Genetic Requirements for Signaling from an Autoactive Plant NB-LRR Intracellular Innate Immune Receptor

Autor: Vera Bonardi, Anna Stallmann, Melinda Roberts, Saijun Tang, Jeffery L. Dangl
Jazyk: angličtina
Rok vydání: 2013
Předmět:
Zdroj: PLoS Genetics
PLoS Genetics, Vol 9, Iss 4, p e1003465 (2013)
ISSN: 1553-7404
1553-7390
Popis: 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.
Author Summary Plants possess an active, inducible disease resistance system, and induction of these responses depends in part on plant resistance proteins. Present understanding of these resistance proteins likens them to molecular switches that bind nucleotides to activate disease resistance responses. Previously it was shown that Activated Disease Resistance 1-like 2 (ADR1-L2), a plant disease resistance protein, is important in the immune response, but can function in the contexts analysed independently of what is currently considered the canonical nucleotide switch activation. Here, we show that, in addition to these previously reported functions, ADR1-L2 also works as a typical, activated disease resistance protein. We use an autoactive mutant form of the protein and show that it promotes disease resistance. We find that ADR1-L2 works in an EDS1-dependent feedback loop with salicylic acid, a hormone known to be essential for plant disease resistance. This work allows us to broaden the understanding of how plant disease resistance proteins function to generate defense against pathogens.
Databáze: OpenAIRE
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