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   Genetic Requirements for Signaling from an Autoactive Plant NB-LRR Intracellular Innate Immune Receptor  
   
نویسنده roberts m. ,tang s. ,stallmann a. ,dangl j.l. ,bonardi v.
منبع plos genetics - 2013 - دوره : 9 - شماره : 4
چکیده    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. © 2013 roberts et al.
آدرس department of biology,university of north carolina,chapel hill,nc, United States, college of biological sciences,china agricultural university,beijing, China, department of biology,university of north carolina,chapel hill,nc, United States, department of biology,university of north carolina,chapel hill,nc,united states,howard hughes medical institute,university of north carolina,chapel hill,nc,united states,curriculum in genetics and molecular biology,university of north carolina,chapel hill,nc,united states,department of microbiology and immunology,university of north carolina,chapel hill,nc,united states,carolina center for genome sciences,university of north carolina,chapel hill,nc, United States, department of biology,university of north carolina,chapel hill,nc, United States
 
     
   
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