic and photometric properties of the camera network be obtained from live images? What is changing about the environment in which the network is embedded? How much information can be obtained from dynamic events that are observed by the network? What if the camera network consists of a random collection of sensors that happened to observe a particular event (think hand-held cell phone cameras)? Do we need synchronization? Those questions become even more challenging if one considers active camera networks that can adapt to the vision task at hand. How should resources be prioritized for different tasks? Can we derive optimal strategies to control camera parameters such as pan, tilt and zoom, trade-off resolution, frame-rate and bandwidth? More fundamentally, seeing cameras as points that sample incoming light rays and camera networks as a distributed sensor, how does one decide which rays should be sampled? Many of those issues are particularly interesting when we consider time-varying events. Both spatial and temporal resolution are important and heterogeneous frame-rates and resolution can offer advantages. Prior knowledge or information obtained from earlier samples can be used to restrict the possible range of solutions (e.g. smoothness assumption and motion prediction). My goal is to obtain fundamental answers to many of those question based on thorough theoretical analysis combined with practical algorithms that are proven on real applications.
Summary
The focus of this project is the development of algorithms that allow one to capture and analyse dynamic events taking place in the real world. For this, we intend to develop smart camera networks that can perform a multitude of observation tasks, ranging from surveillance and tracking to high-fidelity, immersive reconstructions of important dynamic events (i.e. 4D videos). There are many fundamental questions in computer vision associated with these problems. Can the geometric, topologic and photometric properties of the camera network be obtained from live images? What is changing about the environment in which the network is embedded? How much information can be obtained from dynamic events that are observed by the network? What if the camera network consists of a random collection of sensors that happened to observe a particular event (think hand-held cell phone cameras)? Do we need synchronization? Those questions become even more challenging if one considers active camera networks that can adapt to the vision task at hand. How should resources be prioritized for different tasks? Can we derive optimal strategies to control camera parameters such as pan, tilt and zoom, trade-off resolution, frame-rate and bandwidth? More fundamentally, seeing cameras as points that sample incoming light rays and camera networks as a distributed sensor, how does one decide which rays should be sampled? Many of those issues are particularly interesting when we consider time-varying events. Both spatial and temporal resolution are important and heterogeneous frame-rates and resolution can offer advantages. Prior knowledge or information obtained from earlier samples can be used to restrict the possible range of solutions (e.g. smoothness assumption and motion prediction). My goal is to obtain fundamental answers to many of those question based on thorough theoretical analysis combined with practical algorithms that are proven on real applications.
Max ERC Funding
1 757 422 €
Duration
Start date: 2008-08-01, End date: 2013-11-30
Project acronym ADIPODIF
Project Adipocyte Differentiation and Metabolic Functions in Obesity and Type 2 Diabetes
Researcher (PI) Christian Wolfrum
Host Institution (HI) EIDGENOESSISCHE TECHNISCHE HOCHSCHULE ZUERICH
Call Details Starting Grant (StG), LS6, ERC-2007-StG
Summary Obesity associated disorders such as T2D, hypertension and CVD, commonly referred to as the “metabolic syndrome”, are prevalent diseases of industrialized societies. Deranged adipose tissue proliferation and differentiation contribute significantly to the development of these metabolic disorders. Comparatively little however is known, about how these processes influence the development of metabolic disorders. Using a multidisciplinary approach, I plan to elucidate molecular mechanisms underlying the altered adipocyte differentiation and maturation in different models of obesity associated metabolic disorders. Special emphasis will be given to the analysis of gene expression, postranslational modifications and lipid molecular species composition. To achieve this goal, I am establishing several novel methods to isolate pure primary preadipocytes including a new animal model that will allow me to monitor preadipocytes, in vivo and track their cellular fate in the context of a complete organism. These systems will allow, for the first time to study preadipocyte biology, in an in vivo setting. By monitoring preadipocyte differentiation in vivo, I will also be able to answer the key questions regarding the development of preadipocytes and examine signals that induce or inhibit their differentiation. Using transplantation techniques, I will elucidate the genetic and environmental contributions to the progression of obesity and its associated metabolic disorders. Furthermore, these studies will integrate a lipidomics approach to systematically analyze lipid molecular species composition in different models of metabolic disorders. My studies will provide new insights into the mechanisms and dynamics underlying adipocyte differentiation and maturation, and relate them to metabolic disorders. Detailed knowledge of these mechanisms will facilitate development of novel therapeutic approaches for the treatment of obesity and associated metabolic disorders.
