title: Knockout of Arabidopsis accelerated-cell-death11 encoding a sphingosine transfer protein causes activation of programmed cell death and defense.
abstract: We describe the lethal, recessive accelerated-cell-death11 Arabidopsis mutant (acd11). Cell death in acd11 exhibits characteristics of animal apoptosis monitored by flow cytometry, and acd11 constitutively expresses defense-related genes that accompany the hypersensitive response normally triggered by avirulent pathogens. Global transcriptional changes during programmed cell death (PCD) and defense activation in acd11 were monitored by cDNA microarray hybridization. The PCD and defense pathways activated in acd11 are salicylic acid (SA) dependent, but do not require intact jasmonic acid or ethylene signaling pathways. Light is required for PCD execution in acd11, as application of an SA-analog to SA-deficient acd11 induced death in the light, but not in the dark. Epistatic analysis showed that the SA-dependent pathways require two regulators of SA-mediated resistance responses, PAD4 and EDS1. Furthermore, acd11 PR1 gene expression, but not cell death, depends on the SA signal tranducer NPR1, suggesting that the npr1-1 mutation uncouples resistance responses and cell death in acd11. The acd11 phenotype is caused by deletion of the ACD11 gene encoding a protein homologous to a mammalian glycolipid transfer protein (GLTP). In contrast to GLTP, ACD11 accelerates the transfer of sphingosine, but not of glycosphingolipids, between membranes in vitro.
authors.affiliation: Institute of Molecular Biology, Copenhagen University, 1353 Copenhagen K, Denmark.
authors.forename: Peter
authors.initials: P
authors.lastname: Brodersen
authors.forename: Morten
authors.initials: M
authors.lastname: Petersen
authors.forename: Helen M
authors.initials: HM
authors.lastname: Pike
authors.forename: Brian
authors.initials: B
authors.lastname: Olszak
authors.forename: Søren
authors.initials: S
authors.lastname: Skov
authors.forename: Niels
authors.initials: N
authors.lastname: Odum
authors.forename: Lise Bolt
authors.initials: LB
authors.lastname: Jørgensen
authors.forename: Rhoderick E
authors.initials: RE
authors.lastname: Brown
authors.forename: John
authors.initials: J
authors.lastname: Mundy
mesh_terms: D000595:Amino Acid Sequence; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D051017:Apoptosis Regulatory Proteins; D017360:Arabidopsis / Q000235:genetics*; D029681:Arabidopsis Proteins / Q000235:genetics / Q000502:physiology*; D002265:Carboxylic Ester Hydrolases / Q000502:physiology; D002462:Cell Membrane / Q000378:metabolism; D003001:Cloning, Molecular; D020869:Gene Expression Profiling; D018506:Gene Expression Regulation, Plant / Q000502:physiology; D005804:Genes, Lethal; D005808:Genes, Recessive; D006028:Glycosphingolipids / Q000378:metabolism; D008027:Light; D026901:Membrane Transport Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D008969:Molecular Sequence Data; D010641:Phenotype; D010935:Plant Diseases / Q000235:genetics; D010940:Plant Proteins / Q000235:genetics / Q000502:physiology*; D030821:Plants, Genetically Modified; D020156:Salicylic Acid / Q000378:metabolism; D016415:Sequence Alignment; D017386:Sequence Homology, Amino Acid; D015398:Signal Transduction / Q000502:physiology; D013110:Sphingosine / Q000378:metabolism*; D013830:Thiadiazoles / Q000494:pharmacology
chemical_list: C451029:ACD11 protein, Arabidopsis; D051017:Apoptosis Regulatory Proteins; D029681:Arabidopsis Proteins; D006028:Glycosphingolipids; D026901:Membrane Transport Proteins; D010940:Plant Proteins; D013830:Thiadiazoles; C099403:S-methyl benzo(1,2,3)thiadiazole-7-carbothioate; D002265:Carboxylic Ester Hydrolases; C400766:PAD4 protein, Arabidopsis; D013110:Sphingosine; D020156:Salicylic Acid