A chemical screen for suppressors of the avrRpm1-RPM1-dependent hypersensitive cell death response in Arabidopsis thaliana

Abstract Plant nucleotide-binding domain, leucine-rich repeat receptor (NLR) proteins play important roles in recognition of pathogen-derived effectors. However, the mechanism by which plant NLRs activate immunity is still largely unknown. The paired Arabidopsis NLRs RRS1-R and RPS4, that confer recognition of bacterial effectors AvrRps4 and PopP2, are well studied, but how the RRS1/RPS4 complex activates early immediate downstream responses upon effector detection is still poorly understood. To study RRS1/RPS4 responses without the influence of cell surface receptor immune pathways, we generated an Arabidopsis line with inducible expression of the effector AvrRps4. Induction does not lead to hypersensitive cell death response (HR) but can induce electrolyte leakage, which often correlates with plant cell death. Activation of RRS1 and RPS4 without pathogens cannot activate mitogen-associated protein kinase cascades, but still activates up-regulation of defence genes, and therefore resistance against bacteria.

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A MYB Transcription Factor Regulates Very-Long-Chain Fatty Acid Biosynthesis for Activation of the Hypersensitive Cell Death Response in Arabidopsis

The Plant Cell ◽

10.1105/tpc.107.054858 ◽

2008 ◽

Vol 20 (3) ◽

pp. 752-767 ◽

Cited By ~ 207

Author(s):

Sylvain Raffaele ◽

Fabienne Vailleau ◽

Amandine Léger ◽

Jérôme Joubès ◽

Otto Miersch ◽

...

Keyword(s):

Cell Death ◽

Transcription Factor ◽

Fatty Acid Biosynthesis ◽

Chain Fatty Acid ◽

Myb Transcription Factor ◽

Acid Biosynthesis ◽

Long Chain Fatty Acid ◽

Hypersensitive Cell Death ◽

Cell Death Response ◽

Long Chain

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OsJAZ13 Negatively Regulates Jasmonate Signaling and Activates Hypersensitive Cell Death Response in Rice

International Journal of Molecular Sciences ◽

10.3390/ijms21124379 ◽

2020 ◽

Vol 21 (12) ◽

pp. 4379

Author(s):

Xiujing Feng ◽

Lei Zhang ◽

Xiaoli Wei ◽

Yun Zhou ◽

Yan Dai ◽

...

Keyword(s):

Cell Death ◽

Splice Variants ◽

Adaptor Protein ◽

Dependent Manner ◽

Hypersensitive Cell Death ◽

Cell Death Response ◽

Jaz Proteins ◽

Localization Analysis ◽

And Function

Jasmonate ZIM-domain (JAZ) proteins belong to the subgroup of TIFY family and act as key regulators of jasmonate (JA) responses in plants. To date, only a few JAZ proteins have been characterized in rice. Here, we report the identification and function of rice OsJAZ13 gene. The gene encodes three different splice variants: OsJAZ13a, OsJAZ13b, and OsJAZ13c. The expression of OsJAZ13 was mainly activated in vegetative tissues and transiently responded to JA and ethylene. Subcellular localization analysis indicated OsJAZ13a is a nuclear protein. Yeast two-hybrid assays revealed OsJAZ13a directly interacts with OsMYC2, and also with OsCOI1, in a COR-dependent manner. Furthermore, OsJAZ13a recruited a general co-repressor OsTPL via an adaptor protein OsNINJA. Remarkably, overexpression of OsJAZ13a resulted in the attenuation of root by methyl JA. Furthermore, OsJAZ13a-overexpressing plants developed lesion mimics in the sheath after approximately 30–45 days of growth. Tillers with necrosis died a few days later. Gene-expression analysis suggested the role of OsJAZ13 in modulating the expression of JA/ethylene response-related genes to regulate growth and activate hypersensitive cell death. Taken together, these observations describe a novel regulatory mechanism in rice and provide the basis for elucidating the function of OsJAZ13 in signal transduction and cell death in plants.

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The helper NLR immune protein NRC3 mediates the hypersensitive cell death caused by the cell-surface receptor Cf-4

10.1101/2021.09.28.461843 ◽

2021 ◽

Author(s):

Jiorgos Kourelis ◽

Mauricio P. Contreras ◽

Adeline Harant ◽

Hiroaki Adachi ◽

Lida Derevnina ◽

...

Keyword(s):

Cell Death ◽

Cell Surface ◽

Immune Responses ◽

Coiled Coil ◽

Chimeric Protein ◽

Cell Surface Receptor ◽

Surface Pattern ◽

Hypersensitive Cell Death ◽

Cell Death Response ◽

Surface Receptor

Cell surface pattern recognition receptors (PRRs) activate immune responses that can include the hypersensitive cell death. However, the pathways that link PRRs to the cell death response are poorly understood. Here, we show that the cell surface receptor-like protein Cf-4 requires the intracellular nucleotide-binding domain leucine-rich repeat containing receptor (NLR) NRC3 to trigger a confluent cell death response upon detection of the fungal effector Avr4 in leaves of Nicotiana benthamiana. This NRC3 activity requires an intact N-terminal MADA motif, a conserved signature of coiled-coil (CC)-type plant NLRs that is required for resistosome-mediated immune responses. A chimeric protein with the N-terminal α1 helix of Arabidopsis ZAR1 swapped into NRC3 retains the capacity to mediate Cf-4 hypersensitive cell death. Pathogen effectors acting as suppressors of NRC3 can suppress Cf-4-triggered hypersensitive cell-death. Our findings link the NLR resistosome model to the hypersensitive cell death caused by a cell surface PRR.

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