Author
WEI, FUSHENG - IOWA STATE UNIVERSITY | |
Halterman, Dennis | |
Gobelman Werner, Karin | |
MAO, LONG - CLEMSON UNIVERSITY | |
KURTH, JOACHIM - SAINSBURY LABORATORY | |
SCHULZE-LEFERT, PAUL - SAINSBURY LABORATORY | |
WING, ROD - CLEMSON UNIVERSITY | |
Wise, Roger |
Submitted to: Keystone Symposia
Publication Type: Abstract Only Publication Acceptance Date: 2/25/2000 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Powdery mildew of barley, caused by Erysiphe graminis f. sp. hordei, is a model system for investigating the mechanisms of gene-for-gene interactions between large-genome cereals and obligate-fungal pathogens. The Mla (powdery mildew) resistance-gene cluster is positioned on the short arm of chromosome 5 (1H). AFLP-, RAPD-, and RFLP-derived markers were used to saturate the Mla region in a recombinant population segregating for the [Mla6 + Mla14] and [Mla13 + Ml-Ru3] resistance specificities. The Mla cluster has been delimited to a 240-kb interval bridged by two overlapping BAC clones. Complete sequencing of one of these BACs revealed seven NBS- LRR resistance gene homologs (RGHs), six chymotrypsin inhibitor (CI) genes, and several BARE-1 copia-like retro elements in two gene islands. Pairwise GAP similarity analyses indicate that the RGHs comprise three dissimilar families. cDNA library screening was used to identify members of expressed dRGH families from both Mla6 and Mla13 backgrounds. Fast-neutron derived, accelerated cell-death mutants are being used to target signaling events in the barley-powdery mildew interaction. Research supported in part by USDA- NRI/CGP grant 98-35300-6169. |