Summary
Obesity associated disorders such as T2D, hypertension and CVD, commonly referred to as the “metabolic syndrome”, are prevalent diseases of industrialized societies. Deranged adipose tissue proliferation and differentiation contribute significantly to the development of these metabolic disorders. Comparatively little however is known, about how these processes influence the development of metabolic disorders. Using a multidisciplinary approach, I plan to elucidate molecular mechanisms underlying the altered adipocyte differentiation and maturation in different models of obesity associated metabolic disorders. Special emphasis will be given to the analysis of gene expression, postranslational modifications and lipid molecular species composition. To achieve this goal, I am establishing several novel methods to isolate pure primary preadipocytes including a new animal model that will allow me to monitor preadipocytes, in vivo and track their cellular fate in the context of a complete organism. These systems will allow, for the first time to study preadipocyte biology, in an in vivo setting. By monitoring preadipocyte differentiation in vivo, I will also be able to answer the key questions regarding the development of preadipocytes and examine signals that induce or inhibit their differentiation. Using transplantation techniques, I will elucidate the genetic and environmental contributions to the progression of obesity and its associated metabolic disorders. Furthermore, these studies will integrate a lipidomics approach to systematically analyze lipid molecular species composition in different models of metabolic disorders. My studies will provide new insights into the mechanisms and dynamics underlying adipocyte differentiation and maturation, and relate them to metabolic disorders. Detailed knowledge of these mechanisms will facilitate development of novel therapeutic approaches for the treatment of obesity and associated metabolic disorders.
Max ERC Funding
1 607 105 €
Duration
Start date: 2008-07-01, End date: 2013-06-30
Project acronym ATOMKI-PPROCESS
Project Nuclear reaction studies relevant to the astrophysical p-process nucleosynthesis
Researcher (PI) György Gyürky
Host Institution (HI) Magyar Tudomanyos Akademia Atommagkutato Intezete
Call Details Starting Grant (StG), PE2, ERC-2007-StG
Summary The astrophysical p-process, the stellar production mechanism of the heavy, proton rich isotopes (p-isotopes), is one of the least studied processes in nucleosynthesis. The astrophysical site(s) for the p-process could not yet be clearly identified. In order to reproduce the natural abundances of the p-isotopes, the p-process models must take into account a huge nuclear reaction network. A precise knowledge of the rate of the nuclear reactions in this network is essential for a reliable abundance calculation and for a clear assignment of the astrophysical site(s). For lack of experimental data the nuclear physics inputs for the reaction networks are based on statistical model calculations. These calculations are largely untested in the mass and energy range relevant to the p-process and the uncertainties in the reaction rate values result in a correspondingly uncertain prediction of the p-isotope abundances. Therefore, experiments aiming at the determination of reaction rates for the p-process are of great importance. In this project nuclear reaction cross section measurements will be carried out in the mass and energy range of p-process to check the reliability of the statistical model calculations and to put the p-process models on a more reliable base. The accelerators of the Institute of Nuclear Research in Debrecen, Hungary provide the necessary basis for such studies. The p-process model calculations are especially sensitive to the rates of reactions involving alpha particles and heavy nuclei. Because of technical difficulties, so far there are practically no experimental data available on such reactions and the uncertainty in these reaction rates is presently one of the biggest contributions to the uncertainty of p-isotope abundance calculations. With the help of the ERC grant the alpha-induced reaction cross sections can be measured on heavy isotopes for the first time, which could contribute to a better understanding of the astrophysical p-process.
