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ARS Home » Midwest Area » Ames, Iowa » Corn Insects and Crop Genetics Research » Research » Publications at this Location » Publication #226010
Title: Genetical Genomic Dissection of Stem Rust Infection in Barley

Author
item Lauter, Nicholas
item MOSCOU, MATTHEW - IOWA STATE UNIVERSITY
item Rodriguez, Jose
item Fuerst, Gregory
item STEFFENSON, BRIAN - UNIVERSITY OF MINNESOTA
item Jin, Yue
item Szabo, Les
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: Lauter, N.C., Moscou, M.J., Rodriguez, J.E., Fuerst, G.S., Steffenson, B.J., Jin, Y., Szabo, L.J., Wise, R.P. 2007. Genetical Genomic Dissection of Stem Rust Infection in Barley [abstract]. Annual International Plant & Animal Genome Conference. Book of Abstracts. p. 17.

Interpretive Summary:

Technical Abstract: To identify breeding and biochemical targets that will mitigate a stem rust epidemic currently threatening barley and wheat crops worldwide, we have performed QTL and eQTL mapping experiments to connect genetic loci that confer stem rust resistance with gene expression networks that are responsive to infection. Barley1 GeneChips have been used to profile the transcriptome of inoculated and mock-inoculated leaves of Q21861, SM89010, and seventy-five Q21861 x SM89010 doubled haploid lines that vary both qualitatively and quantitatively in their reaction to P. graminis f.sp. tritici, race TTKS. The linkage map of the QSM population was built using Single Feature Polymorphism (SFP) markers derived from our GeneChip hybridizations. These were placed onto a skeletal map initially populated by markers with coincident occurrence in the Steptoe x Morex doubled haploid SFP map (Potokina et al. 2007, Plant Journal). Our eQTL analyses thus far have focused on probesets that show differential expression between inoculated and mock-inoculated leaves, allowing identification of loci that regulate the genes and gene networks most relevant to disease defense. We will discuss the extent to which QTL and eQTL positions are coincident and will address whether or not the major effect QTL for TTKS resistance is identified as a trans-eQTL hotspot likely to be coordinately regulating a large number of genes that reside throughout the genome.