Additional Sources of Resistance to Tan Spot of Wheat

Riede, Carlos Roberto; Francl, L. J.; Anderson, James A.; Jordahl, James G.; Meinhardt, Steven W.

doi:10.2135/cropsci1996.0011183x003600030040x

Cited by 55 publications

(32 citation statements)

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“…However, resistance occurs at different levels in many spring and winter types especially in Brazilian spring wheats. High levels of resistance in bread wheat and synthetic wheat have been observed by other researchers (Tadesse et al 2006a, b;Riede et al 1996). In a recent evaluation of 126 adapted durum and hard red spring wheat cultivars and breeding lines from the Prairie region of North America, observed ten genotypes showing high level of resistance to multiple races of P. tritici-repentis and their toxins.…”

Section: Sources Of Resistancementioning

confidence: 61%

Genetics of wheat–Pyrenophora tritici-repentis interactions

Singh

Duveiller

et al. 2009

Euphytica

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Tan spot, caused by an ascomycete fungus Pyrenophora tritici-repentis, is one of the most devastating foliar diseases of wheat. This fungus induces two distinct symptoms, tan necrosis and extensive chlorosis, on susceptible wheat cultivars. Besides causing average yield losses of 5-10%, tan spot also causes significant losses in grain quality by grain shriveling, red smudge, and black point. Conservation agriculture in combination with wheat monoculture involving cultivation of susceptible cultivars has resulted in frequent onset of tan spot epidemics worldwide. Development of new resistant wheat cultivars, in conjunction with crop rotation, will provide an effective, economical, and environmentally safe means of controlling tan spot. Presently, eight races of P. tritici-repentis have been identified worldwide based on the ability to induce necrosis and chlorosis symptoms on a set of differential wheat cultivars. P. tritici-repentis is a homothallic fungus having both sexual and asexual reproduction resulting in high genetic diversity worldwide. Both quantitative and qualitative mode of inheritance for resistance to tan spot of wheat has been reported. The tan spot fungus produces multiple host-specific toxins and host resistance is highly correlated to insensitivity to toxins. Genetic studies have further confirmed that wheat-P. tritici-repentis follows the toxin model of gene-for-gene hypothesis although other mechanism of host-pathogen interaction may exist and exploitation of all resistance phenomenon is to be adopted to develop durable resistant cultivars.

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Section: Sources Of Resistancementioning

confidence: 61%

Genetics of wheat–Pyrenophora tritici-repentis interactions

Singh

Duveiller

et al. 2009

Euphytica

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“…are major foliar diseases of wheat in North America (Fernandez et al 1998;Gilbert and Woods 2001). Leaf spots on average cause yield losses of 10-15%, however, under conditions favorable for disease development, losses can be as high as 50% (King et al 1983;Riede et al 1996). Leaf spots also cause signiWcant losses in grain quality by grain shriveling, red smudge, and black point (Fernandez et al 1998;McKendry et al 1995).…”

Section: Introductionmentioning

confidence: 99%

A quantitative trait locus on chromosome 5B controls resistance of Triticum turgidum (L.) var. diccocoides to Stagonospora nodorum blotch

et al. 2008

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Stagonospora nodorum blotch (SNB) is an important foliar disease of durum wheat (Triticum turgidum var. durum) worldwide. The combined eVects of SNB and tan spot, considered as components of the leaf spotting disease complex, result in signiWcant damage to wheat production in the northern Great Plains of North America. The main objective of this study was the genetic analysis of resistance to SNB caused by Phaeosphaeria nodorum in tetraploid wheat, and its association with tan spot caused by Pyrenophora tritici-repentis race 2. The 133 recombinant inbred chromosome lines (RICL) developed from the cross LDN/LDN(Dic-5B) were evaluated for SNB reaction at the seedling stage under greenhouse conditions. Molecular markers were used to map a quantitative trait locus (QTL) on chromosome 5B, explaining 37.6% of the phenotypic variation in SNB reaction. The location of the QTL was 8.8 cM distal to the tsn1 locus coding for resistance to P. tritici-repentis race 2. The presence of genes for resistance to both SNB and tan spot in close proximity in tetraploid wheat and the identiWcation of molecular markers linked to these genes or QTLs will be useful for incorporating resistance to these diseases in wheat breeding programs.

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“…Cloning of the gene encoding Ptr ToxA demonstrated that toxin production is sufficient for the pathogenicity of P. triticirepentis on wheat (Ciuffetti et al 1997). However, it was observed that under growth chamber conditions, a Ptr ToxA insensitive line can be highly susceptible to P. tritici-repentis when inoculated with conidia of the necrosis-inducing only race (race 2) and a Ptr ToxA sensitive line can be resistant to conidial inoculation (Riede et al 1996). The inconsistency between Ptr ToxA sensitivity and susceptibility to conidial inoculation may suggest that other factors besides toxin sensitivity may be involved in the hostpathogen interaction.…”

mentioning

confidence: 99%