Specific projects:

The role of plant regulators of programmed cell death in plant-microbe interactions

Plant programmed cell death is crucial for the outcome of plant-microbe interactions. Cell survival is required for establishment and maintenance of biotrophic interactions, such as that of plants with powdery mildew fungi. Consequently, cell death is part of the plant’s defense machinery against biotrophs. In contrast, plant programmed cell death is corrupted by necrotrophic microbes, which depend on host cell death for nutrition. Therefore, the timely induction of cell death reactions such as the hypersensitive response (HR) can control infection by biotrophs, whereas its suppression might impair propagation of necrotrophs.

One of our projects focused on BAX INHIBITOR-1 (BI-1) and related proteins, which are conserved regulators of stress- and pathogenesis-related cell-death in plants and animals. We have shown that abundance of the plant cell death suppressor BAX INHIBITOR-1 (BI-1) is crucial for susceptibility to biotrophic powdery mildew fungi but can support basal resistance to necrotrophs (Eichmann et al. 2010; Babaeizad et al. 2009). Currently, we are studying the mechanism by which BI-1 and interacting proteins modulate cell death and susceptibility to powdery mildew. This reveals new insights into BI-1 function and regulation of cell death in plants. Data are transferable into application for providing disease-resistant plants (Babaeizad et al. 2009). More recently, we identified BI-1-like Lifeguard proteins and BI-1-interacting proteins that also act in susceptibility to powdery mildew (Weis et al. 2013a; Weis et al. 2013b, Weis et al. 2014). We further described the barley NADPH oxidase RBOHF2 and the Arabidopsis CONSTITUTIVE EXPRESSION of PR GENES 5, CPR5, as regulators of cell death and of susceptibility to powdery mildew (Torres et al. 2017; Höwing et al. 2017).

Cell death of pathogen-attacked Arabidopsis cells as indicated by collapse of membranes and cytoskeleton (left) or whole cell deposition of callose (right).