Zhang Jianping, Zhang Peng, Karaoglu Haydar, Park Robert F
First, second, third, and fourth authors: University of Sydney, Plant Breeding Institute Cobbitty, Cobbitty, NSW 2570, Australia; first author: CSIRO Agriculture, GPO Box 1600, Canberra, ACT 2601, Australia; and first author: Henan Tianmin Seed Company Ltd., South Industrial District, Lankao, Henan, 475300, P. R. China.
Phytopathology. 2017 Sep;107(9):1032-1038. doi: 10.1094/PHYTO-09-16-0334-R. Epub 2017 Jun 29.
Long-term surveys of pathogenicity in Puccinia graminis f. sp. tritici in Australia have implicated mutation as a major source of virulence, at times leading to the demise of stem-rust-resistant wheat cultivars and substantial yield losses. Since 1925, these surveys have identified at least four occasions on which exotic isolates of P. graminis f. sp. tritici appeared in Australia, with each acting as a founding isolate that gave rise sequentially to derivative pathotypes via presumed single-step mutation. The current study examined the relationship between virulence and molecular patterns using simple-sequence repeat (SSR) markers on selected isolates of P. graminis f. sp. tritici collected in Australia during a 52-year period in order to propose an evolutionary pathway involving these isolates. Studies of SSR variability among this collection of isolates within a putative clonal lineage based on pathotype 21-0, first detected in 1954 (the "21/34 lineage"), provided compelling evidence of clonality over the 52-year period, coupled with single-step acquisition of virulence for resistance genes. It also supported the postulation that two triticale-attacking pathotypes (34-2,12 and 34-2,12,13) detected in the early 1980s were derived from pathotype 21-0 via stepwise sequential acquisition of virulence for Sr5, Sr11, Sr27, and then SrSatu. Some of the isolates examined that were regarded as members of the race 21/34 lineage based on pathogenicity differed significantly in their SSR genotypes, indicating that they may have originated from processes more complex than simple mutation. This included two isolates of pathotype 21-0, which were collected in 1994 and 2006. Given that sexual recombination in P. graminis is rare or absent in Australia, the cryptic complexity observed could indicate that one or more of these isolates arose as a consequence of asexual recombination.
对澳大利亚小麦条锈病菌致病性的长期调查表明，突变是毒力的主要来源，有时会导致抗茎锈病小麦品种的消亡和产量大幅损失。自1925年以来，这些调查已确定至少有四次小麦条锈病菌的外来分离株出现在澳大利亚，每一次这些分离株都作为创始分离株，通过假定的单步突变依次产生衍生致病型。本研究使用简单序列重复（SSR）标记，对在52年期间收集的澳大利亚小麦条锈病菌选定分离株的毒力与分子模式之间的关系进行了研究，以提出涉及这些分离株的进化途径。基于1954年首次检测到的致病型21-0（“21/34谱系”），对这一假定克隆谱系内的分离株集合进行SSR变异性研究，提供了52年期间克隆性的有力证据，以及抗锈基因毒力的单步获得。这也支持了这样的推测，即20世纪80年代初检测到的两种攻击小黑麦的致病型（34-2,12和34-2,12,13）是通过对Sr5、Sr11、Sr27，然后是SrSatu的毒力逐步顺序获得，从致病型21-0衍生而来。一些基于致病性被视为21/34小种谱系成员的检测分离株，其SSR基因型存在显著差异，表明它们可能起源于比简单突变更复杂的过程。这包括1994年和2006年收集的两个致病型21-0分离株。鉴于在澳大利亚小麦条锈病菌中很少发生或不存在有性重组，观察到的这种隐秘复杂性可能表明这些分离株中的一个或多个是无性重组的结果。
