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Plant J. 2009 May;58(3):401-12. doi: 10.1111/j.1365-313X.2009.03791.x. Epub 2009 Jan 8.

Genetic analysis of acd6-1 reveals complex defense networks and leads to identification of novel defense genes in Arabidopsis.

Author information

1
Department of Biological Sciences, University of Maryland Baltimore County, 1000 Hilltop Circle, Baltimore, MD 21250, USA. hualu@umbc.edu

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.

PMID:
19144005
PMCID:
PMC2727925
DOI:
10.1111/j.1365-313X.2009.03791.x
[Indexed for MEDLINE]
Free PMC Article

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