Summary
The astrophysical p-process, the stellar production mechanism of the heavy, proton rich isotopes (p-isotopes), is one of the least studied processes in nucleosynthesis. The astrophysical site(s) for the p-process could not yet be clearly identified. In order to reproduce the natural abundances of the p-isotopes, the p-process models must take into account a huge nuclear reaction network. A precise knowledge of the rate of the nuclear reactions in this network is essential for a reliable abundance calculation and for a clear assignment of the astrophysical site(s). For lack of experimental data the nuclear physics inputs for the reaction networks are based on statistical model calculations. These calculations are largely untested in the mass and energy range relevant to the p-process and the uncertainties in the reaction rate values result in a correspondingly uncertain prediction of the p-isotope abundances. Therefore, experiments aiming at the determination of reaction rates for the p-process are of great importance. In this project nuclear reaction cross section measurements will be carried out in the mass and energy range of p-process to check the reliability of the statistical model calculations and to put the p-process models on a more reliable base. The accelerators of the Institute of Nuclear Research in Debrecen, Hungary provide the necessary basis for such studies. The p-process model calculations are especially sensitive to the rates of reactions involving alpha particles and heavy nuclei. Because of technical difficulties, so far there are practically no experimental data available on such reactions and the uncertainty in these reaction rates is presently one of the biggest contributions to the uncertainty of p-isotope abundance calculations. With the help of the ERC grant the alpha-induced reaction cross sections can be measured on heavy isotopes for the first time, which could contribute to a better understanding of the astrophysical p-process.
Max ERC Funding
750 000 €
Duration
Start date: 2008-07-01, End date: 2013-06-30
Project acronym BCLYM
Project Molecular mechanisms of mature B cell lymphomagenesis
Researcher (PI) Almudena Ramiro
Host Institution (HI) CENTRO NACIONAL DE INVESTIGACIONESCARDIOVASCULARES CARLOS III (F.S.P.)
Call Details Starting Grant (StG), LS3, ERC-2007-StG
Summary Most of the lymphomas diagnosed in the western world are originated from mature B cells. The hallmark of these malignancies is the presence of recurrent chromosome translocations that usually involve the immunoglobulin loci and a proto-oncogene. As a result of the translocation event the proto-oncogene becomes deregulated under the influence of immunoglobulin cis sequences thus playing an important role in the etiology of the disease. Upon antigen encounter mature B cells engage in the germinal center reaction, a complex differentiation program of critical importance to the development of the secondary immune response. The germinal center reaction entails the somatic remodelling of immunoglobulin genes by the somatic hypermutation and class switch recombination reactions, both of which are triggered by Activation Induced Deaminase (AID). We have previously shown that AID also initiates lymphoma-associated c-myc/IgH chromosome translocations. In addition, the germinal center reaction involves a fine-tuned balance between intense B cell proliferation and program cell death. This environment seems to render B cells particularly vulnerable to malignant transformation. We aim at studying the molecular events responsible for B cell susceptibility to lymphomagenesis from two perspectives. First, we will address the role of AID in the generation of lymphomagenic lesions in the context of AID specificity and transcriptional activation. Second, we will approach the regulatory function of microRNAs of AID-dependent, germinal center events. The proposal aims at the molecular understanding of a process that lies in the interface of immune regulation and oncogenic transformation and therefore the results will have profound implications both to basic and clinical understanding of lymphomagenesis.
Summary
Most of the lymphomas diagnosed in the western world are originated from mature B cells. The hallmark of these malignancies is the presence of recurrent chromosome translocations that usually involve the immunoglobulin loci and a proto-oncogene. As a result of the translocation event the proto-oncogene becomes deregulated under the influence of immunoglobulin cis sequences thus playing an important role in the etiology of the disease. Upon antigen encounter mature B cells engage in the germinal center reaction, a complex differentiation program of critical importance to the development of the secondary immune response. The germinal center reaction entails the somatic remodelling of immunoglobulin genes by the somatic hypermutation and class switch recombination reactions, both of which are triggered by Activation Induced Deaminase (AID). We have previously shown that AID also initiates lymphoma-associated c-myc/IgH chromosome translocations. In addition, the germinal center reaction involves a fine-tuned balance between intense B cell proliferation and program cell death. This environment seems to render B cells particularly vulnerable to malignant transformation. We aim at studying the molecular events responsible for B cell susceptibility to lymphomagenesis from two perspectives. First, we will address the role of AID in the generation of lymphomagenic lesions in the context of AID specificity and transcriptional activation. Second, we will approach the regulatory function of microRNAs of AID-dependent, germinal center events. The proposal aims at the molecular understanding of a process that lies in the interface of immune regulation and oncogenic transformation and therefore the results will have profound implications both to basic and clinical understanding of lymphomagenesis.
