Plants mount highly elaborate, layered, and complex defenses against constantly invading pathogens. These multi-layered defenses, broadly termed PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI), account for responses to the perception of conserved molecular patterns present on a pathogen surface or to a specific pathogen effector secreted and sensed within the plant cell by a cognate resistance (R) protein, respectively.

Although genetic screens and subsequent molecular approaches have identified several key immune players, our present understanding clearly suggests that signaling in ETI defies the conventional step-wise linear arrangements of signal receivers and transducers. Instead, effector activities that cause alterations in the dynamics of protein interactomes between the R protein with positive and negative regulators directly mediate the sensing and transduction of signals. 

The broad goal of our research group is to unravel this mystery at a molecular level. We utilize various pathosystems to identify routes for defense signal transduction and how pathogen effectors are intercepted or escape perception by the plant immune sentinels.

Broadly, we investigate the role of inositol compounds in the assembly of defense players and in the downstream signaling. This includes elucidation of inositol metabolite profiles in mutants altered in defense responses in order to identify specific signalling routes and also explore the synergistic and antagonistic cross-talk between hormonal pathways and how pathogen effectors or induced ETI impinge on this network.

In parallel, we also investigate the molecular understanding of pathogen effector evolution that often challenges the biotechnological effort to improve plant resistance. Our goal is to identify molecular hubs in diverse plant hosts that are targeted by unrelated pathogen effectors. We aim to engineer these immune hubs to facilitate broad-spectrum defenses in crop plants.