ERC Grants

The European Research Council (ERC) supports pioneering research by awarding highly endowed grants to outstanding scientists for groundbreaking projects.

ERC Starting Grants

The ERC Starting Grants (up to 2.5 million euros over a maximum of five years) are aimed at outstanding young researchers from all disciplines who are at the beginning of an independent scientific career in Europe and would like to set up their own research group or have already done so and would like to establish it on a longer-term basis.

The following ERC Starting Grants are currently being funded at the BMC:

ERC Starting Grant
EpiCblood - Towards early cancer detection and tumor classification using epigenomic biomarkers in blood
Project leader
Dr. Rodrigo Villaseñor
Institution
Division of Molecular Biology,
Biomedical Center (BMC)
Funding period
2024 to 2028
Website
Project description in CORDIS
Project description
Detecting cancer at an early stage can improve the chances of successful treatment and long-term survival. Dying cells release small DNA fragments wrapped around a core of histone proteins into the bloodstream, called circulating nucleosomes. These carry DNA sequence information and chemical modifications that are stable in the blood, reflecting promising disease biomarkers. The EpiCblood project, funded by the European Research Council, will explore the diagnostic potential of circulating nucleosomes for early cancer detection and tumour classification. The goal is to use several abundant histone modifications and cancer-specific combinatorial histone marks to predict the tissue of origin of the tumour and its gene expression pattern noninvasively. The results may advance liquid biopsy assays for personalised cancer management and early detection.

Source: CORDIS

ERC Starting Grant
oxDOPAMINE - Unraveling the mystery of preferential degeneration of midbrain neurons in neurodegerative diseases

Project leader
Prof. Dr. Lena Burbulla
Institution
Division of Metabolic Biochemistry, Biomedical Center (BMC)
Funding period
2021 to 2026
Website
Project description in CORDIS
Project description
In Parkinson's disease (PD), oxidised dopamine and alpha-synuclein serve as key mediators of mitochondrial and lysosomal dysfunction in midbrain dopaminergic neurons that preferentially degenerate in this progressive movement disorder. The working hypothesis of the EU-funded oxDOPAMINE project is that oxidation of dopamine aberrantly increases in PD. Scientists will investigate pathways of dopamine oxidation that predisposes human neurons to selective vulnerability and degeneration. Based on recent data implicating defective synaptic dopamine metabolism and iron dyshomeostasis in the oxidation of dopamine early in disease pathogenesis, they will study disorders associated with iron accumulation and progressive dopamine neuron degeneration to find common pathogenic mechanisms. Results may lead to novel strategies for restoring synaptic dysfunction and iron homeostasis as a means of preventing neurodegeneration.

Source: CORDIS
ERC Starting Grant
Baby DCs - Age-dependent regulation of dendritic cell development and function
Project leader
Prof. Dr. Barbara Schraml
Institution
Institute for Immunology, Biomedical Center (BMC)
Funding period
2017 to 2024
Website
Project description in CORDIS
Project description
Early life immune balance is essential for survival and establishment of healthy immunity in later life. We aim to define how age-dependent regulation of dendritic cell (DC) development contributes to this crucial immune balance. DCs are versatile controllers of immunity that in neonates are qualitatively distinct from adults. Why such age-dependent differences exist is unclear but newborn DCs are considered underdeveloped and functionally immature.
Using ontogenetic tracing of conventional DC precursors, I have found a previously unappreciated developmental heterogeneity of DCs that is particularly prominent in young mice. Preliminary data indicate that distinct waves of DC poiesis contribute to the functional differences between neonatal and adult DCs. I hypothesize that the neonatal DC compartment is not immature but rather that DC poiesis is developmentally regulated to create essential age-dependent immune balance. Further, I have identified a unique situation in early life to address a fundamental biological question, namely to what extent cellular function is pre-programmed by developmental origin (nature) versus environmental factors (nurture).
In this proposal, we will first use novel models to fate map the origin of the DC compartment with age. We will then define to what extent cellular origin determines age-dependent functions of DCs in immunity. Using innovative comparative gene expression profiling and integrative epigenomic analysis the cell intrinsic mechanisms regulating the age-dependent functions of DCs will be characterized. Because environmental factors in utero and after birth critically influence immune balance, we will finally define the impact of maternal infection and metabolic disease, as well as early microbial encounter on DC poiesis. Characterizing how developmentally regulated DC poiesis shapes the unique features of early life immunity will provide novel insights into immune development that are vital to advance vaccine strategies.

Source: CORDIS

ERC Consolidator Grants

The ERC Consolidator Grants (up to three million euros over a maximum of five years) are aimed at outstanding young researchers from all disciplines whose own independent working group is in the consolidation phase.