Max ERC Funding
1 596 000 €
Duration
Start date: 2008-12-01, End date: 2014-11-30
Project acronym CANCER SIGNALOSOMES
Project Spatially and temporally regulated membrane complexes in cancer cell invasion and cytokinesis
Researcher (PI) Johanna Ivaska
Host Institution (HI) TEKNOLOGIAN TUTKIMUSKESKUS VTT
Call Details Starting Grant (StG), LS1, ERC-2007-StG
Summary Cancer progression, characterized by uncontrolled proliferation and motility of cells, is a complex and deadly process. Integrins, a major cell surface adhesion receptor family, are transmembrane proteins known to regulate cell behaviour by transducing extracellular signals to cytoplasmic protein complexes. We and others have shown that recruitment of specific protein complexes by the cytoplasmic domains of integrins is important in tumorigenesis. Here our aim is to study three interrelated processes in cancer progression which involve integrin signalling, but which have not been elucidated earlier at all. 1) Integrins in cell division (cytokinesis). Since coordinated action of the cytoskeleton and membranes is needed both for cell division and motility, shared integrin functions can regulate both events. 2) Dynamic integrin signalosomes at the leading edge of invading cells. Spatially and temporally regulated, integrin-protein complexes at the front of infiltrating cells are likely to dictate the movement of cancer cells in tissues. 3) Transmembrane segments of integrins as scaffolds for integrin signalling. In addition to cytosolic proteins, integrins most likely interact with proteins within the membrane resulting into new signalling modalities. In this proposal we will use innovative, modern and even unconventional techniques (such as RNAi and live-cell arrays detecting integrin traffic, cell motility and multiplication, laser-microdissection, proteomics and bacterial-two-hybrid screens) to unravel these new integrin functions, for which we have preliminary evidence. Each project will give fundamentally novel mechanistic insight into the role of integrins in cancer. Moreover, these interdisciplinary new openings will increase our understanding in cancer progression in general and will open new possibilities for therapeutic intervention targeting both cancer proliferation and dissemination in the body.
Summary
Cancer progression, characterized by uncontrolled proliferation and motility of cells, is a complex and deadly process. Integrins, a major cell surface adhesion receptor family, are transmembrane proteins known to regulate cell behaviour by transducing extracellular signals to cytoplasmic protein complexes. We and others have shown that recruitment of specific protein complexes by the cytoplasmic domains of integrins is important in tumorigenesis. Here our aim is to study three interrelated processes in cancer progression which involve integrin signalling, but which have not been elucidated earlier at all. 1) Integrins in cell division (cytokinesis). Since coordinated action of the cytoskeleton and membranes is needed both for cell division and motility, shared integrin functions can regulate both events. 2) Dynamic integrin signalosomes at the leading edge of invading cells. Spatially and temporally regulated, integrin-protein complexes at the front of infiltrating cells are likely to dictate the movement of cancer cells in tissues. 3) Transmembrane segments of integrins as scaffolds for integrin signalling. In addition to cytosolic proteins, integrins most likely interact with proteins within the membrane resulting into new signalling modalities. In this proposal we will use innovative, modern and even unconventional techniques (such as RNAi and live-cell arrays detecting integrin traffic, cell motility and multiplication, laser-microdissection, proteomics and bacterial-two-hybrid screens) to unravel these new integrin functions, for which we have preliminary evidence. Each project will give fundamentally novel mechanistic insight into the role of integrins in cancer. Moreover, these interdisciplinary new openings will increase our understanding in cancer progression in general and will open new possibilities for therapeutic intervention targeting both cancer proliferation and dissemination in the body.
