Leptosphaeria maculans vs. Leptosphaeria biglobosa – The oilseed rape battle
Maria R Eckert1, Bruce D.L. Fitt1, Andrew Selley2, Stephen Rossall3
1Rothamsted Research, Harpenden, UK, 2DuPont UK Ltd., Stevenage, UK, 3Division of Plant Science, University of Nottingham, UK
Phoma stem canker, a serious disease of oilseed rape world-wide, is caused by Leptosphaeria maculans and L. biglobosa, a fungal species complex which has only recently been defined. The two pathogens vie for the same host, but L. biglobosa is regarded as less damaging than L. maculans. Environmental factors and cultural practices are known to influence disease epidemiology, but little is understood of the effects fungicides have on the two pathogens. A population survey within England was based on both cultural and molecular techniques. Results showed that both pathogens are present in all areas surveyed, but indicated a difference in geographical distribution between the two pathogens. In vitro screening of 120 isolates obtained dur ing the survey showed a significant difference in susceptibility to triazole fungicides between L. maculans and L. biglobosa. ED50 values obtained in this screen indicate that L. biglobosa maybe less susceptible to both flusilazole and tebuconazole than L. maculans. A field experiment at Rothamsted in 2002/2003 showed that timing of fungicide application can influence the population structure; early application of Punch C (full field rate) reduced the proportion of the less damaging L. biglobosa isolates found at the end of the growing season. To better understand the effect fungicides have on the pathogens during the infection process, isolates of L. maculans and L. biglobosa have been transformed with the genes encoding GFP and dsRed. The suitability of using these transformants to visualize the infection pathway is currently being assessed.
Genetic analysis of yellow rust resistance in the UK
Clare M Lewis and Lesley A Boyd
Disease and Stress Biology Department, John Innes Centre, Colney, Norwich, Norfolk. NR4 7UH.
Due to the ability of the yellow rust pathogen (Puccinia striiformis) to rapidly overcome race-specific resistance genes in wheat there has been an increased interest in recent years in the exploitation of partial, adult plant resistance (APR). This is based on the opinion that such forms of resistance may present as potentially more durable, as is the case for the yellow rust APR gene Yr18 (Singh and Rajaram, 1994, Euphytica 72: 1-7), where durability is defined as the situation where a cultivar has been grown for many years over considerable acreage, in an environment suitable for the disease and maintained adequate resistance (Johnson, 1992, Euphytica 63: 3-22). The German wheat Carstens V has long been attributed as the source of at least some of the genes that confer yellow rust APR in modern Western European cultivars. Of the many resistance genes Carstens V is thought to carry (Chen & Line, 1993, Euphytica 71: 107-113; Calonnec et al., 2002, Plant Pathology 51: 777-786) only two have been assigned a chromosomal location. A dominant, race-specific resistance gene, YrCv (Stubbs, 1985, The Cereal Rusts II; 61-101) was first located on chromosome 2A (Afshari, 2000, Phd thesis). Subsequently, a seedling, race-specific resistance gene was mapped to 2AL in the cultivar Senat, and has been designated Yr32 (Eriksen et al., 2004, TAG 108: 576-575). However, it is believed that Yr32 and YrCV may actually be the same gene, but this has yet to be confirmed. The UK biscuit wheat Claire (released in 1999 by Nickersons Seeds) is very resistant to Puccinia striiformis and currently the market leader of its type. It is believed to have Carstens V in its pedigree (P. Fenwick, personal communication) and is being studied to determine the genetics of its yellow rust resistance, and to trace the resistance within its pedigree (Claire family - Carstens V, Carstens VIII, Caribo and Buster). Claire has been postulated to carry the race-specific, seedling resistance genes Yr2 and Yr3. Its adult plant resistance is first observed at growth stage 22, and has been tentatively attributed to QTLs located on chromosomes 2AS, 2DS, 3DL, 4AS and 5DL using a F2 population. These QTLs are currently being mapped more precisely and will be confirmed with F3 family field trials. Buster, a distant sib of Claire has been postulated to have a recessive, seedling resistance to which virulence is not present in the UK P.striiformis f. sp. tritici population. Other family members were postulated to carry the race-specific resistances YrCv (Carstens V), Yr3 (Carstens VIII) and Yr2 (Caribo). Preliminary segregation analysis of the yellow rust APR of Carstens V (x Lemhi/Kharchia local), Carstens VIII (x Kharchia local) and Caribo (x Kharchia local) in F2 populations suggests that at least one major gene confers resistance in each cross. DNA markers and QTL mapping software are currently being used to fine map the resistance in Claire and this Claire family.