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Molecular Plant Advance Access originally published online on April 15, 2008
Molecular Plant 2008 1(3):510-527; doi:10.1093/mp/ssn011
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© The Author 2008. Published by the Molecular Plant Shanghai Editorial Office in association with Oxford University Press on behalf of CSPP and IPPE, SIBS, CAS.

A Lesion-Mimic Syntaxin Double Mutant in Arabidopsis Reveals Novel Complexity of Pathogen Defense Signaling

Ziguo Zhanga, Andrea Lenka, Mats X. Anderssona, Torben Gjettingb, Carsten Pedersena, Mads E. Nielsena,d, Mari-Anne Newmanc, Bi-Huei Houb, Shauna C. Somervilleb and Hans Thordal-Christensena,1

a Plant and Soil Science, Dept of Agricultural Sciences, Faculty of Life Sciences, University of Copenhagen, Thorvaldsensvej 40, DK-1871 Frederiksberg C, Denmark
b Dept of Plant Biology, Carnegie Institution, Stanford, CA 94305, USA
c Plant Pathology, Dept of Plant Biology, Faculty of Life Sciences, University of Copenhagen, Thorvaldsensvej 40, DK-1871 Frederiksberg C, Denmark
d Research Laboratory, Carlsberg Research Center, Gl. Carlsbergvej 10, DK-2500 Valby, Copenhagen, Denmark

1 To whom correspondence should be addressed. E-mail htc{at}life.ku.dk, fax +45 35333460, tel +45 35333443.

The lesion-mimic Arabidopsis mutant, syp121 syp122, constitutively expresses the salicylic acid (SA) signaling pathway and has low penetration resistance to powdery mildew fungi. Genetic analyses of the lesion-mimic phenotype have expanded our understanding of programmed cell death (PCD) in plants. Inactivation of SA signaling genes in syp121 syp122 only partially rescues the lesion-mimic phenotype, indicating that additional defenses contribute to the PCD. Whole genome transcriptome analysis confirmed that SA-induced transcripts, as well as numerous other known pathogen-response transcripts, are up-regulated after inactivation of the syntaxin genes. A suppressor mutant analysis of syp121 syp122 revealed that FMO1, ALD1, and PAD4 are important for lesion development. Mutant alleles of EDS1, NDR1, RAR1, and SGT1b also partially rescued the lesion-mimic phenotype, suggesting that mutating syntaxin genes stimulates TIR-NB-LRR and CC-NB-LRR-type resistances. The syntaxin double knockout potentiated a powdery mildew-induced HR-like response. This required functional PAD4 but not functional SA signaling. However, SA signaling potentiated the PAD4-dependent HR-like response. Analyses of quadruple mutants suggest that EDS5 and SID2 confer separate SA-independent signaling functions, and that FMO1 and ALD1 mediate SA-independent signals that are NPR1-dependent. These studies highlight the contribution of multiple pathways to defense and point to the complexity of their interactions.


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