CHARACTERIZATION OF STRESS RESISTANCE GENES AND MECHANISMS, & IMPROVEMENT AND GENOTYPING OF WHEAT AND BARLEY GERMPLASM FOR THE WESTERN U.S.
Location: Wheat Genetics, Quality Physiology and Disease Research
Title: Mapping QTL for resistance to eyespot of wheat in Aegilops longissima
Submitted to: Theoretical and Applied Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 27, 2012
Publication Date: N/A
Interpretive Summary: Eyespot is caused by the soilborne fungi Oculimacula yallundae (syn: Tapesia yallundae, Wallwork & Spooner) Crous & W. Gams and O. acuformis Crous & W. Gams (syn: T. acuformis) (Crous et al. 2003). These two pathogens were formerly known as the W- and R- pathotypes of Pseudocercosporella herpotrichoides (Fron.) Deighton, respectively, before the teleomorph was discovered (Lucas et al. 2000). These fungi infect the stem base of wheat and other cereals and grasses, causing eye-shaped elliptical
lesions that result in lodging of infected plants and yield loss (Murray 2010). When eyespot is severe, yield loss of up to 50 % can occur in susceptible cultivars (Murray and Bruehl 1986). Eyespot has been reported in several wheat-growing areas of the world with cool, wet autumn and winter weather including North and South America, Australia, New Zealand, Europe, and Africa (Lucas et al. 2000). In the US, eyespot is a yield-limiting disease mainly in the Pacific Northwest (PNW) even though the pathogens are
widespread. The most economical and environmentally friendly control method for eyespot is growing resistant wheat cultivars. Cappelle Desprez was the first source of eyespot resistance reported from hexaploid wheat (Law et al. 1976).
Eyespot is an economically important disease of wheat caused by the soilborne fungi Oculimacula yal- lundae and O. acuformis. These pathogens infect and colonize the stem base, which results in lodging of diseased plants and reduced grain yield. Disease resistant cultivars are the most desirable control method, but resistance genes are limited in the wheat gene pool. Some accessions of the wheat wild relative Aegilops longissima are resistant to eyespot, but nothing is known about the genetic control of
resistance. A recombinant inbred line population was developed from the cross PI 542196 (R) PI 330486
(S) to map the resistance genes and better understand resistance in Ae. longissima. A genetic linkage map of the Sl genome was constructed with 169 wheat microsatellite markers covering 1261.3 cM in 7 groups. F5 lines (189) were tested for reaction to O. yallundae and four QTL were detected in chromosomes 1Sl, 3Sl , 5Sl , and 7Sl. These QTL explained 44 % of the total phenotypic variation in reaction to eyespot based on GUS scores and 63 % for visual disease ratings. These results demonstrate that genetic control of O. yallundae resistance in Ae. longissima is polygenic. This is the first report of multiple QTL conferring resistance to eyespot in Ae. longissima. Markers cfd6, wmc597, wmc415, and cfd2 are tightly linked to Q.Pch. wsu-1Sl, Q.Pch.wsu-3Sl, Q.Pch.wsu-5Sl, and Q.Pch.wsu-7Sl, respectively. These markers may be useful in marker-assisted selection for transferring resistance genes to wheat to increase the effectiveness of resistance and broaden the genetic diversity of eyespot resistance.