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+<HTML><HEAD><TITLE>Barley1 Leaf INOC Pgt TTKS (aka isolate Ug99) RMA (Aug09)</TITLE>
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+ <P class="title">Barley1 Leaf INOC Pgt TTKS (aka isolate Ug99) RMA (Aug09) (accession number: <A HREF="/webqtl/main.py?FormID=sharinginfo&GN_AccessionId=236">GN236</A>) <A HREF="/webqtl/main.py?FormID=editHtml">
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+<Blockquote>
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+<P>
+Leaf mRNA data was generated by Roger Wise and colleagues. Please reference the key publications below that describes these data and the experimental design in more detail:
+
+<BR><BR>Moscou MJ, Lauter N, Steffenson B, Wise RP (2011) Quantitative and qualitative stem rust resistance factors in barley are associated with transcriptional suppression of defense regulons. PLoS Genet 7:e1002208
+<A HREF="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1002208">PDF</A>
+
+<P>Data were entered into GeneNetwork by Roger Wise, Rob Williams, and colleagues. All MIAME-compliant GeneChip profiling data are available as accession BB64 at the PLEXdb expression resource for plants and plant pathogens (www.plexdb.org), accession GSE20416 at NCBI-GEO, as well as accessions GN235, GN236, GN237, GN238 at GeneNetwork (www.genenetwork.org).
+
+<P>
+<B>Abstract </B>
+<BR>
+Stem rust (Puccinia graminis f. sp. tritici; Pgt) is a devastating fungal disease of wheat and barley. Pgt race TTKSK (isolate Ug99) is a serious threat to these Triticeae grain crops because resistance is rare. In barley, the complex Rpg-TTKSK locus on chromosome 5H is presently the only known source of qualitative resistance to this aggressive Pgt race. Segregation for resistance observed on seedlings of the Q21861 × SM89010 (QSM) doubled-haploid (DH) population was found to be predominantly qualitative, with little of the remaining variance explained by loci other than Rpg-TTKSK. In contrast, analysis of adult QSM DH plants infected by field inoculum of Pgt race TTKSK in Njoro, Kenya, revealed several additional quantitative trait loci that contribute to resistance. To molecularly characterize these loci, Barley1 GeneChips were used to measure the expression of 22,792 genes in the QSM population after inoculation with Pgt race TTKSK or mock-inoculation. Comparison of expression Quantitative Trait Loci (eQTL) between treatments revealed an inoculation-dependent expression polymorphism implicating Actin depolymerizing factor3 (within the Rpg-TTKSK locus) as a candidate susceptibility gene. In parallel, we identified a chromosome 2H trans-eQTL hotspot that co-segregates with an enhancer of Rpg-TTKSK-mediated, adult plant resistance discovered through the Njoro field trials. Our genome-wide eQTL studies demonstrate that transcript accumulation of 25% of barley genes is altered following challenge by Pgt race TTKSK, but that few of these genes are regulated by the qualitative Rpg-TTKSK on chromosome 5H. It is instead the chromosome 2H trans-eQTL hotspot that orchestrates the largest inoculation-specific responses, where enhanced resistance is associated with transcriptional suppression of hundreds of genes scattered throughout the genome. Hence, the present study associates the early suppression of genes expressed in this host–pathogen interaction with enhancement of R-gene mediated resistance.
+
+</P>
+
+<P>Corresponding data on Q/SM resistance to UG99 infection has been generated by Brian Steffenson. The key publication on phenotyping is (not yet entered into GeneNetwork)
+
+<BR><BR>Steffenson BJ, Jin Y, Brueggeman RS, Kleinhofs A, Sun Y (2009) Resistance to stem rust race TTKSK maps to the rpg4/Rpg5 complex of chromosome 5H of barley. Phytopathology 99:1135-41
+
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+<Blockquote class="subtitle">Acknowledgment of Data Use and Disclaimer:
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+<Blockquote><P>Availability of this data and information does not constitute scientific publication. We request that information derived from it not be published prior to our publication without permission (see below) or 12 months from the time of display whichever is the sooner.<p>
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+Our policy is to release data in a timely and prompt manner to aid the progress of research in plant-pathogen interactions. However, it is not intended to allow others to preempt our scientific publications by rushing to publication in advance of our own efforts.
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