title: Ethylene signaling pathway and MAPK cascades are required for AAL toxin-induced programmed cell death.
abstract: Programmed cell death (PCD), known as hypersensitive response cell death, has an important role in plant defense response. The signaling pathway of PCD remains unknown. We employed AAL toxin and Nicotiana umbratica to analysis plant PCD. AAL toxin is a pathogenicity factor of the necrotrophic pathogen Alternaria alternata f. sp. lycopersici. N. umbratica is sensitive to AAL toxin, susceptible to pathogens, and effective in Tobacco rattle virus-based virus-induced gene silencing (VIGS). VIGS analyses indicated that AAL toxin-triggered cell death (ACD) is dependent upon the mitogen-activated protein (MAP) kinase kinase MEK2, which is upstream of both salicylic acid-induced protein kinase (SIPK) and wound-induced protein kinase (WIPK) responsible for ethylene (ET) synthesis. ET treatment of MEK2-silenced N. umbratica re-established ACD. In SIPK- and WIPK-silenced N. umbratica, ACD was compromised and ET accumulation was not observed. However, in contrast to the case of MEK2-silenced plants, ET treatment did not induce cell death in SIPK- and WIPK-silenced plants. This work showed that ET-dependent pathway and MAP kinase cascades are required in ACD. Our results suggested that MEK2-SIPK/WIPK cascades have roles in ET biosynthesis; however, SIPK and WIPK have other roles in ET signaling or another pathway leading to cell death by AAL toxin.
authors.affiliation: Nagoya University, Nagoya, Japan.
authors.forename: Keisuke
authors.initials: K
authors.lastname: Mase
authors.forename: Takahito
authors.initials: T
authors.lastname: Mizuno
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Ishihama
authors.forename: Takayuki
authors.initials: T
authors.lastname: Fujii
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Mori
authors.forename: Motoichiro
authors.initials: M
authors.lastname: Kodama
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Yoshioka
mesh_terms: D000528:Alternaria / Q000472:pathogenicity; D016923:Cell Death / Q000187:drug effects / Q000235:genetics; D004198:Disease Susceptibility; D005030:Ethylenes / Q000378:metabolism* / Q000494:pharmacology; D018506:Gene Expression Regulation, Plant; D020868:Gene Silencing; D048370:MAP Kinase Kinase 2 / Q000235:genetics / Q000378:metabolism; D020935:MAP Kinase Signaling System; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D010935:Plant Diseases / Q000382:microbiology; D018515:Plant Leaves / Q000187:drug effects / Q000382:microbiology; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism; D030821:Plants, Genetically Modified; D015398:Signal Transduction; D013110:Sphingosine / Q000494:pharmacology*; D014026:Nicotiana / Q000166:cytology* / Q000187:drug effects / Q000235:genetics / Q000378:metabolism* / Q000382:microbiology
chemical_list: C047996:Alternaria alternata pathotoxin TA; D005030:Ethylenes; D010940:Plant Proteins; C036216:ethylene; D020928:Mitogen-Activated Protein Kinases; C106405:SA-induced protein kinase; C113423:WIPK protein, Nicotiana tabacum; D048370:MAP Kinase Kinase 2; D013110:Sphingosine