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A regulon conserved in monocot and dicot plants defines a functional module in antifungal plant immunity
Edited by Jeffery L. Dangl, University of North Carolina, Chapel Hill, NC, and approved October 29, 2010 (received for review March 30, 2010)

Abstract
At least two components that modulate plant resistance against the fungal powdery mildew disease are ancient and have been conserved since the time of the monocot–dicot split (≈200 Mya). These components are the seven transmembrane domain containing MLO/MLO2 protein and the syntaxin ROR2/PEN1, which act antagonistically and have been identified in the monocot barley (Hordeum vulgare) and the dicot Arabidopsis thaliana, respectively. Additionally, syntaxin-interacting N-ethylmaleimide sensitive factor adaptor protein receptor proteins (VAMP721/722 and SNAP33/34) as well as a myrosinase (PEN2) and an ABC transporter (PEN3) contribute to antifungal resistance in both barley and/or Arabidopsis. Here, we show that these genetically defined defense components share a similar set of coexpressed genes in the two plant species, comprising a statistically significant overrepresentation of gene products involved in regulation of transcription, posttranslational modification, and signaling. Most of the coexpressed Arabidopsis genes possess a common cis-regulatory element that may dictate their coordinated expression. We exploited gene coexpression to uncover numerous components in Arabidopsis involved in antifungal defense. Together, our data provide evidence for an evolutionarily conserved regulon composed of core components and clade/species-specific innovations that functions as a module in plant innate immunity.
Footnotes
- 5To whom correspondence should be addressed. E-mail: panstrug{at}mpiz-koeln.mpg.de.
Author contributions: M.H., P.S.-L., S.S., and R.P. designed research; M.H., P.B., B.K., S.K., M.S., and M.P.-B. performed research; M.H., P.B., B.K., S.K., M.S., U.G., K.S., A.L., and R.P. analyzed data; and M.H., P.B., P.S.-L., and R.P. wrote the paper.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission.
This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1003619107/-/DCSupplemental.
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