Open AccessPriming of the A rabidopsis pattern‐triggered immunity response upon infection by necrotrophic P ectobacterium carotovorum bacteria
Author(s) -
PoWen Chen,
Singh Prashant,
Zimmerli Laurent
Publication year - 2013
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.1364-3703.2012.00827.x
Subject(s) - pectobacterium carotovorum , biology , arabidopsis , microbiology and biotechnology , systemic acquired resistance , plant disease resistance , phytoalexin , callose , mutant , gene , pathogen , genetics , biochemistry , resveratrol
Summary Boosted responsiveness of plant cells to stress at the onset of pathogen‐ or chemically induced resistance is called priming. The chemical β‐aminobutyric acid ( BABA ) enhances A rabidopsis thaliana resistance to hemibiotrophic bacteria through the priming of the salicylic acid ( SA ) defence response. Whether BABA increases A rabidopsis resistance to the necrotrophic bacterium P ectobacterium carotovorum ssp . carotovorum ( P cc ) is not clear. In this work, we show that treatment with BABA protects A rabidopsis against the soft‐rot pathogen P cc . BABA did not prime the expression of the jasmonate/ethylene‐responsive gene PLANT DEFENSIN 1.2 ( PDF 1.2 ), the up‐regulation of which is usually associated with resistance to necrotrophic pathogens. Expression of the SA marker gene PATHOGENESIS RELATED 1 ( PR 1 ) on P cc infection was primed by BABA treatment, but SA ‐defective mutants demonstrated a wild‐type level of BABA ‐induced resistance against Pcc . BABA primed the expression of the pattern‐triggered immunity (PTI)‐responsive genes FLG22‐INDUCED RECEPTOR‐LIKE KINASE 1 ( FRK1 ), ARABIDOPSIS NON‐RACE SPECIFIC DISEASE RESISTANCE GENE (NDR1)/HAIRPIN‐INDUCED GENE (HIN1)‐LIKE 10 ( NHL10 ) and CYTOCHROME P450, FAMILY 81 ( CYP81F2 ) after inoculation with P cc or after treatment with purified bacterial microbe‐associated molecular patterns, such as flg22 or elf26. PTI ‐mediated callose deposition was also potentiated in BABA ‐treated A rabidopsis, and BABA boosted A rabidopsis stomatal immunity to P cc . BABA treatment primed the PTI response in the SA ‐defective mutants SA induction deficient 2‐1 ( sid2‐1 ) and phytoalexin deficient 4‐1 ( pad4‐1 ). In addition, BABA priming was associated with open chromatin configurations in the promoter region of PTI marker genes. Our data indicate that BABA primes the PTI response upon necrotrophic bacterial infection and suggest a role for the PTI response in BABA ‐induced resistance.