4.7 Article

Mapping of powdery mildew resistance genes in melon (Cucumis melo L.) by bulked segregant analysis

Journal

SCIENTIA HORTICULTURAE
Volume 220, Issue -, Pages 160-167

Publisher

ELSEVIER
DOI: 10.1016/j.scienta.2017.04.001

Keywords

Bulked segregant analysis; Powdery mildew; Resistance gene; Melon

Categories

Funding

  1. National Nature Science Foundation of China [31301791, 31672177]
  2. Academic Backbone Project of Northeast Agricultural University [16XG06]
  3. Young Talents Project of Northeast Agricultural University [14QC09]
  4. China Agriculture Research System [CARS-26-02]

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The fungus Podosphaera xanthii causes powdery mildew, a disease that has serious negative effects on the production of melon (Cucumis melo L.) worldwide. In this study, an F-2 melon population, derived from a cross between a resistant (MR-1) and a susceptible cultivar (Top Mark), was used for excavation of major powdery mildew resistance genes by bulked segregant analysis (BSA). The resistant and susceptible DNA bulks were constructed using 30 plants selected from the F-2 population. Next-generation sequencing (NGS) was applied for the resequencing of the parental materials and two bulks. A total of 237.6 million paired reads were obtained that were used to calculate the Delta single nucleotide polymorphisms (SNP)-index. A 0.6-Mb region on chromosome 12 was identified and further narrowed by 424 identified SNPs and quantitative trait locus (QTL) mapping in the F-2 progeny with 25 screened polymorphic cleaved amplified polymorphic sequences (CAPS) markers. A major effective QTL named BPm12.1 was detected between the CAPS markers BSA12-LI3ECORI and BSA12-LI4HINFI which was tightly linked to the resistance gene for powdery mildew with genetic distances 0.02 cM and 0.28 cM, Seventeen candidate genes were identified, seven of which were predicted as candidate genes related to the resistance of melon to powdery mildew. The results of candidate gene analysis provided a potential target for further cloning and functional identification of the resistance gene in MR-1.

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