Max ERC Funding
1 529 369 €
Duration
Start date: 2008-08-01, End date: 2013-07-31
Project acronym CDSIF
Project Contour dynamics and singularities in incompressible flows
Researcher (PI) Diego Cordoba
Host Institution (HI) AGENCIA ESTATAL CONSEJO SUPERIOR DEINVESTIGACIONES CIENTIFICAS
Call Details Starting Grant (StG), PE1, ERC-2007-StG
Summary The search of singularities in incompressible flows has become a major challenge in the area of non-linear partial differential equations and is relevant in applied mathematics, physics and engineering. The existence of such singularities would have important consequences for the understanding of turbulence. One way to make progress in this direction, is to study plausible scenarios for the singularities supported by experiments or numerical analysis. With the more sophisticated numerical tools now available, the subject has recently gained considerable momentum. The main goal of this project is to study analytically several incompressible fluid models. In particular solutions that involve the possible formation of singularities or quasi-singular structures.
Summary
The search of singularities in incompressible flows has become a major challenge in the area of non-linear partial differential equations and is relevant in applied mathematics, physics and engineering. The existence of such singularities would have important consequences for the understanding of turbulence. One way to make progress in this direction, is to study plausible scenarios for the singularities supported by experiments or numerical analysis. With the more sophisticated numerical tools now available, the subject has recently gained considerable momentum. The main goal of this project is to study analytically several incompressible fluid models. In particular solutions that involve the possible formation of singularities or quasi-singular structures.
Max ERC Funding
650 000 €
Duration
Start date: 2008-09-01, End date: 2013-08-31
Project acronym CHROMOREPAIR
Project Genome Maintenance in the Context of Chromatin
Researcher (PI) Oscar Fernández-Capetillo Ruiz
Host Institution (HI) FUNDACION CENTRO NACIONAL DE INVESTIGACIONES ONCOLOGICAS CARLOS III
Call Details Starting Grant (StG), LS1, ERC-2007-StG
Summary With the availability of the essentially complete sequence of the human genome, as well as a rapid development of massive sequencing techniques, the research efforts to understand genetics and disease from a cis standpoint will soon reach an endpoint. However, our emerging knowledge of gene regulation networks reveals that epigenetic regulation of the hereditary information plays crucial roles in various biological events through its influence on processes such as transcription, DNA replication and chromosome architecture. Another scenario in which the control of chromatin structure is crucial is the repair of lesions in genomic DNA. There is mounting evidence, particularly from model organisms such as Saccharomyces cerevisiae, that histone modifying enzymes (acetylases, deacetylases, kinases, …) are essential components of the machinery that maintains genome integrity and thereby guards against cancer, degenerative diseases and ageing. However, little is known about the specific “code” of histone tail modifications that coordinate DNA repair, and the impact that an aberrant “histone code” may have on human health. In CHROMOREPAIR we will systematically analyze the chromatin remodelling process that undergoes at DNA lesions and evaluate the impact that chromatin alterations have on the access, signaling and repair of DNA damage. Furthermore, we propose to translate our in vitro knowledge to the development of mouse models that help us evaluate how modulation of chromatin status impinges on genome maintenance and therefore on cancer and aging. As a provocative line of research and based on our preliminary data, we propose that certain chromatin alterations could not only impair but also in some cases promote a more robust response to DNA breaks, which could be a novel and not yet explored way to potentiate the elimination of pre-cancerous cells.
