ERC FUNDED PROJECTS

In the recent years in advanced democracies there has been a wave of electoral successes of populist politicians supporting extreme messages. Is populism caused by negative economic shocks? If so, what are the mechanisms? What explains heterogeneity in responses to such shocks? In this project, I will test empirically if personal experiences, information environment, and their interaction with aggregate economic shocks shape people’s political decisions. The project consists of three parts. First, I will study how personal employment histories, potentially affected by globalization and technological shocks, individual predispositions, and information environment influenced voting for Trump. I will use a unique database of more than 40 million resumes for the period 2010-2016, the largest available repository of resumes of job-seekers in the US, which was not previously used in academic research, and match it with zipcode-level economic and voting variables. Second, I will study how negative social experiences during the formative years affect subsequent labor market outcomes, antisocial behavior, and the support of populist agenda. I will examine how corporal punishment in schools in UK affected subsequent educational attainment, employment, antisocial behavior, and voting for UKIP and Brexit. I will digitize archival records on regulations and practice of corporal punishment in different educational authorities in the UK during 1970-80s, combining it with contemporary outcomes. Third, I will examine what makes people actively resist extremist regimes even when it is associated with high personal costs. I will study a historical example of resistance to Nazi regime in Germany during the WWII, which provides unique methodological opportunity to study determinants of resistance to extremism in a high stake environment. I will use a self-collected dataset on treason cases to measure resistance, combining it with data on bombing and exposure to foreign propaganda.

1 467 736 €

Start date: 2019-01-01, End date: 2023-12-31

Discriminating differences in day length is critical for many organisms to synchronize reproduction with the most favourable season of the year. Plants have evolved sophisticated time-keeping mechanisms that largely work in leaves, to measure the duration of the day. Upon perception of favourable day lengths, a leaf-borne signal moves to the shoot apical meristem to induce flower formation. Rice is a crop whose yield heavily depends on flowering at the right time, and genetic variation within leaf regulators contributes to diversification of flowering responses among different rice varieties. However, how the shoot apical meristem responds to changes in day length and initiates flowering is currently unknown. High-yielding European rice varieties flower within a limited range of days and expanding such range would prove beneficial to increase yield and expand cultivation to different environments. Our goal is to identify novel genes that modify meristem sensitivity to day length, and breed them into high-yielding cultivars. Together with the gene pool controlling day length responses in the leaves, these novel alleles will allow to design varieties with diverse sensitivities to photoperiod and will distribute the reproductive phase over a broader period of time. This knowledge-based breeding will require preliminary studies in order to identify regulators acting in the shoot apical meristem. To this extent, rice provides an excellent biological model for the availability of powerful genetic and molecular tools. I am proposing a number of genetic and biochemical screens that will allow us to explore the rice genome for genes required at the shoot apical meristem to drive reproductive phase transitions. We will investigate genetic variation in these components, relate it to flowering and adaptation, and use it for introgressing novel alleles into elite germplasm.

1 499 880 €

Start date: 2011-04-01, End date: 2016-03-31

"Financial economics is at a crossroads: Academics are struggling to redefine the theory of finance and practitioners and regulators to restructure the financial industry. The current financial crisis will have significant impact on how we regulate financial markets and how we manage risk in companies and financial institutions. It will continue to inspire an intense discussion and research agenda over the next decade in academics, in industry, and among financial regulators and a central focus will be the role of frictions in financial markets. Nowhere are these issues more pertinent than in Europe right now. To take up the challenge presented by this crossroad of financial economics, my research project seeks to contribute to the knowledge of financial frictions and what to do about them. FRICTIONS will explore how financial frictions affect asset prices and the economy, and the implications of frictions for financial risk management, the optimal regulation, and the conduct of monetary policy. Whereas economists have traditionally focused on the assumption of perfect markets, a growing body of evidence is leading to a widespread recognition that markets are plagued by significant financial frictions. FRICTIONS will model key financial frictions such as leverage constraints, margin requirements, transaction costs, liquidity risk, and short sale constraints. The objective is to develop theories of the origins of these frictions, study how these frictions change over time and across markets, and, importantly, how they affect the required return on assets and the economy. The project will test these theories using data from global equity, bond, and derivative markets. In particular, the project will measure these frictions empirically and study the empirical effect of frictions on asset returns and economic dynamics. The end result is an empirically-validated model of economic behavior subject to financial frictions that yields qualitative and quantitative insights."

1 307 160 €

Start date: 2013-01-01, End date: 2017-12-31

Gadd45 family proteins play a critical role in genomic stability, cell cycle regulation proliferation and apoptosis. Gadd45a is activated by the tumor suppressor gene p53, which is mutated in >50% of human tumors. The lack of GADD45a in mice leads to spontaneous development of an autoimmune disease similar to systemic lupus erythematosus. The molecular mechanisms that cause autoimmunity are poorly understood. Recent evidence suggests that p38 activation is involved in autoimmune development and tumor suppression. We found that Gadd45a negatively regulates p38 activity in T cells by preventing phosphorylation on Tyr323. Inhibition of Tyr323p38 phosphorylation is a potential therapeutic target in several types of leukemia and autoimmune diseases, including lupus and rheumatoid arthritis. The main goals of this project are a) to study the in vivo function of the Gadd45 family and p38 in tumor suppression and autoimmunity, and b) to analyze their molecular mechanisms to identify targets for disease treatment. We will dissect the signaling pathways involved in development of autoimmunity and cancer using a multidisciplinary approach that combines mouse genetic, human epigenetic, biochemical, molecular biological and immunological techniques. Our project involves the characterization of murine models deficient in each member of the Gadd45 family (Gadd45a, Gadd45b, Gadd45g), as well as double- and triple-knockout mice, development of a knock-in model for p38a, in vivo and in vitro analysis of T cell activation, proliferation, apoptosis and differentiation, epigenetic studies of potential targets, and finally, validation of these results in autoimmune disease and cancer patients. The results of this project will help identify new therapeutic targets for autoimmune diseases and/or cancer.

1 755 805 €

Start date: 2008-09-01, End date: 2014-08-31