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|Title: ||Non-host resistance: is it really a durable source of resistance?|
|Authors: ||Rodrigues, Paula|
|Keywords: ||Non-host resistance|
|Issue Date: ||2004|
|Publisher: ||The British Society for Plant Pathology|
|Citation: ||Conference of the EFPP. 7th. BSPP Presidential Meeting. Aberdeen, 2004|
|Abstract: ||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.|
|Appears in Collections:||BB - Posters em Encontros Científicos Internacionais|
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