New Insights into the Roles of Host Gene-Necrotrophic Effector Interactions in Governing Susceptibility of Durum Wheat to Tan Spot and Septoria nodorum Blotch

被引:50
|
作者
Virdi, Simerjot K. [1 ]
Liu, Zhaohui [2 ]
Overlander, Megan E. [3 ]
Zhang, Zengcui [3 ]
Xu, Steven S. [3 ]
Friesen, Timothy L. [2 ,3 ]
Faris, Justin D. [3 ]
机构
[1] North Dakota State Univ, Dept Plant Sci, Fargo, ND 58108 USA
[2] North Dakota State Univ, Dept Plant Pathol, Fargo, ND 58108 USA
[3] ARS, USDA, Cereal Cops Res Unit, Northern Crop Sci Lab, Fargo, ND 58102 USA
来源
G3-GENES GENOMES GENETICS | 2016年 / 6卷 / 12期
基金
美国农业部;
关键词
durum wheat; tan spot; Septoria nodorum; necrotrophic pathogen; disease resistance; PYRENOPHORA-TRITICI-REPENTIS; QUANTITATIVE TRAIT LOCI; RACE-NONSPECIFIC RESISTANCE; STAGONOSPORA-NODORUM; TETRAPLOID WHEAT; SELECTIVE TOXINS; SEEDLING RESISTANCE; HEXAPLOID WHEAT; PTR TOXB; TRIGGERED SUSCEPTIBILITY;
D O I
10.1534/g3.116.036525
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Tan spot and Septoria nodorum blotch (SNB) are important diseases of wheat caused by the necrotrophic fungi Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively. The P. tritici-repentis necrotrophic effector (NE) Ptr ToxB causes tan spot when recognized by the Tsc2 gene. The NE ToxA is produced by both pathogens and has been associated with the development of both tan spot and SNB when recognized by the wheat Tsn1 gene. Most work to study these interactions has been conducted in common wheat, but little has been done in durum wheat. Here, quantitative trait loci (QTL) analysis of a segregating biparental population indicated that the Tsc2-Ptr ToxB interaction plays a prominent role in the development of tan spot in durum. However, analysis of two biparental populations indicated that the Tsn1-ToxA interaction was not associated with the development of tan spot, but was strongly associated with the development of SNB. Pa. nodorum expressed ToxA at high levels in infected Tsn1 plants, whereas ToxA expression in P. tritici-repentis was barely detectable, suggesting that the differences in disease levels associated with the Tsn1-ToxA interaction were due to differences in pathogen expression of ToxA. These and previous results together indicate that: (1) the effects of Tsn1-ToxA on tan spot in common wheat can range from nonsignificant to highly significant depending on the host genetic background; (2) Tsn1-ToxA is not a significant factor for tan spot development in durum wheat; and (3) Tsn1-ToxA plays a major role in SNB development in both common and durum wheat. Durum and common wheat breeders alike should strive to remove both Tsc2 and Tsn1 from their materials to achieve disease resistance.
引用
收藏
页码:4139 / 4150
页数:12
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