Summary
With the availability of the essentially complete sequence of the human genome, as well as a rapid development of massive sequencing techniques, the research efforts to understand genetics and disease from a cis standpoint will soon reach an endpoint. However, our emerging knowledge of gene regulation networks reveals that epigenetic regulation of the hereditary information plays crucial roles in various biological events through its influence on processes such as transcription, DNA replication and chromosome architecture. Another scenario in which the control of chromatin structure is crucial is the repair of lesions in genomic DNA. There is mounting evidence, particularly from model organisms such as Saccharomyces cerevisiae, that histone modifying enzymes (acetylases, deacetylases, kinases, …) are essential components of the machinery that maintains genome integrity and thereby guards against cancer, degenerative diseases and ageing. However, little is known about the specific “code” of histone tail modifications that coordinate DNA repair, and the impact that an aberrant “histone code” may have on human health. In CHROMOREPAIR we will systematically analyze the chromatin remodelling process that undergoes at DNA lesions and evaluate the impact that chromatin alterations have on the access, signaling and repair of DNA damage. Furthermore, we propose to translate our in vitro knowledge to the development of mouse models that help us evaluate how modulation of chromatin status impinges on genome maintenance and therefore on cancer and aging. As a provocative line of research and based on our preliminary data, we propose that certain chromatin alterations could not only impair but also in some cases promote a more robust response to DNA breaks, which could be a novel and not yet explored way to potentiate the elimination of pre-cancerous cells.
Max ERC Funding
948 426 €
Duration
Start date: 2008-12-01, End date: 2013-11-30
Project acronym COSMO@LHC
Project Cosmology at the CERN Large Hadron Collider
Researcher (PI) Geraldine Servant
Host Institution (HI) EUROPEAN ORGANIZATION FOR NUCLEAR RESEARCH
Call Details Starting Grant (StG), PE2, ERC-2007-StG
Summary The Large Hadron Collider (LHC), a 7 + 7 TeV proton-proton collider under completion at CERN, the European Laboratory for Particle Physics in Geneva, will take experiments into a new energy domain beyond the Standard Model of strong and electroweak interactions. As the LHC will unveil the mysteries of the electroweak symmetry breaking, this will also have far-reaching implications for cosmology. The aim of this project is to work out what we may learn about the Early Universe from discoveries at the LHC. This concerns in particular the two fundamental questions of the nature of the Dark Matter and the origin of the matter-antimatter asymmetry of the Universe. The LHC-Cosmology interplay has been a topic of active research in the last years. However, studies have essentially focussed on a single class of models: supersymmetry. The original and innovative directions of this project are: 1) To investigate dark matter particle physics models that have not been explored yet and confront theoretical predictions with existing and upcoming observational constraints. Measuring the properties of the dark matter will require a complementarity between the LHC searches and the other numerous ongoing dark matter experiments such as gamma ray telescopes, neutrino telescopes, cosmic positron detectors ... etc. 2) To work out the details of the electroweak phase transition in extensions of the Standard Model. One of the best-motivated mechanism for generating the baryon asymmetry of the universe relies on a first-order electroweak phase transition. Interestingly, this has strong implications for Gravity Wave physics. We will explore thoroughly how the planned gravity wave detector and space interferometer LISA, which turns out to be a completely independent window on the electroweak scale, could complement the information provided by the LHC. This project will also serve as a solid basis for future research at the Internatinal electron-positron Linear Collider.
Summary
The Large Hadron Collider (LHC), a 7 + 7 TeV proton-proton collider under completion at CERN, the European Laboratory for Particle Physics in Geneva, will take experiments into a new energy domain beyond the Standard Model of strong and electroweak interactions. As the LHC will unveil the mysteries of the electroweak symmetry breaking, this will also have far-reaching implications for cosmology. The aim of this project is to work out what we may learn about the Early Universe from discoveries at the LHC. This concerns in particular the two fundamental questions of the nature of the Dark Matter and the origin of the matter-antimatter asymmetry of the Universe. The LHC-Cosmology interplay has been a topic of active research in the last years. However, studies have essentially focussed on a single class of models: supersymmetry. The original and innovative directions of this project are: 1) To investigate dark matter particle physics models that have not been explored yet and confront theoretical predictions with existing and upcoming observational constraints. Measuring the properties of the dark matter will require a complementarity between the LHC searches and the other numerous ongoing dark matter experiments such as gamma ray telescopes, neutrino telescopes, cosmic positron detectors ... etc. 2) To work out the details of the electroweak phase transition in extensions of the Standard Model. One of the best-motivated mechanism for generating the baryon asymmetry of the universe relies on a first-order electroweak phase transition. Interestingly, this has strong implications for Gravity Wave physics. We will explore thoroughly how the planned gravity wave detector and space interferometer LISA, which turns out to be a completely independent window on the electroweak scale, could complement the information provided by the LHC. This project will also serve as a solid basis for future research at the Internatinal electron-positron Linear Collider.
