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Plos Genetics : Genetic Requirements for Signaling from an Autoactive Plant Nb-lrr Intracellular Innate Immune Receptor, Volume 9

By McDowell, John M.

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Book Id: WPLBN0003952954
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Reproduction Date: 2015

Title: Plos Genetics : Genetic Requirements for Signaling from an Autoactive Plant Nb-lrr Intracellular Innate Immune Receptor, Volume 9  
Author: McDowell, John M.
Volume: Volume 9
Language: English
Subject: Journals, Science, Genetics
Collections: Periodicals: Journal and Magazine Collection (Contemporary), PLoS Genetics
Historic
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Publisher: Plos

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Mcdowell, J. M. (n.d.). Plos Genetics : Genetic Requirements for Signaling from an Autoactive Plant Nb-lrr Intracellular Innate Immune Receptor, Volume 9. Retrieved from http://www.nationalpubliclibrary.com/


Description
Description : Plants react to pathogen attack via recognition of, and response to, pathogen-specific molecules at the cell surface and inside the cell. Pathogen effectors (virulence factors) are monitored by intracellular nucleotide-binding leucine-rich repeat (NB-LRR) sensor proteins in plants and mammals. Here, we study the genetic requirements for defense responses of an autoactive mutant of ADR1-L2, an Arabidopsis coiled-coil (CC)-NB-LRR protein. ADR1-L2 functions upstream of salicylic acid (SA) accumulation in several defense contexts, and it can act in this context as a ‘‘helper’’ to transduce specific microbial activation signals from ‘‘sensor’’ NB-LRRs. This helper activity does not require an intact P-loop. ADR1-L2 and another of two closely related members of this small NB-LRR family are also required for propagation of unregulated runaway cell death (rcd) in an lsd1 mutant. We demonstrate here that, in this particular context, ADR1-L2 function is P-loop dependent. We generated an autoactive missense mutation, ADR1-L2D484V, in a small homology motif termed MHD. Expression of ADR1- L2D848V leads to dwarfed plants that exhibit increased disease resistance and constitutively high SA levels. The morphological phenotype also requires an intact P-loop, suggesting that these ADR1-L2D484V phenotypes reflect canonical activation of this NB-LRR protein. We used ADR1-L2D484V to define genetic requirements for signaling. Signaling from ADR1- L2D484V does not require NADPH oxidase and is negatively regulated by EDS1 and AtMC1. Transcriptional regulation of ADR1-L2D484V is correlated with its phenotypic outputs: these outputs are both SA–dependent and –independent. The genetic requirements for ADR1-L2D484V activity resemble those that regulate an SA–gradient-dependent signal amplification of defense and cell death signaling initially observed in the absence of LSD1. Importantly, ADR1-L2D484V autoactivation signaling is controlled by both EDS1 and SA in separable, but linked pathways. These data allows us to propose a genetic model that provides insight into an SA–dependent feedback regulation loop, which, surprisingly, includes ADR1-L2.

 

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