|Gobelman Werner, Karin|
Submitted to: Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/10/1999
Publication Date: N/A
Citation: Interpretive Summary: Fungal diseases cause widespread damage to crop plants. The most efficient way to control these diseases is by the incorporation of genetic resistance to the pathogens that cause these diseases. Genes that confer resistance to pathogens are often clustered together on a single chromosome. In barley, a large number of genes, which confer resistance to the powdery mildew fungus, Erysiphe graminis f. sp. hordei, are clustered together at locus designated Mla. We are interested in understanding how these genes trigger an active defense response. In order to do this, it is necessary to clone the Mla gene. By doing so, we can begin to understand the signaling processes involved to confer resistance to disease. This research will facilitate the development of plants with resistance to diseases which in turn will be more productive for growers.
Technical Abstract: Powdery mildew of barley, caused by Erysiphe graminis f. sp. hordei, is a model system for investigating the mechanism of gene-for-gene interaction between large-genome cereals and obligate-fungal pathogens. A large number of loci that confer resistance to this disease are located on the short arm of chromosome 5(1H). The Mla resistance-gene cluster is positioned near the telomeric end of this chromosome arm. AFLP-, RAPD-, and RFLP-derived markers were used to saturate the Mla region in a high-resolution recombinant population segregating for the (Mla6 + Mla14) and (Mla13 + Ml- Ru3) resistance specificities. These tightly linked genetic markers were used to identify and develop a physical contig of YAC and BAC clones spanning the Mla cluster. Three distinct NBS-LRR resistance-gene homologue (RGH) families were revealed via computational analysis of low-pass and BAC-end sequence data derived from Mla-spanning clones. Genetic and physical mapping delimited the Mla-associated, NBS-LRR gene families to a 240-kb interval. Recombination within the RGH families was at least ten- fold less frequent than between markers directly adjacent to the Mla cluster.