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Project 32
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Project 32

Kenichi Tsuda

Molecular basis of network robustness during effector-triggered immunity

Max-Planck-Institute for Plant Breeding Research, Department of Plant Microbe Interactions, Cologne

Brief description in German
Die Beständigkeit eines Netzwerks ist eine maßgebende Eigenschaft immunaler Signalnetzwerke. Der Hauptteil der durch Salicylsäure regulierten pflanzlichen Immunsignalwege kann durch langanhaltende Aktivierung einer MAPK, beispielsweise vorkommend während der Effektor-induzierten Immunität, kompensiert werden, wodurch eine Netzwerkrobustheit gewährleistet wird.

Die MAPK-Aktivierungsdauer dient damit als molekularer Kontrollpunkt über die Robustheit des Immunsignalnetzwerks, wodurch der durch ausgedehnte MAPK-Aktivität ermöglichte Mechanismus einen Ansatz für die Widerstandsfähigkeit in ETI darstellt. Ziel unserer Studie ist die molekularen Mechanismen der Netzwerkrobustheit in der Effektor-induzierten Immunität zu definieren.

Summary
Network robustness is a crucial property of immune signaling networks because pathogens attack network components to dampen immune responses. In addition to being robust, immune signaling network should be tunable since unnecessary induction of immunity negatively impact fitness.

Nevertheless, modulation of network robustness is an area of biology that has rarely been explored. Like animals, plants recognize conserved molecular patterns and virulence effectors deribed from microbes.These modes of immunity are called PAMP/pattern- triggered immunity (PTI) and effector-triggered immunity (ETI), respectively.

In plants, while these two modes of immunity extensively share signaling machinery, ETI is much more robust than PTI, suggesting modulation of network components. In Arabidopsis, transcriptiome changes in wild-type plants during PTI and ETI are very similar.

However, transcriptome is more amenable to perturbations during PTI than that during ETI. For example, salicylic acid (SA) signaling, which regulates a major portion of the plant immune response, was required for the proper regulation of the vast majority of SA-responsive genes during PTI.

However, we found that during ETI, most SA-responsive genes were still responsive in SA-deficient mutants as in wild-type plants, suggesting a robust gene reguratory mechasnism during ETI. The activation of the two immune-related MAPKs, MPK3 and MPK6, persisted for several hours during ETI but less than one hour during PTI.

Sustained MAPK activation was sufficient to confer SA-independent regulation of most SA-responsive genes. Furthermore, the MPK3 and SA signaling sectors were compensatory in bacterial resistance during ETI.These results indicate that the duration of the MAPK activation is a critical determinant for modulation of robustness of the immune signaling network.

Our major goals the SFB670 are identifying
1) the gene regulatory mechanism controlled by sustained MAPK activation and
2) the molecular mechanism to modulate duration of MAPK activation during ETI.

Results from these studies should advance our understanding of fundamental processes governing plant defense reprograming and modulation of biological networks. It is reported that a biphasic innate immune MAPK response descriminates between a non-pathogenic and pathogenic fungus in animals although the molecular mechanism is not known. Thus, plants and animals employ MAPK signaling as a molecular switch to fine-tune innate immune responses, providing us with opportunity to understand innate immune responses and network modulation in a borader context.

List of publications resulting from the project

Peer-reviewed publications:

Sreekanta S, Bethke G, Hatsugai N, Tsuda K, Thao A, Wang L, Katagiri F, Glazebrook J. 2015. The Receptor-Like Cytoplasmic Kinase PCRK1 Contributes to Pattern-Triggered Immunity against Pseudomonas syringae in Arabidopsis thaliana. New Phytologist, 207, 78-90

Cui H, Tsuda K, Parker JE. 2015. Effector-Triggered Immunity: From Pathogen Perception to Robust Defense. Annual Review of Plant Biology, 66, 487-511

Tsuda K and Somssich IE. 2015. Transcriptional networks in plant immunity. New Phytologist, 206, 932-947

Seyfferth C and Tsuda K. 2014. Salicylic acid signal transduction: the initiation of biosynthesis, perception and transcriptional reprogramming. Frontiers in Plant Science, 5, 697.

Mine A, Sato M, and Tsuda K. 2014. Toward a systems understanding of plant-microbe interactions. Frontiers in Plant Science, 5, 423.

Kim Y, Tsuda K, Igarashi D, Hillmer RA, Sakakibara H, Myers CL, and Katagiri F. 2014. Mechanisms underlying robustness and tunability in a plant immune signaling network. Cell Host & Microbe, 15, 84-94.

Ross A, Yamada K, Hiruma K, Yamashita-Yamada M, Lu Xunli, Takano Y, Tsuda K, and Saijo Y. 2014. The Arabidopsis PEPR pathway couples local and systemic plant immunity. The EMBO Journal, 33, 62-75.

Tsuda K, Mine A, Bethke G, Igarashi D, Botanga CJ, Tsuda Y, Glazebrook J, Sato M, Katagiri F. 2013. Dual regulation of gene expression mediated by extended MAPK activation and salicylic acid contributes to robust innate immunity in Arabidopsis thaliana. PLoS Genetics, 9, e1004015

Heidrich K, Tsuda K, Blanvillain-Baufumé S, Wirthmueller L, Bautor J, and Parker JE. 2013. Arabidopsis TNL-WRKY domain receptor RRS1 contributes to temperature-conditioned RPS4 auto-immunity. Frontiers in Plant Science, 4, 403.

Tintor N, Ross A, Kanehara K, Yamada K, Fan L, Kemmerling B, Nurnberger T, Tsuda K, Saijo Y. 2013. Layered pattern receptor signaling via ethylene and endogenous elicitor peptides during Arabidopsis immunity to bacterial infection. Proceedings of the National Academy of Sciences USA, 110, 6211-6216.

Non peer-reviewed publications:

Anver S and Tsuda K. 2014. Ethylene and Plant Immunity. In Ethylene in Plants. Ed.: Chi-Kuang Wen. Springer Science+Business Media, Dordrecht Heidelberg New York London, 205-221.