Genetic relationships between race-nonspecific and race-specific interactions in the wheat–Pyrenophora tritici-repentis pathosystem

Abstract

We identified a major QTL conferring race-nonspecific resistance and revealed its relationships with race-specific interactions in the wheat- Pyrenophora tritici-repentis pathosystem. Tan spot, caused by the fungus Pyrenophora tritici-repentis (Ptr), is a destructive disease of wheat worldwide. The disease system is known to include inverse gene-for-gene, race-specific interactions involving the recognition of fungal-produced necrotrophic effectors (NEs) by corresponding host sensitivity genes. However, quantitative trait loci (QTLs) conferring race-nonspecific resistance have also been identified. In this work, we identified a major race-nonspecific resistance QTL and characterized its genetic relationships with the NE-host gene interactions Ptr ToxA-Tsn1 and Ptr ToxC-Tsc1 in a recombinant inbred wheat population derived from the cross between 'Louise' and 'Penawawa.' Both parental lines were sensitive to Ptr ToxA, but Penawawa and Louise were highly resistant and susceptible, respectively, to conidial inoculations of all races. Resistance was predominantly governed by a major race-nonspecific QTL on chromosome arm 3BL for resistance to all races. Another significant QTL was detected at the distal end of chromosome arm 1AS for resistance to the Ptr ToxC-producing isolates, which corresponded to the known location of the Tsc1 locus. The effects of the 3B and 1A QTLs were largely additive, and the 3B resistance QTL was epistatic to the Ptr ToxA-Tsn1 interaction. Resistance to race 2 in F1 plants was completely dominant; however, race 3-inoculated F1 plants were only moderately resistant because they developed chlorosis presumably due to the Ptr ToxC-Tsc1 interaction. This work provides further understanding of genetic resistance in the wheat-tan spot system as well as important guidance for tan spot resistance breeding.

Population Structure and Genomewide Association Analysis of Resistance to Disease and Insensitivity to Ptr Toxins in Canadian Spring Wheat Using 90K SNP Array

“…Results from different studies, however, suggest the possible role of other genes and/or QTLs for three reasons. Second, there are different reports that suggest the complexity of the Ptr pathosystem in wheat (Chu et al, 2008a;Kariyawasam et al, 2016), which could be due to the role of other genes and/or QTLs. Second, there are different reports that suggest the complexity of the Ptr pathosystem in wheat (Chu et al, 2008a;Kariyawasam et al, 2016), which could be due to the role of other genes and/or QTLs.…”

Evaluating the importance of the tan spot ToxA–Tsn1 interaction in Australian wheat varieties

“…This lack of association of the ToxA– Tsn1 interaction with disease demonstrates the complexities underlying the tan spot pathosystem, and may be due to the presence of race‐nonspecific resistance. Such a QTL was identified on chromosome 3B in a RIL population derived from a cross between a highly susceptible and a highly resistant wheat line (both sensitive to ToxA) (Kariyawasam et al ., ). The 3B QTL appeared to prohibit the effector‐triggered susceptibility from the ToxA– Tsn1 interaction, thus it appears that this QTL has an epistatic effect on the ToxA– Tsn1 interaction in certain host backgrounds.…”

Vavilov wheat accessions provide useful sources of resistance to tan spot (syn. yellow spot) of wheat

“…Numerous studies have also reported quantitative resistance to P. tritici‐repentis that is effective against multiple races of the pathogen, thus deemed non‐race‐specific forms of resistance (Singh et al ., ; Faris et al ., ; Kariyawasam et al ., ). These studies highlight the complexity of host resistance to P. tritici‐repentis .…”