title: Runaway cell death, but not basal disease resistance, in lsd1 is SA- and NIM1/NPR1-dependent.
abstract: LSD1 was defined as a negative regulator of plant cell death and basal disease resistance based on its null mutant phenotypes. We addressed the relationship between lsd1-mediated runaway cell death and signaling components required for systemic acquired resistance (SAR), namely salicylic acid (SA) accumulation and NIM1/NPR1. We present two important findings. First, SA accumulation and NIM1/NPR1 are required for lsd1-mediated runaway cell death following pathogen infection or application of chemicals that mimic SA action. This implies that lsd1-dependent cell death occurs 'downstream' of the accumulation of SA. As SA application triggers runaway cell death in lsd1 but not wild-type plants, we infer that LSD1 negatively regulates an SA-dependent signal leading to cell death. Thus SA is both a trigger and a required mediator of lsd1 runaway cell death. Second, neither SA accumulation nor NIM1/NPR1 function is required for the basal resistance operating in lsd1. Therefore LSD1 negatively regulates a basal defense pathway that can act upstream or independently of both NIM1/NPR1 function and SA accumulation following avirulent or virulent pathogen challenge. Our data, together with results from other studies, point to the existence of an SA-dependent 'signal potentiation loop' controlling HR. Continued escalation of signaling in the absence of LSD1 leads to runaway cell death. We propose that LSD1 is a key negative regulator of this signal potentiation.
authors.affiliation: Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, NC 27599-3280, USA.
authors.forename: Daniel H
authors.initials: DH
authors.lastname: Aviv
authors.forename: Christine
authors.initials: C
authors.lastname: Rustérucci
authors.forename: Ben F
authors.initials: BF
authors.lastname: Holt
authors.forename: Robert A
authors.initials: RA
authors.lastname: Dietrich
authors.forename: Jane E
authors.initials: JE
authors.lastname: Parker
authors.forename: Jeffery L
authors.initials: JL
authors.lastname: Dangl
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D017360:Arabidopsis / Q000187:drug effects / Q000382:microbiology / Q000502:physiology; D029681:Arabidopsis Proteins; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D004268:DNA-Binding Proteins / Q000187:drug effects / Q000378:metabolism; D005658:Fungi / Q000254:growth & development; D006861:Hydrogen Peroxide / Q000378:metabolism; D007113:Immunity, Innate / Q000187:drug effects; D018384:Oxidative Stress; D018515:Plant Leaves / Q000187:drug effects / Q000382:microbiology / Q000502:physiology; D010940:Plant Proteins / Q000378:metabolism*; D020156:Salicylic Acid / Q000378:metabolism* / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects; D014157:Transcription Factors / Q000187:drug effects / Q000378:metabolism
chemical_list: D029681:Arabidopsis Proteins; D004268:DNA-Binding Proteins; C104920:LSD1 protein, Arabidopsis; C105496:NPR1 protein, Arabidopsis; D010940:Plant Proteins; D014157:Transcription Factors; D006861:Hydrogen Peroxide; D020156:Salicylic Acid