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首页> 外文期刊>G3: Genes, Genomes, Genetics >New Insights into the Roles of Host Gene-Necrotrophic Effector Interactions in Governing Susceptibility of Durum Wheat to Tan Spot and Septoria nodorum Blotch
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New Insights into the Roles of Host Gene-Necrotrophic Effector Interactions in Governing Susceptibility of Durum Wheat to Tan Spot and Septoria nodorum Blotch

机译:宿主基因坏死性效应物相互作用在控制硬质小麦对棕褐色斑点和Nodorum斑点的敏感性中的作用的新见解

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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.
机译:棕褐色斑点病和黑斑病菌(SNB)是小麦的坏死病菌,主要由坏死性真菌Pyrenophora-tritici-repentis和稻瘟病菌引起。当被Tsc2基因识别时,P。tritici-repentis坏死性营养效应子(NE)Ptr ToxB引起棕褐色斑点。 NE ToxA由两种病原体共同产生,并在被小麦Tsn1基因识别时与棕褐色斑点和SNB的发展有关。研究这些相互作用的大多数工作是在普通小麦中进行的,但在硬粒小麦中却很少进行。在这里,对隔离的双亲种群的数量性状基因座(QTL)分析表明,Tsc2-Ptr ToxB相互作用在硬粒棕褐色斑的形成中起着重要作用。然而,对两个双亲种群的分析表明,Tsn1-ToxA的相互作用与棕褐色斑点的发展无关,但与SNB的发展密切相关。 Pa。nodorum在受感染的Tsn1植物中高水平表达ToxA,而在小麦假单胞菌中ToxA的表达几乎无法检测到,这表明与Tsn1-ToxA相互作用相关的疾病水平的差异是由于ToxA病原体表达的差异所致。这些结果和先前的结果共同表明:(1)Tsn1-ToxA对普通小麦棕褐色斑点的影响范围从无显着到高度显着,具体取决于宿主的遗传背景; (2)Tsn1-ToxA不是硬质小麦中棕褐色斑点发展的重要因素; (3)Tsn1-ToxA在普通小麦和硬质小麦的SNB发育中都起着重要作用。硬粒小麦和普通小麦育种者都应努力从其材料中去除Tsc2和Tsn1,以实现抗病性。

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