Phytopathology. 2003 Apr;93(4):397-401. doi: 10.1094/PHYTO.2003.93.4.397.
ABSTRACT Pyrenophora tritici-repentis race 2 produces Ptr ToxA, a host-selective toxin previously described as a pathogenicity factor for tan spot on wheat. The objective of this research was to evaluate the role of host sensitivity to toxin, conditioned by a single dominant gene on chromosome 5BL, in the disease development by race 2. An F(2)-derived F(6) recombinant inbred population of 108 wheat lines, produced from crosses of toxin-sensitive, disease-susceptible cv. Kulm with the toxin-insensitive, disease-resistant cv. Erik segregated 1:1 for toxin reaction. However, the population was skewed toward resistance to race 2 of the fungus. Toxin reaction accounted for 24.4% of the genetic variance for disease. Heritability estimates suggested the presence of four to five genes that influence disease reaction in the population. Toxin-insensitive mutants, previously derived Kulm, were susceptible to race 2, although disease developed more slowly on the mutants than it did on the wild-type Kulm. The data indicate that sensitivity to Ptr ToxA influences disease severity in some host genotypes without defining susceptibility.
摘要 禾旋孢腔菌 2 号生理小种产生 Ptr ToxA,该毒素是以前描述的引起小麦叶枯病的致病性因子。本研究的目的是评估由第 5BL 染色体上单个显性基因决定的对毒素的宿主敏感性在 2 号生理小种引起的疾病发展中的作用。由毒素敏感、感病品种 Kulm 与毒素不敏感、抗病品种 Erik 杂交产生的 F2 衍生 F6 重组自交系群体 108 个品系,对毒素反应呈 1:1 分离。然而,该群体对真菌的 2 号生理小种具有抗药性的偏倚。毒素反应占疾病遗传方差的 24.4%。遗传力估计表明,该群体中有四到五个基因影响疾病反应。先前从 Kulm 中分离出的对毒素不敏感的突变体对 2 号生理小种敏感,尽管突变体上的疾病发展比野生型 Kulm 上的疾病发展缓慢。这些数据表明,对 Ptr ToxA 的敏感性影响了某些宿主基因型的疾病严重程度,但并未定义易感性。