Abstract
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.
Highlights
Plants encounter a wide variety of pathogens
Present understanding of these resistance proteins likens them to molecular switches that bind nucleotides to activate disease resistance responses
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
Summary
Plants encounter a wide variety of pathogens. Plants rely on their organ surfaces as pre-formed barriers to infection. Plants have evolved an active, two-layered immune system [1]. The first branch utilizes transmembrane receptors (PRRs, or pattern recognition receptors) which detect microbe-associated molecular patterns (MAMPs) of various pathogens [2]. MAMP detection elicits a rapid, relatively lowamplitude host transcriptional response resulting in MAMPtriggered immunity (MTI) which is sufficient to halt growth of many microbes [1,3]. Successful pathogens can suppress or delay MTI via delivery of effector molecules into host cells. Effectors are typically virulence proteins [4]. Gram-negative bacterial pathogens deliver effectors via injection into the plant cell by the Type
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