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Runaway cell death, but not basal disease resistance, in lsd1 is SA‐ and NIM1/NPR1 ‐dependent
Author(s) -
Aviv Daniel H.,
Rustérucci Christine,
Iii Ben F. Holt,
Dietrich Robert A.,
Parker Jane E.,
Dangl Jeffery L.
Publication year - 2002
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.0960-7412.2001.01225.x
Subject(s) - programmed cell death , microbiology and biotechnology , biology , npr1 , signal transduction , regulator , genetics , natriuretic peptide , medicine , apoptosis , gene , heart failure
Summary 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.