College of Horticulture and Landscape Architecture, Northeast Agricultural University, Mucai Street 59, Xiangfang District, Harbin, 150030, China.
Department of Plant and Microbial Biology, University of Minnesota, St. Paul, MN, 55108, USA.
Theor Appl Genet. 2022 May;135(5):1467-1476. doi: 10.1007/s00122-022-04047-6. Epub 2022 Feb 15.
Gray leaf spot (GLS) resistance in tomato is controlled by one major dominant locus, Sm. Sm was fine mapped, and the nucleotide-binding site-leucine-rich repeat (NBS-LRR) gene Solyc11g020100 was identified as a candidate gene for Sm. Further functional analysis indicated that this gene confers high resistance to Stemphylium lycopersici in tomato. Tomato (Solanum Lycopersicum) is widely consumed and cultivated in the world. Gray leaf spot (GLS), caused by Stemphylium lycopersici (S. lycopersici), is one of the most devastating diseases in tomato production. To date, only one resistance gene, Sm, which confers high resistance against GLS disease, has been identified in the wild tomato species Solanum pimpinellifolium. This resistance locus (comprising the Sm gene) has been transferred into the cultivated variety 'Motelle'. Although several studies have reported the mapping of the Sm gene, it has not been cloned, limiting the utilization in tomato breeding. Here, we cloned Sm using a map-based cloning strategy. The Sm gene was mapped in a region of 160 kb at chromosome 11 between two markers, namely, M390 and M410, by using an F population from a cross between the resistant cultivar 'Motelle' (Mt) and susceptible line 'Moneymaker' (Mm). Three clustered NBS-LRR (nucleotide-binding site-leucine-rich repeat) resistance genes, namely, Solyc11g020080 (R1), Solyc11g020090 (R2), and Solyc11g020100 (R3) were identified in this interval. Nonsynonymous SNPs were identified in only the open reading frame (ORF) of R3, suggesting it as a strong candidate for the Sm gene. Furthermore, gene silencing of R3 abolished the high resistance to S. lycopersici in Motelle, demonstrating that this gene confers high resistance to S. lycopersici. The cloning of Sm may speed up its utilization for breeding resistant tomato varieties and represents an important step forward in our understanding of the mechanism underlying the resistance to GLS.
番茄的灰斑病（GLS）抗性由一个主要的显性基因位点 Sm 控制。Sm 被精细定位，并且核苷酸结合位点-富含亮氨酸重复（NBS-LRR）基因 Solyc11g020100 被鉴定为 Sm 的候选基因。进一步的功能分析表明，该基因赋予番茄对茎枯病菌的高抗性。番茄（Solanum Lycopersicum）在世界范围内广泛食用和种植。由茎枯病菌（S. lycopersici）引起的灰斑病（GLS）是番茄生产中最具破坏性的病害之一。迄今为止，在野生番茄物种 Solanum pimpinellifolium 中仅发现了一个抗性基因 Sm，该基因赋予对 GLS 病的高抗性。该抗性基因座（包含 Sm 基因）已被转移到栽培品种 'Motelle' 中。尽管有几项研究报道了 Sm 基因的图谱，但尚未对其进行克隆，限制了其在番茄育种中的利用。在这里，我们使用基于图谱的克隆策略克隆了 Sm。通过使用来自抗性品种 'Motelle'（Mt）和易感系 'Moneymaker'（Mm）杂交的 F 群体，将 Sm 基因映射到位于染色体 11 上两个标记 M390 和 M410 之间的 160kb 区域内。在这个区间内鉴定出三个聚集的 NBS-LRR（核苷酸结合位点-富含亮氨酸重复）抗性基因，分别是 Solyc11g020080（R1）、Solyc11g020090（R2）和 Solyc11g020100（R3）。仅在 R3 的开放阅读框（ORF）中发现了非同义 SNPs，表明它是 Sm 基因的强候选基因。此外，R3 的基因沉默消除了 Motelle 对 S. lycopersici 的高抗性，表明该基因赋予了对 S. lycopersici 的高抗性。Sm 的克隆可能会加速其在培育抗灰斑病番茄品种中的利用，并代表着我们对 GLS 抗性机制理解的重要一步。
