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ARS Home » Midwest Area » Ames, Iowa » Corn Insects and Crop Genetics Research » Research » Publications at this Location » Publication #226006

Title: Gene-For-Gene-Mediated Transcriptome Reprogramming in Barley-Powdery Mildew Interactions

item MOSCOU, M
item Lauter, Nicholas
item CALDO, R
item Wise, Roger

Submitted to: Annual International Plant & Animal Genome Conference
Publication Type: Abstract Only
Publication Acceptance Date: 12/7/2007
Publication Date: 12/7/2007
Citation: Moscou, M.J., Lauter, N.C., Caldo, R.A., Wise, R.P. 2007. Gene-For-Gene-Mediated Transcriptome Reprogramming in Barley-Powdery Mildew Interactions [abstract]. Annual International Plant & Animal Genome Conference. Abstract Book. p. 88.

Interpretive Summary:

Technical Abstract: Barley has a complex interaction with powdery mildew [Blumeria graminis f. sp. hordei (Bgh)] that begins with early recognition of microbe-associated molecular patterns (MAMPs) from the pathogen. During Bgh invasion of the epidermis, the fate of cells is decided by the presence of resistance (R) genes that mediate an immediate response, which halts the progress of the pathogen. To understand the regulatory role and response associated with R-gene-mediated defense, we surveyed the transcriptional response of barley upon pathogen inoculation using three Manchuria NILs carrying allelic variants at the Mla locus, null mutations mla1-m508 and mla6-m9472, as well as Sultan 5 (Mla12) and mutants derived there from, mla12-m66, rar-1-1, rar1-2, and rom1. Each experiment consisted of sampling at 0, 8, 16, 20, 24, and 32 hours after inoculation with three replications, varying only in the inclusion of non-inoculated material. We found that the resistance response manifests itself via dynamic reprogramming of the transcriptome, which includes over 5,000 genes and may likely exceed 10,000. In addition, the same genes that are coordinately expressed in resistant versus susceptible reactions are differentially expressed between inoculated and non-inoculated tissue. By contrast, the quantitative nature of the Mla control becomes apparent when we observe null mutations, where early signaling effects are compromised by this gene loss. Collectively, our results confirm the high-level regulatory control of Mla in gene-for-gene-mediated resistance and point to an essential early regulatory role as observed via massive transcriptome reprogramming.