Abstract
Powdery mildew (PM) is a very important disease of cucumber (Cucumis sativus L.). Resistant cultivars have been deployed in production for a long time, but the genetic mechanisms of PM resistance in cucumber are not well understood. A 3-year QTL mapping study of PM resistance was conducted with 132 F2:3 families derived from two cucumber inbred lines WI 2757 (resistant) and True Lemon (susceptible). A genetic map covering 610.4 cM in seven linkage groups was developed with 240 SSR marker loci. Multiple QTL mapping analysis of molecular marker data and disease index of the hypocotyl, cotyledon and true leaf for responses to PM inoculation identified six genomic regions in four chromosomes harboring QTL for PM resistance in WI 2757. Among the six QTL, pm1.1 and pm1.2 in chromosome 1 conferred leaf resistance. Minor QTL pm3.1 (chromosome 3) and pm4.1 (chromosome 4) contributed to disease susceptibility. The two major QTL, pm5.1 and pm5.2 were located in an interval of ~40 cM in chromosome 5 with each explaining 21.0–74.5 % phenotypic variations. Data presented herein support two recessively inherited, linked major QTL in chromosome 5 plus minor QTL in other chromosomes that control the PM resistance in WI 2757. The QTL pm5.2 for hypocotyl resistance plays the most important role in host resistance. Multiple observations in the same year revealed the importance of scoring time in the detection of PM resistance QTL. Results of this study provided new insights into phenotypic and genetic mechanisms of powdery mildew resistance in cucumber.
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Acknowledgments
The authors thank Linda Crubaugh for technical assistance and two anonymous reviewers for critical reading and valuable suggestions to improve an early version of the manuscript. XH was supported by the Guangdong Academy of Agricultural Sciences, China. YL was supported by China Scholarship Council. MP was supported by a training grant from Punjab Agricultural University, Ludhiana, India. SP was supported by a training grant from the Indian Council of Agricultural Research, New Delhi, India. The authors greatly appreciate the support of these sponsors.
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Communicated by I. Paran.
X. He and Y. Li contributed equally to the work.
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Fig. S1 Frequency distribution of DI for hypocotyl (A), cotyledons (B) and true leaf (C) PM resistances in EXPT1 (2010), EXPT2 (2011) and second observation of EXPT3. DI means for parental lines, F1 and controls are shown in the table.
Fig. S2 Frequency distribution of DI for hypocotyl (HY, A), cotyledons (CL, B) and true leaf (TL, C) PM resistance from three observations of EXPT3 (EXPT3-1, EXPT3-2 and EXPT3-3). Data of the three observations were collected at four-day intervals.
Fig. S3 A SSR-based linkage map developed with 132 WI 2757 × True Lemon F2 plants. Numbers on top of the map are chromosomes numbers. Cumulative map distance (cM) is shown to the left of each linkage group and marker designation is on the right. The gene pm-h at 83.3 cM in Chr5 is for hypocotyl PM resistance in WI 2757 based on EXPT2 data.
Fig. S4 LOD curves of QTL for PM resistance based on phenotypic data from three observations in EXPT3 demonstrating effects of scoring time on QTL detection. A global view of map locations of ten QTL is presented in A. LOD curves of seven QTLs mapped in chromosome 5 are shown in B. LOD profiles were based on simple interval mapping, which differed slightly from MQM profiles shown in Table 2 for some QTL. The dashed line is LOD threshold (3.5) based on 10,000 permuted samples.
Table S1. Major statistics of a linkage map developed with 132 F2 plants of WI 2757 × True Lemon.
Table S2. Information of 240 markers placed on the WI2757 × True Lemon F2 genetic map. Marker loci are arranged by increasing order of map locations in each linkage group (LG). The physical location of each marker in the Gy14 scaffold assembly is also shown.
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He, X., Li, Y., Pandey, S. et al. QTL mapping of powdery mildew resistance in WI 2757 cucumber (Cucumis sativus L.). Theor Appl Genet 126, 2149–2161 (2013). https://doi.org/10.1007/s00122-013-2125-6
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DOI: https://doi.org/10.1007/s00122-013-2125-6