title: Pattern-triggered immunity suppresses programmed cell death triggered by fumonisin b1.
abstract: Programmed cell death (PCD) is a crucial process for plant innate immunity and development. In plant innate immunity, PCD is believed to prevent the spread of pathogens from the infection site. Although proper control of PCD is important for plant fitness, we have limited understanding of the molecular mechanisms regulating plant PCD. Plant innate immunity triggered by recognition of effectors (effector-triggered immunity, ETI) is often associated with PCD. However pattern-triggered immunity (PTI), which is triggered by recognition of elicitors called microbe-associated molecular patterns (MAMPs), is not. Therefore we hypothesized that PTI might suppress PCD. Here we report that PCD triggered by the mycotoxin fumonisin B1 (FB1) can be suppressed by PTI in Arabidopsis. FB1-triggered cell death was suppressed by treatment with the MAMPs flg22 (a part of bacterial flagellin) or elf18 (a part of the bacterial elongation factor EF-Tu) but not chitin (a component of fungal cell walls). Although plant hormone signaling is associated with PCD and PTI, both FB1-triggered cell death and suppression of cell death by flg22 treatment were still observed in mutants deficient in jasmonic acid (JA), ethylene (ET) and salicylic acid (SA) signaling. The MAP kinases MPK3 and MPK6 are transiently activated and inactivated within one hour during PTI. We found that FB1 activated MPK3 and MPK6 about 36-48 hours after treatment. Interestingly, this late activation was attenuated by flg22 treatment. These results suggest that PTI suppression of FB1-triggered cell death may involve suppression of MPK3/MPK6 signaling but does not require JA/ET/SA signaling.
authors.affiliation: Department of Plant Biology, Microbial and Plant Genomics Institute, University of Minnesota, St. Paul, Minnesota, USA.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Igarashi
authors.forename: Gerit
authors.initials: G
authors.lastname: Bethke
authors.forename: Yuan
authors.initials: Y
authors.lastname: Xu
authors.forename: Kenichi
authors.initials: K
authors.lastname: Tsuda
authors.forename: Jane
authors.initials: J
authors.lastname: Glazebrook
authors.forename: Fumiaki
authors.initials: F
authors.lastname: Katagiri
mesh_terms: D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics / Q000276:immunology*; D029681:Arabidopsis Proteins / Q000235:genetics / Q000276:immunology; D001426:Bacterial Proteins / Q000494:pharmacology; D016923:Cell Death / Q000187:drug effects / Q000276:immunology; D002686:Chitin / Q000494:pharmacology; D003517:Cyclopentanes / Q000378:metabolism; D005030:Ethylenes / Q000378:metabolism / Q000494:pharmacology; D005408:Flagellin / Q000494:pharmacology; D037341:Fumonisins / Q000494:pharmacology*; D018506:Gene Expression Regulation, Plant / Q000187:drug effects* / Q000276:immunology; D020929:Mitogen-Activated Protein Kinase Kinases / Q000235:genetics / Q000276:immunology; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000276:immunology; D009183:Mycotoxins / Q000494:pharmacology*; D054883:Oxylipins / Q000378:metabolism; D010444:Peptide Elongation Factor Tu / Q000494:pharmacology; D010446:Peptide Fragments / Q000494:pharmacology; D010937:Plant Growth Regulators / Q000378:metabolism / Q000494:pharmacology; D057865:Plant Immunity / Q000187:drug effects*; D020156:Salicylic Acid / Q000378:metabolism / Q000494:pharmacology; D015398:Signal Transduction
chemical_list: D029681:Arabidopsis Proteins; D001426:Bacterial Proteins; D003517:Cyclopentanes; D005030:Ethylenes; D037341:Fumonisins; D009183:Mycotoxins; D054883:Oxylipins; D010446:Peptide Fragments; D010937:Plant Growth Regulators; D005408:Flagellin; D002686:Chitin; C056933:fumonisin B1; C011006:jasmonic acid; C036216:ethylene; C458516:AtMPK3 protein, Arabidopsis; C436293:MPK6 protein, Arabidopsis; D020928:Mitogen-Activated Protein Kinases; D020929:Mitogen-Activated Protein Kinase Kinases; D010444:Peptide Elongation Factor Tu; D020156:Salicylic Acid
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