research.knit

Our Research

Plant immunity is governed by intricate physiological mechanisms that enable plants to detect, respond to, and defend against a wide range of pathogens. These defense strategies involve a coordinated network of interactions and responses at both the cellular and molecular levels.

Our Lab is particularly interested in:

Cellular recognition mechanisms, including how immune receptor proteins detect pathogen-derrived signals.
Signal transduction pathways that link receptor-mediated recognition to host physiology.
Pathogen strategies for immune evasion and effector-mediated immune suppression.

To dissect the physiological processes that underpin plant immunity—and how these are exploited by pathogens—we use the interaction between the cereal crop barley (Hordeum vulgare) and the barley powdery mildew fungus Blumeria hordei (Bh) as a primary model. This system allows us to investigate how host-associated microbes manipulate plant biology to establish successful infections. To broaden our understanding of immune mechanisms across plant lineages, we complement our work in barley with studies in established model systems such as Arabidopsis thaliana and Nicotiana benthamiana. This comparative approach enables us to explore both conserved and lineage-specific features of immunity in monocots and dicots, using a diverse array of fungal and bacterial pathogens that interact with each plant type.

Here some examples of our ongoing projects:

Emmy Noether Project

Quantification of virulence function and identification of key residues

We investigate the virulence functions of Blumeria hordei (Bh) avirulence (AVRA) effectors and their naturally occurring variants that have lost avirulence activity (AVRA-V). Specifically, we quantify how both avirulent and virulent effector forms influence Bh proliferation rates in host plants. In addition, we assess whether AVRA effectors affect the growth of other pathogens or influence disease outcomes in other plant species. This approach allows us to determine whether avirulence and virulence functions are linked or operate independently, whether the loss of avirulence also compromises virulence, and whether effector functions are conserved across different plant hosts.

CEPLAS & EN Project

Identification of intrinsic functions of effectors from cereal infecting fungal pathogens

Assigning biological functions to pathogen effectors is essential for understanding the development of barley powdery mildew disease. To this end, we biochemically identify the host targets of Bh AVRA effectors within barley cells. We employ state-of-the-art proximity-dependent protein labeling techniques to capture in situ interactions, enabling us to characterize the molecular context of AVRA effector activity and to elucidate the biochemical pathways in which their host targets are involved.

SFB1403 Project

Identification of the host cell death pathways affected in the presence of Bh AVRA effectors

As an obligate biotroph, Bh depends on living host tissue for its proliferation, making the suppression of host cell death crucial for successful infection (Saur et al., 2021; Saur & Hückelhoven, 2021). Interestingly, MLA immune receptors in barley recognize effectors from a range of unrelated biotrophic pathogens, suggesting that the AVRA effectors recognized by MLAs are strong candidates for suppressing host cell death—either directly or indirectly—to support Bh colonization. To explore this hypothesis, we examine the ability of AVRA and related virulence effectors to suppress various cell death pathways in barley, providing insights into their potential role in promoting biotrophic.

For5682 Project

The obligate biotrophic powdery mildew fungus - adaptation to the leaf epidermal cell niche by defending against other microbes

In this project, we investigate how Bh influences barley colonization by other microbes—both directly through microbial antagonism and indirectly by triggering physiological changes in the host plant. Our focus lies on members of the native barley microbiota as well as dominant microbial invaders with biotrophic or necrotrophic lifestyles.