College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, China.
Western Barley Genetics Alliance, Western Australian State Agricultural Biotechnology Centre, School of Veterinary and Life Sciences, Murdoch University, Murdoch, WA, Australia.
Theor Appl Genet. 2020 Jul;133(7):2307-2321. doi: 10.1007/s00122-020-03599-9. Epub 2020 May 13.
An effective and stable quantitative resistance locus, QSc.VR4, was fine mapped, characterized and physically anchored to the short arm of 4H, conferring adult plant resistance to the fungus Rhynchosporium commune in barley. Scald caused by Rhynchosporium commune is one of the most destructive barley diseases worldwide. Accumulation of adult plant resistance (APR) governed by multiple resistance alleles is predicted to be effective and long-lasting against a broad spectrum of pathotypes. However, the molecular mechanisms that control APR remain poorly understood. Here, quantitative trait loci (QTL) analysis of APR and fine mapping were performed on five barley populations derived from a common parent Vlamingh, which expresses APR to scald. Two QTLs, designated QSc.VR4 and QSc.BR7, were detected from a cross between Vlamingh and Buloke. Our data confirmed that QSc.VR4 is an effective and stable APR locus, residing on the short arm of chromosome 4H, and QSc.BR7 derived from Buloke may be an allele of reported Rrs2. High-resolution fine mapping revealed that QSc.VR4 is located in a 0.38 Mb genomic region between InDel markers 4H2282169 and 4H2665106. The gene annotation analysis and sequence comparison suggested that a gene cluster containing two adjacent multigene families encoding leucine-rich repeat receptor kinase-like proteins (LRR-RLKs) and germin-like proteins (GLPs), respectively, is likely contributing to scald resistance. Adult plant resistance (APR) governed by QSc.VR4 may confer partial levels of resistance to the fungus Rhynchosporium commune and, furthermore, be an important resource for gene pyramiding that may contribute broad-based and more durable resistance.
一个有效且稳定的数量抗性位点 QSc.VR4 被精细定位、表征,并物理锚定到 4H 短臂上,赋予大麦对 Rhynchosporium commune 真菌的成株期抗性。由 Rhynchosporium commune 引起的叶枯病是世界范围内最具破坏性的大麦病害之一。由多个抗性等位基因控制的成株期抗性 (APR) 的积累预计对广泛的致病型有效且持久。然而,控制 APR 的分子机制仍知之甚少。在这里,对源自表达叶枯病 APR 的共同亲本 Vlamingh 的五个大麦群体进行了 APR 的数量性状位点 (QTL) 分析和精细定位。从 Vlamingh 和 Buloke 的杂交中检测到两个 QTL,分别命名为 QSc.VR4 和 QSc.BR7。我们的数据证实,QSc.VR4 是一个有效且稳定的 APR 位点,位于 4H 染色体的短臂上,而源自 Buloke 的 QSc.BR7 可能是报道的 Rrs2 的一个等位基因。高分辨率精细定位表明,QSc.VR4 位于 4H2282169 和 4H2665106 之间的 0.38 Mb 基因组区域内。基因注释分析和序列比较表明,一个包含两个相邻多基因家族的基因簇可能导致叶枯病抗性,分别编码富含亮氨酸重复受体激酶样蛋白 (LRR-RLKs) 和萌发素样蛋白 (GLPs)。由 QSc.VR4 控制的成株期抗性可能赋予真菌 Rhynchosporium commune 部分水平的抗性,并且是基因聚合的重要资源,可能有助于基础广泛和更持久的抗性。