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基于基因组的甜罗勒枯萎病抗性的高分辨率图谱绘制。

Genome-based high-resolution mapping of fusarium wilt resistance in sweet basil.

机构信息

Newe Ya'ar Research Center, Agricultural Research Organization, Volcani Institute, Ramat Yishay 30095, Israel.

Newe Ya'ar Research Center, Agricultural Research Organization, Volcani Institute, Ramat Yishay 30095, Israel; Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Rehovot 76100, Israel.

出版信息

Plant Sci. 2022 Aug;321:111316. doi: 10.1016/j.plantsci.2022.111316. Epub 2022 May 11.

DOI:10.1016/j.plantsci.2022.111316
PMID:35696916
Abstract

Fusarium wilt of basil is a disease of sweet basil (Ocimum basilicum L.) plants caused by the fungus Fusarium oxysporum f. sp. basilici (FOB). Although resistant cultivars were released > 20 years ago, the underlying mechanism and the genes controlling the resistance remain unknown. We used genetic mapping to elucidate FOB resistance in an F population derived from a cross between resistant and susceptible cultivars. We performed genotyping by sequencing of 173 offspring and aligning the data to the sweet basil reference genome. In total, 23,411 polymorphic sites were detected, and a single quantitative trait locus (QTL) for FOB resistance was found. The confidence interval was < 600 kbp, harboring only 60 genes, including a cluster of putative disease-resistance genes. Based on homology to a fusarium resistance protein from wild tomato, we also investigated a candidate resistance gene that encodes a transmembrane leucine-rich repeat - receptor-like kinase - ubiquitin-like protease (LRR-RLK-ULP). Sequence analysis of that gene in the susceptible parent vs. the resistant parent revealed multiple indels, including an insertion of 20 amino acids next to the transmembrane domain, which might alter its functionality. Our findings suggest that this LRR-RLK-ULP might be responsible for FOB resistance in sweet basil and demonstrate the usefulness of the recently sequenced basil genome for QTL mapping and gene mining.

摘要

罗勒枯萎病是由尖孢镰刀菌茄专化型(FOB)引起的甜罗勒(Ocimum basilicum L.)病害。尽管 20 多年前就已经发布了抗枯萎病的品种,但这种抗性的潜在机制和控制基因仍不清楚。我们利用遗传图谱,从抗枯萎病和易感品种的杂交后代中解析 FOB 抗性。我们对 173 个后代进行了测序基因型分析,并将数据与甜罗勒参考基因组进行比对。总共检测到 23411 个多态性位点,并发现了一个单一的 FOB 抗性数量性状位点(QTL)。置信区间小于 600kbp,仅包含 60 个基因,包括一组假定的抗病基因簇。基于与野生番茄的 Fusarium 抗性蛋白的同源性,我们还研究了一个候选抗性基因,该基因编码跨膜亮氨酸丰富重复-受体样激酶-泛素样蛋白酶(LRR-RLK-ULP)。在易感亲本和抗性亲本中对该基因进行序列分析,发现了多个插入缺失,包括在跨膜结构域旁边插入 20 个氨基酸,这可能改变其功能。我们的研究结果表明,该 LRR-RLK-ULP 可能是甜罗勒 FOB 抗性的原因,并证明了最近测序的罗勒基因组在 QTL 作图和基因挖掘方面的有用性。

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