Agriculture and Agri-Food Canada, Morden Research and Development Centre, Morden, MB, Canada.
Agriculture and Agri-Food Canada, Swift Current Research and Development Centre, Swift Current, SK, Canada.
BMC Plant Biol. 2020 Jul 3;20(1):314. doi: 10.1186/s12870-020-02525-x.
The genetics of resistance to loose smut of wheat (Triticum aestivum L.) caused by the fungus Ustilago tritici (Pers.) Rostr. is not well understood. This study examines loose smut resistance in Sonop (TD-14), a South African spring wheat variety. A doubled haploid (DH) population of 163 lines derived from the cross Diamont/TD-14 was studied. The parents and progenies were inoculated with U. tritici races T2, T9, and T39 individually in growth facilities at Morden and Swift Current, Canada. Loose smut incidence (LSI) and partial loose smut resistance (PLSR) were assessed.
A whole genome linkage map was developed consisting of 11,519 SNP loci found on 31 linkage groups spanning 2845 cM. A new major resistance gene Ut11 was located to the distal end of chromosome arm 7BS. Ut11 conferred resistance to U. tritici race T2, but not races T9 and T39. Quantitative trait locus (QTL) mapping identified four QTL controlling LSI in the Diamont/TD-14 DH population on chromosomes 3B, 4B, 5B, and 7B (at Ut11) with TD-14 contributing the resistance alleles at three of these loci. The major QTL QUt.mrc-5B was effective against all three races and explained up to 81% of the phenotypic variation. The only QTL identified for PLSR coincided with the LSI QTL QUt.mrc-5B indicating that this locus affected both loose smut incidence and partial smutting of spikes.
A race-specific resistance gene Ut11 and a broadly effective resistance QTL QUt.mrc-5B were the main loci controlling loose smut resistance in the differential line TD-14 (cultivar Sonop). This study provides insight into the genetics of loose smut resistance in spring wheat Sonop and the single nucleotide polymorphism (SNP) markers linked to the resistance gene Ut11 and QTL QUt.mrc-5B will be useful for selecting loose smut resistance in breeding programs.
小麦散黑穗病(由真菌 Ustilago tritici(Pers.)Rostr.引起)的抗性遗传机制尚不清楚。本研究考察了南非春小麦品种 Sonop(TD-14)的散黑穗病抗性。用来自 Diamont/TD-14 的杂交后代 163 个双单倍体(DH)系群体在加拿大 Morden 和 Swift Current 的生长设施中分别接种 U. tritici 菌株 T2、T9 和 T39,对亲本和后代进行接种。评估散黑穗病发病率(LSI)和部分散黑穗病抗性(PLSR)。
开发了一个全基因组连锁图谱,包含在 31 个连锁群上的 11519 个 SNP 标记,跨越 2845cM。在 7BS 染色体臂的远端位置鉴定出一个新的主要抗性基因 Ut11。Ut11 对 U. tritici 菌株 T2 具有抗性,但对菌株 T9 和 T39 没有抗性。在 Diamont/TD-14 DH 群体中,定量性状位点(QTL)图谱鉴定出 4 个控制 LSI 的 QTL,位于染色体 3B、4B、5B 和 7B 上(位于 Ut11 处),其中 3 个位点的抗性等位基因来自 TD-14。主要 QTL QUt.mrc-5B 对所有三个菌株均有效,解释了 81%的表型变异。鉴定出的唯一一个与 PLSR 相关的 QTL 与 LSI QTL QUt.mrc-5B 重合,表明该位点影响了散黑穗病发病率和穗部部分黑穗病。
在鉴别品种 TD-14(品种 Sonop)中,一个与特定菌株相关的抗性基因 Ut11 和一个广泛有效的抗性 QTL QUt.mrc-5B 是控制散黑穗病抗性的主要基因。本研究为 Sonop 春小麦散黑穗病抗性的遗传机制提供了见解,与抗性基因 Ut11 和 QTL QUt.mrc-5B 相关的单核苷酸多态性(SNP)标记将有助于在选育计划中选择散黑穗病抗性。