The following ERC Consolidator Grants are currently being funded at the BMC:

ERC Consolidator Grant
switchDecoding - Decoding the path to cellular variation within pathogen populations
Project leader
Prof. Dr. T. Nicolai Siegel
Institution
Division of Physiological Chemistry, Biomedical Center (BMC), and Division of Experimental Parasitology, Faculty of Veterinary Medicine
Funding period
2023 to 2028
Website
Project description in CORDIS
Project description
Heterogeneity amongst isogenic cells is pervasive throughout biology. Recently developed single-cell omics approaches are beginning to systematically reveal the repertoire of functionally distinct cell subpopulations within metazoan tissues. Pathogens frequently encounter changing and often hostile environments. To adapt to these challenges unicellular pathogen populations also exhibit a large degree of cell-to-cell heterogeneity, which often affects the outcome of infections. Yet, despite the importance of this cell-to-cell variation, very little is known about the mechanisms that control the level of heterogeneity in pathogen populations or why some isogenic populations are more heterogeneous than others. The goal of switchDecoding is to unveil the path to cellular variation. To this end I will go beyond identifying and describing new subpopulations of cells and elucidate the molecular pathways that establish them and modulate the level of cellular heterogeneity. As a model I will study the mechanism responsible for creating heterogeneity in surface antigen expression in the unicellular parasite Trypanosoma brucei. Antigenic variation is a widely employed strategy by evolutionarily divergent pathogens to evade the host immune response. Using a multidisciplinary approach, I will develop and combine single-cell multi-omics, lineage tracing and CRISPR-Cas-based genome manipulation strategies to characterize the processes, pathways and molecules regulating antigen switching in T. brucei. A better understanding of the mechanisms affecting the level of heterogeneity within a pathogen population will enable us to better predict how pathogens adapt to environmental challenges, including those that lead to the emergence of drug resistance. In the future this knowledge will enable the development of novel intervention strategies: drugs that modulate cell-to-cell heterogeneity to facilitate the clearance of infections.

Source: CORDIS
ERC Consolidator Grant
EpiCortex - Deciphering the Regulatory Logic of Cortical Development
Project leader
Dr. Boyan Bonev
Institution
Division of Physiological Genomics, Biomedical Center (BMC), and Helmholtz Munich
Funding period
2023 to 2027
Website
Project description in CORDIS
Project description
The mammalian cortex is the most complex region of the brain responsible for higher cognitive functions. Abnormal cortical development often translates into prominent neuropsychiatric diseases, which affect different neuronal subtypes with unique molecular and morphological features. Increasing evidence suggests that epigenetic regulation is essential for cortical development but how multiple regulatory layers are coordinated to specify distinct neuronal lineages in vivo remains unclear.
My team and I recently applied single-cell RNA-seq, single-cell ATAC-seq together with cell-type-specific DNA methylation and 3D genome measurements to map the regulatory landscape of neural differentiation at a single embryonic stage in vivo. However, the process of neuronal subtype specification involves multiple distinct waves of differentiation over several consecutive days. Therefore, to decode the molecular logic of temporal cellular identity in the cortex, I will comprehensively dissect the interplay between gene expression, chromatin topology and epigenetics in specifying cell fate.
In order to accomplish this, I will build upon my extensive experimental and computational expertise to (1) map the regulatory landscape of the developing mouse cortex across multiple regulatory layers and timepoints in single cells; (2) identify and validate cis-regulatory elements via a novel massive parallel cell-type specific reporter assay in vivo and (3) determine the functional consequences of perturbing enhancers and silencers using a highly multiplexed single-cell approach. Collectively, EpiCortex will provide unprecedented insights and establish new paradigms into the interplay between transcription factors, epigenome dynamics and gene expression in development. It will allow us to better understand the molecular logic of lineage specification in the mammalian cortex and more precisely define, compare and ultimately engineer cellular identities for therapeutic and regenerative purposes

Source: CORDIS
ERC Consolidator Grant
ExoDevo - Extracellular vesicles-mediated cross-talk during human brain development and disease
Project leader
Prof. Dr. Silvia Cappello
Institution
Division of Physiological Genomics, Biomedical Center (BMC)
Funding period
2022 to 2027
Website
Project description in CORDIS
Project description
Cellular communication is enabled by many factors including secreted vesicles that transfer nucleic acids, lipids, and proteins. Extracellular vesicles (EVs) are involved in neuron-to-neuron communication, while EV's role in the progenitor-to-neuron and -astrocyte communication during brain development has been poorly investigated. Notably, more than 60% of the genes associated with neurodevelopmental diseases encode proteins carried by EVs. The ERC-funded ExoDevo project aims to investigate the role of EVs during brain development. It will focus on the physiological function of EVs, mediating the cell-to-cell signalling, using transcriptomics, proteomics, imaging, and functional analysis of EVs from human cerebral organoids. This study will provide a better understanding of the fundamental mechanisms in brain development and neurodevelopmental pathologies.

Source: CORDIS

ERC Advanced Grants

The ERC Advanced Grants (up to 3.5 million euros over a maximum of five years) are aimed at established scientists from all disciplines whose highly innovative research goes significantly beyond the current state of research and opens up new areas of research.

The following ERC Advanced Grant is currently being funded at the BMC:

ERC Advanced Grant
NeuroCentro - Novel mechanisms of neurogenesis- from centrosome to engineering migration
Project leader
Prof. Dr. Magdalena Götz
Institution
Division of Physiological Genomics, Biomedical Center (BMC)
Funding period
2020 to 2025
Website
Project description in CORDIS
Project description
The centrosome is an organelle that serves as the microtubule-organising centre of the animal cell and is involved in functions such as cell division, cilia formation and migration. Mutations in centrosome-associated proteins lead to brain diseases, but the mechanisms of this process are not known. The EU-funded NeuroCentro project will study fundamental functions of neural-specific centrosome proteins, aiming to understand the brain-specific phenotype of mutations. The research capitalises on a recent project team discovery of novel centrosome-associated RNA-binding proteins in human neural stem cells with significant and selective associations with periventricular heterotopia (PH), a neuronal migration disorder. In the end, researchers will attempt to apply advanced genetic tools to restore centrosome function and revert defects causing PH.

Source: CORDIS