Identification of non-host resistance genes in wheat to barley yellow rust

Yellow rust, caused by Puccinia striiformis West., is an important foliar disease of wheat and barley throughout the world, and the development of resistant cultivars is the most economical and environmentally friendly method of control. Breeding for resistance to yellow rust has, for decades, been based on the use of race-specific resistance genes, which have shown to be short-lived. Non-host resistance has been studied as a possible source of durable resistance. Two major genes, as well as an undetermined number of minor genes, for non-host resistance to the barley attacking form of yellow rust, P. striiformis f. sp. hordei, have been previously detected in the wheat cultivar ‘Lemhi’. The present study aimed at quantifying and mapping those genes using QTL (quantitative trait loci) mapping procedures. For that purpose, an F2 population of 114 individuals resulting from the cross of resistant ‘Lemhi’ with ‘Chinese 166’, a wheat cultivar susceptible to barley yellow rust, was used as the mapping population. QTL effects and significance were estimated by means of interval mapping and MQM mapping procedures. A map for the F2 population was constructed which included 116 DNA markers (14 SSRs and 102 AFLPs). Two major QTLs have been mapped to chromosome arms 1DS (Psh1) and 2BL (Psh2), with significant LOD values. These two QTLs account for 76.7% of the phenotypic variance for resistance to barley yellow rust. Two other QTLs, with a minor effect, were mapped to chromosome arms 5AL (Psh3) and 6AL (Psh4), explaining 5.1% and 10.9% of the phenotypic variation, respectively. The QTL on 5A was derived from the susceptible variety, ‘Chinese 166’. In all cases the resistance towards P. striiformis f.sp. hordei was associated with a visual chlorosis/necrosis response typical of race-specific, host resistance

Non-host resistance: is it really a durable source of resistance?

Yellow rust, caused by Puccinia striiformis West., is an important foliar disease of wheat and barley throughout the world, and the development of resistant cultivars is the most economical and environmentally friendly method of control. Breeding for resistance to yellow rust has, for decades, been based on the use of race-specific resistance genes, which have shown to be short-lived. Non-host resistance has been studied as a possible source of durable resistance. A non-host resistance associated with hypersensitivity has been detected in the wheat cultivar ‘Lemhi’ to the barley attacking form of yellow rust, P. striiformis f. sp. hordei. Two major genes, as well as an undetermined number of minor genes, have been identified as responsible for this resistance in ‘Lemhi’. The present study aimed at quantifying and mapping those genes using QTL (quantitative trait loci) mapping procedures. For that purpose, an F2 population of 114 individuals resulting from the cross of resistant ‘Lemhi’ with ‘Chinese 166’, a wheat cultivar susceptible to barley yellow rust, was used as the mapping population. QTL effects and significance were estimated by means of interval mapping and MQM mapping procedures. In all individuals showing resistance towards P. striiformis f.sp. hordei, there was a visual chlorosis/necrosis response typical of race-specific, host resistance. QTL analysis resulted in the mapping of two major QTLs on chromosome arms 1DS (Psh1) and 2BL (Psh2) and two other, with a minor effect, on chromosome arms 5AL (Psh3) and 6AL (Psh4). Psh1 and Psh2 have been mapped to segments of the wheat genome where other wheat yellow rust resistance genes (Yr genes) and QTLs had previously been mapped, suggesting an association between host and non-host yellow rust resistance genes. The cloning of both major and minor Psh genes, as well as the Yr genes present in ‘Lemhi’, would allow us to determine the similarity of their structure and function. On the other hand, if a close linkage between major Psh genes and Yr genes is confirmed, it would suggest that these genes could have evolved from the same ancestral R gene. If that is to be the case, then their durability would be similarly perishable. The value of pursuing for non-host resistance genes as a source of durable resistance would therefore have to be seriously reconsidered

The genetics of non-host disease resistance in wheat to barley yellow rust

Non-host resistance is investigated as a potential source of durable resistance. However, the genetics of non-host resistance between closely related plant species and their corresponding pathogens would indicate that in these interactions, non-host resistance primarily involves major genes that operate on a gene-for-gene principal similar to that seen in host resistance. Wheat is a non-host of the barley-attacking form of the fungus responsible for yellow rust, i.e. Puccinia striiformis f. sp. hordei. While P. striiformis f. sp. hordei is generally unable to infect wheat, a partial susceptibility was exhibited by the wheat variety Chinese 166. Consequently, in the cross Lemhi × Chinese 166 two major QTLs for resistance to P. striiformis f. sp. hordei were identified: one on chromosome 1D and a second on 2B. These two QTLs accounted for 43.5% and 33.2% of the phenotypic variance for resistance to barley yellow rust, respectively. In addition, two QTLs of smaller effect were also identified: one on chromosome 5A, contributing 5.1% of the variance and a second on chromosome 6A, contributing 10.9% to the phenotype. The QTL on 6A was derived from the susceptible variety, Chinese 166. In all cases the resistance towards P. striiformis f. sp. hordei was associated with a visual chlorosis/necrosis response typical of race specific host resistance

Arthritis in space and time - To boldly go!

Despite the profound impact of biologics on the treatment of rheumatoid arthritis (RA), long lasting disease remission remains elusive. We propose that this is a consequence of failing to target the right molecular pathway in the most relevant patient group at the appropriate time and place in disease progression. A limitation to testing this approach is the availability of disease models representing the discrete steps in autoimmune pathogenesis. A particular example is the paucity of models to dissect the conditions permissive for the breach of self-tolerance, which would subsequently allow identification and testing of therapeutics for re-establishment of self-tolerance. We conclude that a detailed understanding of the location and timing of events leading to the systemic breach of self-tolerance and subsequent progression to tissue specific pathology are required if rational application of existing drugs and identification of novel targets is to be achieved. This will take the personalised medicine revolution into the realms of contextualised medicine, whereby the right drug is targeted to the right tissue, in the right patient, at the right time. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved