title: Genetic analysis of acd6-1 reveals complex defense networks and leads to identification of novel defense genes in Arabidopsis.
abstract: Pathogen infection leads to the activation of defense signaling networks in plants. To study these networks and the relationships between their components, we introduced various defense mutations into acd6-1, a constitutive gain-of-function Arabidopsis mutant that is highly disease resistant. acd6-1 plants show spontaneous cell death, reduced stature, and accumulate high levels of camalexin (an anti-fungal compound) and salicylic acid (SA; a signaling molecule). Disruption of several defense genes revealed that in acd6-1, SA levels/signaling were positively correlated with the degree of disease resistance and defense gene expression. Salicylic acid also modulates the severity of cell death. However, accumulation of camalexin in acd6-1 is largely unaffected by reducing the level of SA. In addition, acd6-1 shows ethylene- and jasmonic acid-mediated signaling that is antagonized and therefore masked by the presence of SA. Mutant analysis revealed a new relationship between the signaling components NPR1 and PAD4 and also indicated that multiple defense pathways were required for phenotypes conferred by acd6-1. In addition, our data confirmed that the size of acd6-1 was inversely correlated with SA levels/signaling. We exploited this unique feature of acd6-1 to identify two genes disrupted in acd6-1 suppressor (sup) mutants: one encodes a known SA biosynthetic component (SID2) and the other encodes an uncharacterized putative metalloprotease (At5g20660). Taken together, acd6-1 is a powerful tool not only for dissecting defense regulatory networks but also for discovering novel defense genes.
authors.affiliation: Department of Biological Sciences, University of Maryland Baltimore County, 1000 Hilltop Circle, Baltimore, MD 21250, USA. hualu@umbc.edu
authors.forename: Hua
authors.initials: H
authors.lastname: Lu
authors.forename: Sasan
authors.initials: S
authors.lastname: Salimian
authors.forename: Emily
authors.initials: E
authors.lastname: Gamelin
authors.forename: Guoying
authors.initials: G
authors.lastname: Wang
authors.forename: Jennifer
authors.initials: J
authors.lastname: Fedorowski
authors.forename: William
authors.initials: W
authors.lastname: LaCourse
authors.forename: Jean T
authors.initials: JT
authors.lastname: Greenberg
mesh_terms: D017487:Ankyrins / Q000235:genetics*; D017360:Arabidopsis / Q000235:genetics* / Q000378:metabolism; D029681:Arabidopsis Proteins / Q000235:genetics*; D003517:Cyclopentanes / Q000378:metabolism; D005030:Ethylenes / Q000378:metabolism; D017343:Genes, Plant; D007113:Immunity, Innate; D007211:Indoles / Q000378:metabolism; D019751:Intramolecular Transferases / Q000235:genetics / Q000378:metabolism*; D016254:Mutagenesis, Insertional; D009154:Mutation; D054883:Oxylipins / Q000378:metabolism; D020156:Salicylic Acid / Q000378:metabolism; D015398:Signal Transduction; D013844:Thiazoles / Q000378:metabolism; D000094162:Phytoalexins
chemical_list: D017487:Ankyrins; D029681:Arabidopsis Proteins; D003517:Cyclopentanes; D005030:Ethylenes; D007211:Indoles; D019751:Intramolecular Transferases; D054883:Oxylipins; D020156:Salicylic Acid; D013844:Thiazoles; C480953:ACD6 protein, Arabidopsis; C102405:camalexin; D000094162:Phytoalexins; C011006:jasmonic acid; C036216:ethylene; C058486:isochorismate synthase