Phytopathology. 2005 Feb;95(2):144-52. doi: 10.1094/PHYTO-95-0144.
ABSTRACT Pyrenophora tritici-repentis causes necrosis and chlorosis in its wheat host. Susceptibility to races 2 (necrosis) and 5 (chlorosis) of the pathogen is known to be mediated by Ptr ToxA and Ptr ToxB, respectively. Sensitivity to each toxin is controlled by a single dominant and independently inherited gene. We used sensitivity to Ptr ToxA and Ptr ToxB as two genetic markers to investigate the origin and the state of tan spot susceptibility in Canadian Western Red Spring (CWRS) wheat over a period of more than a century. Sensitivity to Ptr ToxA, the toxin produced by nearly all isolates of the pathogen collected in the past 20 years in western Canada, appears to have been present in the first major cultivar, Red Fife, grown massively in the late 1800s. Sensitivity then was transmitted unknowingly into Canadian wheat lines through extensive use of backcrossing to maintain the Marquis-Thatcher breadmaking quality. Sensitivity to Ptr ToxA, which nearly disappeared from cultivars grown in western Canada in the 1950s, was reintroduced in the 1960s and unintentionally bred into many of the present-day cultivars. Sensitivity to Ptr ToxB, a toxin rarely found in isolates from western Canada, appeared with the release of Thatcher in 1934 and was transferred to many cultivars through backcross programs. In spite of large areas planted to Ptr ToxAand Ptr ToxB-sensitive cultivars over decades, tan spot epidemics remained sporadic until the 1970s. The results of this study raise the problem of the narrowing genetic base of CWRS wheat lines and the potential for unanticipated threats from plant pathogens. The intercrossing of genetically diverse material in one Canadian wheat breeding program resulted in the release of several modern cultivars with resistance to tan spot. The absence of wild-type Ptr ToxB-producing isolates in western Canada remains unexplained, given that sensitivity to Ptr ToxB was present continuously in western Canadian cultivars grown on vast areas for more than 70 years.
禾旋孢腔菌引起小麦坏死和黄化。已知该病原菌的 2 号(坏死)和 5 号(黄化)小种分别由 PtrToxA 和 PtrToxB 介导。对每种毒素的敏感性由单个显性且独立遗传的基因控制。我们使用对 PtrToxA 和 PtrToxB 的敏感性作为两个遗传标记,在一个多世纪的时间里研究加拿大西部红春小麦(CWRS)中 tan 斑点易感性的起源和状态。对 PtrToxA 的敏感性,这种毒素几乎存在于过去 20 年在加拿大西部收集的病原菌的所有分离物中,似乎存在于 19 世纪末大规模种植的第一个主要品种 RedFife 中。然后,通过广泛使用回交来维持 Marquis-Thatcher 烘焙质量,加拿大小麦品系在不知不觉中传递了这种敏感性。20 世纪 50 年代在加拿大西部种植的品种中几乎消失的 PtrToxA 敏感性,在 20 世纪 60 年代重新引入,并无意中育成了许多当今的品种。对 PtrToxB 的敏感性,这种毒素在加拿大西部的分离物中很少发现,随着 1934 年 Thatcher 的释放而出现,并通过回交计划转移到许多品种中。尽管数十年来种植了大量对 PtrToxA 和 PtrToxB 敏感的品种,但 tan 斑点的流行仍然是零星的,直到 20 世纪 70 年代。这项研究的结果提出了 CWRS 小麦品种遗传基础狭窄和植物病原体潜在威胁的问题。在一个加拿大小麦育种种质资源中进行遗传多样化的杂交,导致了几种具有 tan 斑点抗性的现代品种的释放。鉴于 PtrToxB 敏感性在加拿大西部种植的大面积品种中连续存在了 70 多年,而在加拿大西部仍然没有发现野生型 PtrToxB 产生的分离物,这仍然是一个未解之谜。