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Author Manuscript
Plant J. Author manuscript; available in PMC 2007 February 14.
NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as:
Plant J. 2005 October ; 44(2): 245–257.
Regulation of plant defense responses in Arabidopsis by EDR2, a
PH and START domain-containing protein
Dingzhong Tang, Jules Ade, Catherine A. Frye†, and Roger W. Innes*
Department of Biology, Indiana University, Bloomington, IN 47405, USA
Summary
We have identified an Arabidopsis mutant that displays enhanced disease resistance (edr2) to the
biotrophic powdery mildew pathogen Erysiphe cichoracearum. Inhibition of fungal growth on
edr2 mutant leaves occurred at a late stage of the infection process and coincided with formation of
necrotic lesions approximately 5 days after inoculation. Double-mutant analysis revealed that edr2-
mediated resistance is suppressed by mutations that inhibit salicylic acid (SA)-induced defense
signaling, including npr1, pad4 and sid2, demonstrating that edr2-mediated disease resistance is
dependent on SA. However, edr2 showed normal responses to the bacterial pathogen Pseudomonas
syringae pv. tomato strain DC3000. EDR2 appears to be constitutively transcribed in all tissues and
organs and encodes a novel protein, consisting of a putative pleckstrin homology (PH) domain and
a steroidogenic acute regulatory protein-related lipid-transfer (START) domain, and contains an N-
terminal mitochondrial targeting sequence. The PH and START domains are implicated in lipid
binding, suggesting that EDR2 may provide a link between lipid signaling and activation of
programmed cell death mediated by mitochondria.
Keywords
defense responses; disease resistance; powdery mildew; programmed cell death; salicylic acid;
senescence
Introduction
Powdery mildews are biotrophic pathogens that infect a large number of plant species, causing
significant economic losses