Erwinia carotovora subsp. carotovora and Erwinia-derived elicitors HrpN and PehA trigger distinct but interacting defense responses and cell death in Arabidopsis.
We have used an hrp-positive strain of the soft rot pathogen Erwinia carotovora subsp. carotovora to elucidate plant responses to this bacterial necrotroph. Purified virulence determinants, harpin (HrpN) and polygalacturonase (PehA), were used as tools to facilitate this analysis. We show that HrpN elicits lesion formation in Arabidopsis and tobacco and triggers systemic resistance in Arabidopsis. Establishment of resistance is accompanied by the expression of salicylic acid (SA)-dependent, but also jasmonate/ethylene (JA/ET)-dependent, marker genes PR1 and PDF1.2, respectively, suggesting that both SA-dependent and JA/ET-dependent defense pathways are activated. Use of pathway-specific mutants and transgenic NahG plants show that both pathways are required for the induction of resistance. Arabidopsis plants treated simultaneously with both elictors PehA, known to trigger only JA/ET-dependent defense signaling, and HrpN react with accelerated and enhanced induction of the marker genes PR1 and PDF1.2 both locally and systemically. This mutual amplification of defense gene expression involves both SA-dependent and JA/ET-dependent defense signaling. The two elicitors produced by E. carotovora subsp. carotovora also cooperate in triggering increased production of superoxide and lesion formation.
Kariola
Tarja
T
Department of Biosciences, Division of Genetics, P.O. Box 56, FIN-00014 University of Helsinki, Finland.
Palomäki
Tiina A
TA
Brader
Günter
G
Palva
E Tapio
ET
D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D017360:Arabidopsis / Q000187:drug effects* / Q000235:genetics / Q000382:microbiology; D001425:Bacterial Outer Membrane Proteins / Q000494:pharmacology*; D003517:Cyclopentanes / Q000494:pharmacology; D023082:Defensins; D004357:Drug Synergism; D005030:Ethylenes / Q000494:pharmacology; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D007113:Immunity, Innate / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D009154:Mutation; D054883:Oxylipins; D016973:Pectobacterium carotovorum / Q000254:growth & development*; D010935:Plant Diseases / Q000382:microbiology; D018515:Plant Leaves / Q000187:drug effects / Q000382:microbiology; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism; D030821:Plants, Genetically Modified; D011096:Polygalacturonase / Q000494:pharmacology*; D020156:Salicylic Acid / Q000494:pharmacology; D015398:Signal Transduction / Q000502:physiology; D013481:Superoxides / Q000378:metabolism; D014026:Nicotiana / Q000187:drug effects / Q000382:microbiology / Q000502:physiology
D001425:Bacterial Outer Membrane Proteins; D003517:Cyclopentanes; D023082:Defensins; D005030:Ethylenes; D054883:Oxylipins; D010940:Plant Proteins; C075462:harpin protein, Erwinia amylovora; C053376:pathogenesis-related proteins, plant; D013481:Superoxides; C087295:HrpZ protein, Pseudomonas syringae; C011006:jasmonic acid; C036216:ethylene; D011096:Polygalacturonase; D020156:Salicylic Acid