Open AccessSalicylic acid (SA)‐dependent gene activation can be uncoupled from cell death‐mediated gene activation: the SA‐inducible NIMIN‐1 and NIMIN‐2 promoters, unlike the PR‐1a promoter, do not respond to cell death signals in tobacco
Author(s) -
GLOCOVA IVANA,
THOR KATHRIN,
ROTH BERNHARD,
BABBICK MAREN,
PFITZNER ARTUR J. P.,
PFITZNER URSULA M.
Publication year - 2005
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/j.1364-3703.2005.00288.x
Subject(s) - promoter , biology , gene , salicylic acid , microbiology and biotechnology , programmed cell death , gene expression , genetics , apoptosis
SUMMARY Tobacco pathogenesis‐related ( PR ) genes of group 1 are induced during pathogen defence (hypersensitive response, HR, and systemic acquired resistance, SAR), after exogenous application of salicylic acid (SA), and by developmental cues. Likewise, SA enhances transcripts for Arabidopsis NIMIN‐1 and NIMIN‐2, which interact with NPR1/NIM1, a key regulator of SAR. To further illuminate gene activation during pathogen defence, reporter gene expression from the NIMIN‐1 and NIMIN‐2 promoters was analysed in transgenic tobacco plants in direct comparison to PR‐1 gene expression. NIMIN[GUS] chimeric genes were highly sensitive to SA, whereas NIMIN[GUS], unlike PR1a[GUS], expression was only weak in necrotic tissue exhibiting HR. Furthermore, PR‐1a , but not NIMIN , promoter constructs were activated systemically in response to local cell death elicited by expression of the proapoptotic Bax gene. Conversely, NIMIN‐1[GUS] expression was completely suppressed during pathogen defence in plants depleted from SA, whereas PR‐1 proteins still accumulated in necrotic tissue. These findings demonstrate that SA‐dependent gene activation can be uncoupled from cell death‐induced gene activation. Whereas PR‐1a induction during the HR and SAR responses is mediated by HR‐associated signals and SA, activation of the NIMIN‐1 and NIMIN‐2 promoters in infected tobacco relies on SA, but not on cell death signals.