Project 19
Toll-related intracellular receptors in plant innate immunity
Max-Planck-Institute for Plant Breeding Research, Cologne
Brief description in German:
Angeborene Immunantworten einzelner Tier- und Pflanzenzellen stellen eine wichtige Abwehrlinie gegenüber Pathogenen dar. Von aktivierten Rezeptoren generierte Signale werden in der Zelle integriert und konvergieren auf trankriptionelle Programme im Kern. Der pflanzliche, Toll-Rezeptor-ähnliche intrazelluläre Rezeptor RPS4 agiert im Kern, um mittels des Regulators EDS1 die Reprogrammierung von Abwehrgenen zu steuern. Wir werden die Prozesse, die durch den Immunrezeptor im Kern ausgelöst werden, charakterisieren. Dies wird unser Verständnis der Dynamik von Transkriptionsfaktor-Netzwerken in Pflanzenimmunität verbessern.
Innate immune responses of individual animal and plant cells constitute a major barrier to pathogen infection. Signals generated by activated receptors are integrated inside the cell and converge on transcriptional programmes in the nucleus. Arabidopsis Toll-related intracellular receptor RPS4 operates inside nuclei to trigger resistance and defence gene reprogramming through the stress response regulator, EDS1. We will characterize immune receptor-activated processes in the host nucleoplasm and at the chromatin in order to advance understanding of transcription network dynamics needed for a balanced cell-autonomous immune response.
In mammals and plants, Nucleotide Binding/Oligomerization Domain-Leucine Rich Repeat (NOD-LRR) proteins act as sensors of pathogen-induced stress inside cells, linking perception of specific molecules to the activation of basal defence and cell death pathways. Common regulatory principles apply in both systems to mechanisms of NOD-LRR receptor activation and the convergence of cell-autonomous immune signalling on transcriptional programmes in the nucleus.
Fine control of innate immune pathways allows a timely local response to be mounted against pathogens and priming of tissues against further infection. The nature of host targets of pathogen effectors in promoting disease and processes by which activated immune receptors intersect with the basal defence machinery still need to be resolved.
Our aim was to characterize mechanisms of activation and downstream signalling of the Arabidopsis intracellular Toll-related NOD-LRR (TIR-NB-LRR) receptor, RPS4, that recognizes a bacterial Type-III secreted effector (AvrRps4) and requires the nucleo-cytoplasmic basal defence regulator, EDS1.
We established that a nuclear pool of RPS4 is necessary to trigger immunity and cell death and that EDS1 is an indispensible component of RPS4 signalling, acting downstream of receptor activation but upstream of transcriptional reprogramming and cell death.
We also found that a pathogen-induced increased accumulation of EDS1 complexes specifically in nuclei is a key early step in RPS4-triggered defence. Our goals in the next round of the SFB are:
1) to elucidate functions of RPS4 and EDS1 complexes inside nuclei and investigate the relevance of recently discovered interactions with transcription factors (TFs) in immune response activation,
2) examine whether RPS4 and/or EDS1 complexes are associated with specific regions or states of chromatin in Arabidopsis defence gene regulation, by performing Ch-IP/seq analyses,
3) explore the genetic and molecular relationship between RPS4 and a second WRKY (TF motif)-containing TIR-NB-LRR protein RRS1 that also recognizes AvrRps4 and uncover the mode of AvrRps4 virulence and recognition in host cells,
4) test whether the EDS1 pathway is important for defence reprogramming in Arabidopsis responses to Microbe-Associated Molecular Patterns (MAMPs).
Results from these studies should advance our understanding of processes governing plant cell-autonomous immunity and modes of infection by host-adapted pathogens. Interactions within the CRC 670 are planned with the groups of T. Kufer (sub-project N01), P. Schulze-Lefert (sub-project 18) in analysis of NOD-LRR receptor signalling, I. Somssich (sub-project 24) and P. Schulze-Lefert (sub-project 18) in processing Ch-IP/seq data and characterizing transcription regulatory complexes, and with Y. Saijo (sub-project 24) in defining MAMP-triggered transcriptional outputs.
List of publications resulting from the project
Peer-reviewed publications:
Cheng, Y.T, Wiermer, M., Germain, H., Bi, D., Xu, F., Garcia, A.V., Wirthmüller, L., Depres, C., Parker, J.E., Zhang, Y. and Li, X. (2009). Nuclear pore complex component MOS7/Nup88 is required for plant innate immunity and nuclear accumulation of defense regulators. Plant Cell 21: 2503-2516.
Birker, D., Heidrich, K., Takahara, H., Narusaka, M., Deslandes, L., Narusaka, Y., Reymond, M., *Parker, J.E. and *O’Connell, R. (2009). A locus conferring resistance to Colletotrichum higginsianum is shared by four geographically distinct Arabidopsis accessions. Plant J. 60(4):602-13. * joint corresponding author.
Kwon, C., Neu, C., Pajonk, S., Yun, H.-S., Lipka, U., Humphry, M.E., Bau, S., Straus, M., Rampelt, H., El Kasmi, F., Jürgens, G., Parker, J., Panstruga, R., Lipka, V. and Schulze-Lefert, P. (2008). Co-option of a default secretory pathway for plant immune responses, Nature 451: 835-840.
Mühlenbock, P., Szechyńska-Hebda, M., Płaszczyca, M., Baudo, M., Mullineaux. P.M., Parker, J.E., Karpińska, B. and Karpiński, S. (2008). Chloroplast signalling and LESION SIMULATING DISEASE 1 regulate crosstalk between light acclimation and immunity in Arabidopsis. Plant Cell 20: 2339-2356.
Wirthmüller, L., Zhang, Y., Jones, J.D.G. and Parker, J.E. (2007). Nuclear accumulation of the Arabidopsis immune receptor RPS4 is necessary for triggering EDS1-dependent defence. Curr. Biol. 17: 2023-2029.
Reviews:
Garcia, A.V. and Parker, J.E. (2009). Heaven’s Gate: Nuclear accessibility and activities of plant immune regulators. Trends Plant Sci. 19: 479-487.
J.E. Parker. (2009). The quest for long-distance signals in plant systemic immunity. Science Signalling 2: pe31.
Panstruga, R., Parker, J.E. and Schulze-Lefert, P. (2009). Cell SnapShot: Plant immune response pathways. Cell 135: 978.e1-978.e3.
