This project addresses the question of how people incorporate increasingly prevalent nonelectoral political acts into individual-level repertoires of participation; and how well represented these different types of political participators are. At a time of growing concern about unequal representation in democracies, two conflicting global trends over the last several decades highlight the importance of these questions: a clear decline in voter turnout, especially among lower status groups; and evidence of increased nonelectoral participation, especially among higher status groups. To assess how these trends in political participation affect patterns of representation, PRD’s theoretical framework integrates new approaches for investigating the links between individuals’ participation repertoires (i.e., how individuals combine voting, protest, online activism) and objective and subjective representational outcomes. PRD’s work packages employ a multi-method approach: “Political acts and political participators” (WP1) analyzes separate surveys and a harmonized dataset and includes methodological innovations using new techniques for identifying participation repertoires. “Participation-representation connection” (WP2) investigates the connections between the political acts and political participators analyzed in WP1 and representational outcomes, and integrates these findings with qualitative fieldwork with activists who focus on unequal representation. Finally, “Mobilizing and organizing low-status groups” (WP3) conducts novel experimental studies using Twitter panel data and field experiments to identify interventions with the potential to produce more equal representational outcomes in the future. By combining an original theoretical framework and methodological innovations, PRD will conduct a uniquely comprehensive empirical investigation of participation repertoires, with a focus on mechanisms that can reduce inequalities in participation and representation.
DNA safekeeping is one of the most important functions of the cell. Since DNA damage occurs in the context of chromatin, it affects both the DNA itself, but also the epigenetic landscape. While the repair mechanism of the DNA has been extensively studied, questions abound regarding the restoration of the epigenetic landscape, and the long-term effects that damage leaves in the region. In this proposal I aim to address these questions using modified DSBs repair sensors from different pathways such as “homologous recombination” and “non-homologous end joining” to map the repair process. Our method will allow us to investigate the influence of the natural epigenetic landscape on pathway choice, the dynamic process of repair and the restoration of the region. Moreover, we will investigate whether certain repair processes leave long- lasting effects at the site of damage or even “epigenetic scars”. The advantage of our method is that it allows us to map each sensor repair time-line in an unbiased and high throughput manner over extended periods of time, even once the damage is already repaired. These questions are especially important for our understanding of ageing, and age-related diseases that are driven by DNA damage. Last, we will test the long-lasting effects of past damage in two different contexts: animal models of neurodegeneration, where DNA damage accumulates, and in the efficiency of reprograming to produce healthy induced pluripotent stem cells (IPCs).