Topology of the network integrating salicylate and jasmonate signal transduction derived from global expression phenotyping

Jane Glazebrook, Wenqiong Chen, Bram Estes, Hur Song Chang, Christiane Nawrath, Jean Pierre Métraux, Tong Zhu, Fumiaki Katagiri

Research output: Contribution to journalArticlepeer-review

411 Scopus citations


The signal transduction network controlling plant responses to pathogens includes pathways requiring the signal molecules salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). The network topology was explored using global expression phenotyping of wild-type and signaling-defective mutant plants, including eds3, eds4, eds5, eds8, pad1, pad2, pad4, NahG, npr1, sid2, ein2, and coi1. Hierarchical clustering was used to define groups of mutations with similar effects on gene expression and groups of similarly regulated genes. Mutations affecting SA signaling formed two groups: one comprised of eds4, eds5, sid2, and npr1-3 affecting only SA signaling; and the other comprised of pad2, eds3, npr1-1, pad4, and NahG affecting SA signaling as well as another unknown process. Major differences between the expression patterns in NahG and the SA biosynthetic mutant sid2 suggest that NahG has pleiotropic effects beyond elimination of SA. A third group of mutants comprised of eds8, pad1, ein2, and coi1 affected ethylene and jasmonate signaling. Expression patterns of some genes revealed mutual inhibition between SA- and JA-dependent signaling, while other genes required JA and ET signaling as well as the unknown signaling process for full expression. Global expression phenotype similarities among mutants suggested, and experiments confirmed, that EDS3 affects SA signaling while EDS8and PAD1 affect JA signaling. This work allowed modeling of network topology, definition of co-regulated genes, and placement of previously uncharacterized regulatory genes in the network.

Original languageEnglish (US)
Pages (from-to)217-228
Number of pages12
JournalPlant Journal
Issue number2
StatePublished - Apr 2003


  • Arabidopsis
  • Disease resistance
  • Microarray
  • Mutants
  • Pseudomonas syringae
  • Signal network


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