Max ERC Funding
800 000 €
Duration
Start date: 2008-07-01, End date: 2013-06-30
Project acronym COSPSENA
Project Coherence of Spins in Semiconductor Nanostructures
Researcher (PI) Dominik Max Zumbühl
Host Institution (HI) UNIVERSITAT BASEL
Call Details Starting Grant (StG), PE3, ERC-2007-StG
Summary Macroscopic control of quantum states is a major theme in much of modern physics because quantum coherence enables study of fundamental physics and has promising applications for quantum information processing. The potential significance of quantum computing is recognized well beyond the physics community. For electron spins in GaAs quantum dots, it has become clear that decoherence caused by interactions with the nuclear spins is a major challenge. We propose to investigate and reduce hyperfine induced decoherence with two complementary approaches: nuclear spin state narrowing and nuclear spin polarization. We propose a new projective state narrowing technique: a large, Coulomb blockaded dot measures the qubit nuclear ensemble, resulting in enhanced spin coherence times. Further, mediated by an interacting 2D electron gas via hyperfine interaction, a low temperature nuclear ferromagnetic spin state was predicted, which we propose to investigate using a quantum point contact as a nuclear polarization detector. Estimates indicate that the nuclear ferromagnetic transition occurs in the sub-Millikelvin range, well below already hard to reach temperatures around 10 mK. However, the exciting combination of interacting electron and nuclear spin physics as well as applications in spin qubits give ample incentive to strive for sub-Millikelvin temperatures in nanostructures. We propose to build a novel type of nuclear demagnetization refrigerator aiming to reach electron temperatures of 0.1 mK in semiconductor nanostructures. This interdisciplinary project combines Microkelvin and nanophysics, going well beyond the status quo. It is a challenging project that could be the beginning of a new era of coherent spin physics with unprecedented quantum control. This project requires a several year commitment and a team of two graduate students plus one postdoctoral fellow.
Summary
Macroscopic control of quantum states is a major theme in much of modern physics because quantum coherence enables study of fundamental physics and has promising applications for quantum information processing. The potential significance of quantum computing is recognized well beyond the physics community. For electron spins in GaAs quantum dots, it has become clear that decoherence caused by interactions with the nuclear spins is a major challenge. We propose to investigate and reduce hyperfine induced decoherence with two complementary approaches: nuclear spin state narrowing and nuclear spin polarization. We propose a new projective state narrowing technique: a large, Coulomb blockaded dot measures the qubit nuclear ensemble, resulting in enhanced spin coherence times. Further, mediated by an interacting 2D electron gas via hyperfine interaction, a low temperature nuclear ferromagnetic spin state was predicted, which we propose to investigate using a quantum point contact as a nuclear polarization detector. Estimates indicate that the nuclear ferromagnetic transition occurs in the sub-Millikelvin range, well below already hard to reach temperatures around 10 mK. However, the exciting combination of interacting electron and nuclear spin physics as well as applications in spin qubits give ample incentive to strive for sub-Millikelvin temperatures in nanostructures. We propose to build a novel type of nuclear demagnetization refrigerator aiming to reach electron temperatures of 0.1 mK in semiconductor nanostructures. This interdisciplinary project combines Microkelvin and nanophysics, going well beyond the status quo. It is a challenging project that could be the beginning of a new era of coherent spin physics with unprecedented quantum control. This project requires a several year commitment and a team of two graduate students plus one postdoctoral fellow.
Max ERC Funding
1 377 000 €
Duration
Start date: 2008-06-01, End date: 2013-05-31
