Investigation of plant immunity activated by enforced nuclear localization of EDS1 (Enhanced Disease Susceptibility1) in Arabidopsis

• Applicant: Dr. Johannes Stuttmann
• Subject Area: Organismic Interactions, Chemical Ecology and Microbiomes of Plant Systems ; Plant Genetics and Genomics
• Term: from 2016 to 2021
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 298818891

Nucleotide-binding leucine-rich repeat (NLR) -type immune receptors can, directly or indirectly, recognize effector molecules secreted into the host cell cytoplasm by pathogenic microbes. Effector recognition and NLR activation induce a rapid resistance response efficiently restricting microbial growth. In plants, NLRs are classified by their N-terminal coiled-coil (CC, CNL) or Toll/interleukin 1-like receptor (TIR, TNLs) domains. CC and TIR domains are assumed to function in signal initiation, but signaling components downstream of activated NLRs and how transcriptional reprogramming inside nuclei is achieved remain largely unknown. Interestingly, TNLs are functionally dependent on the nucleo-cytoplasmic protein Enhanced Disease Sucpetibility1 (EDS1). We discovered that expression of an EDS1-YFPNLS fusion, for enforced nuclear localization, can lead to temperature-dependent induction of autoimmunity in transgenic Arabidopsis. An EDS1-YFPNLS line expressing the fusion protein to high levels and causing seedling lethality at 22°C, was used in a genetic screen. Approximately 50 near death experience (nde) mutants suppressing EDS1-YFPNLS-induced autoimmunity were isolated. Analysis of nde1 alleles identified DM2h, a paralog of the TNL RPP1, as mediator of autoimmunity. The DM2 locus is highly polymorphic between different Arabidopsis accessions, and is causal in several resolved cases of hybrid incompatibility (HI). The introgression of an nde1 allele into different genetic backgrounds provided first genetic evidence on the significance of an individual DM2 gene from accession Landsberg erecta (Ler). We show that DM2hLer is not only essential in two cases of ectopically-induced autoimmunity, but also in HI caused by deleterious epistatic interactions of DM2Ler with SRF3 allelic forms from Central Asian Arabidopsis accessions. In this project, we want to identify and characterize additional NDE loci to understand autoimmunity induced by enforced nuclear EDS1 localization and to identify components of TNL signaling. Furthermore, we want to analyze DM2Ler paralogs to understand how autoimmunity activated by structurally different inducers converges onto a single NLR and how DM2Ler paralogs contribute to plant immunity.

• DFG Programme: Research Grants