The transition towards a society based on 100% renewable energy requires massive deployment of photovoltaics of 30-70 TW until 2050. This requires huge amounts of resources, while their limited availability is already becoming apparent. A major lever to reduce resource consumption is to increase the solar cell efficiency. As best single junction solar cells approach their fundamental limits, higher efficiency can only be reached with so-called tandem solar cells, made of two or more subcells. All tandem technologies so far are based on relatively thick absorber layers, reducing resource demand compared to single junction devices by efficiency increase. There, light trapping strategies are used to maximize absorptance close to the band gap of the materials and improve efficiency by few percent relative. However, by applying advanced light trapping techniques such as nanophotonic metasurfac-es, ultrathin single junction devices with a 5-10-fold decrease in semiconductor material were realized. To reduce resource demand further, the concept of ultrathin solar cells must be extended to tandem devices. This introduces severe challenges, as not only absorption needs to be maximized within the active part, but a spectrally dependent light guiding strategy is required. Metasurfaces have shown the ability to manipulate light e.g. spectrally dependent; however, they have never been implemented into tandem solar cells. Thus, the overarching goal of PHASE is to generate a deep physical understanding of metasurfaces for ultrathin tandem solar cells and to develop process flows to implement nanopho-tonic structures into such devices with efficiencies above 30%. This will proof that the chosen tech-nology pathway can support the urgently needed energy transition. More specific, the goal of PHASE is to realize tandem solar cells, where the resource demanding semiconductor part is 10 times thinner (and thus needs 10 times less semiconductor material) than similar existing devices.

The abusive use of antibiotics has led to multidrug-resistant bacteria and the acute threat of a post-antibiotic era. However, apart from resisters, there is a subgroup of bacteria called persisters that surviveby recalcitrance to antibiotic treatment. Persisters are not resistant to antibiotics but simply survive by metabolic shutdown. Upon withdrawal of antibiotics, these persisters resuscitate and regenerate the colony. They are heavily involved in failure of antibiotic treatment and the development of chronic infections. Bacterial persistence is controlled by the stringent response, which itself is mediated by hyperphosphorylated nucleotides, known as the magic spot (MS) nucleotides or (p)ppGpp. The importance of the stringent response, its omnipresence in the domain of bacteria, its connection to persister formation and tolerance to (antibiotic) stress, and its absence in mammals has led to significant research in microbiology. However, until recently these activities have not been paralleled by the development of chemical biology approaches. The current proposal aims to fill this gap by research into (1) synthetic methodology targeting the magic spot nucleotides and their analogs, (2) tools to identify target proteins of (p)ppGpp, and more generally (p)ppNpp (3) analytical approaches to extract, resolve, and quantify (p)ppGpp, (4) strategies to control the stringent response and persister formation with light (5) inhibitors of the stringent response. These new tools will enable a detailed understanding of the stringent response and thus ultimately help in the design of new antibiotics effective against persisters. The goal is to develop methods to force bacteria into the persistent state or inversely wake them up by using light and small molecules. Forcing bacteria out of persistence and blocking their entry into this state in combination with antibiotic treatment is a highly promising strategy to avoid the development of chronic bacterial infections.

Why are contemporary readers so fascinated by retellings of the Iliad or Beowulf? And why have retellings of premodern – ancient and medieval – texts not been taken seriously as a literary practice to date? In DERIVATE, I investigate the striking surge of retellings in contemporary English literature by setting the contemporary texts in a productive dialogue with practices of writing in the Middle Ages. The medieval period offers a perfect point of departure for theorizing retellings as medieval literature was inherently derivative and medieval authors had developed a system for being inventive within a system of derivations. Taking issue with the privileging of that which is new in literary history, I propose a new paradigm for literary history: literary history as a history of derivations. Starting from the premise that retelling is a transhistorical concept, the project sheds new light on the processes of reception that find their expression in the current interest in and relevance of premodern material. The project triangulates (classical) reception studies, medieval literary studies as well as literary theory, especially postmodernist theory, and scrutinizes the practice of retelling premodern (ancient and medieval) texts in contemporary English literature. DERIVATE thus develops a theory of retelling based on the intense engagement and critical comparison with medieval practices of retelling in order to map the wider cultural, historical, and literary contexts and implications of the current trend in retellings of classical and medieval texts (audiences, canon, literary market) as a springboard for developing a literary history of derivations.

Heart failure is a major cause of death in the Western world, with an estimated prevalence of 2-3\% of the population. A subgroup of heart failure patients is characterised by dilated cardiomyopathy (DCM) which results in substantial morbidity and mortality due to progressive mechanical pump failure (70\%) or sudden cardiac death from ill-predictable electrical disturbances (30\%). DCM is commonly linked to mutations encoding cytoskeletal proteins, but our understanding of why a loss of cardiac myocyte cytoskeletal integrity in inherited DCM phenotypes results in detrimental changes to calcium handling, and how this causes arrhythmias and sudden cardiac death, remains limited. Human studies have associated genetic mutations and loss in the cytoskeletal protein filamin C (FLNC) with arrhythmogenic DCM and sudden death. To explore the biomechanical and mechano-electric mechanisms by which FLNC deficiency leads to mechanical and electrical dysfunction, I will use experimental and mathematical models that span multiple spatial and temporal scales from the protein level up to the whole heart. I hypothesise that FLNC regulates myofilament lattice spacing and that loss of this structure leads to impaired contractile force development by the sarcomere. I postulate that these perturbations in mechanics may contribute to the generation of substrate for the induction and maintenance of lethal ventricular arrhythmias via a variety of mechano-electric coupling mechanisms. Particularly, stretch-induced alterations may affect cardiomyocyte electrophysiology, which may contribute to both the trigger and the substrate for arrhythmias. Thus, altered myocardial mechanics in the FLNC-null mouse model of DCM may contribute to the triggering or maintenance of life-threatening reentrant ventricular arrhythmias via a variety of mechano-electric coupling mechanisms.

In close proximity, plants can sense each other’s presence via a decrease in the red to far-red light ratio (low R:FR) in the nearby surroundings. Low R:FR perception by phytochrome photoreceptors triggers strong and rapid elongation growth allowing plants to grow taller than their neighbors and reach better lit areas. This process, known as shade avoidance is mostly orchestrated by the growth hormone auxin. However, although low R:FR promotes elongation growth, it compromises plant defense against pathogens by dampening defense hormone signaling; a phenomenon referred to as shade-induced susceptibility. Furthermore, I recently found that plants exposed to low R:FR conditions accumulate glucose, which accelerates pathogen development in plants tissue. Yet, the involvement of primary metabolism in regulating the shade-induced susceptibility remains to be explored. In eukaryotes, the TARGET OF RAPAMYCIN (TOR) kinase is a master growth regulator integrating the cell energy and carbohydrate status to regulate growth and defense responses. In plants, TOR activity is promoted by auxin and glucose, both strongly induced by low R:FR. Interestingly, I also found TOR gene expression to be induced by low R:FR in a recent RNA-seq study. In this project, I will study if and how low R:FR regulates TOR signaling to promote growth at the expense of defence. I will use genetic and chemical approaches to (I) identify the spatiotemporal dynamics of TOR gene expression and TOR protein activity in response to shade in the model plant Arabidopsis thaliana, (II) identify the dependency of shade-induced auxin levels and sugar accumulation on TOR dynamics and (III) characterize potential links between TOR signaling and defense hormone signaling. The gained insights will be instrumental for understanding how plants use shade signals to balance growth and defense responses and will help to engineer new pathogen-resilient crop varieties, which can be grown optimally at high densities.