Abstract
A framework genetic map based on genomic DNA-derived SSR, EST-derived SSR, EST-STS and EST-RFLP markers was developed using 181 genotypes generated from D8909-15 (female) × F8909-17 (male), the ‘9621’ population. Both parents are half siblings with a common female parent, Vitis rupestris ‘A. de Serres’, and different male parents (forms of V. arizonica). A total of 542 markers were tested, and 237 of them were polymorphic for the female and male parents. The female map was developed with 159 mapped markers covering 865.0 cM with an average marker distance of 5.4 cM in 18 linkage groups. The male map was constructed with 158 mapped molecular markers covering 1055.0 cM with an average distance of 6.7 cM in 19 linkage groups. The consensus ‘9621’ map covered 1154.0 cM with 210 mapped molecular markers in 19 linkage groups, with average distance of 5.5 cM. Ninety-four of the 210 markers on the consensus map were new. The ‘Sex’ expression locus segregated as single major gene was mapped to linkage group 2 on the consensus and the male map. PdR1, a major gene for resistance to Pierce’s disease, caused by the bacterium Xylella fastidiosa, was mapped to the linkage group 14 between markers VMCNg3h8 and VVIN64, located 4.3 and 2.7 cM away from PdR1, respectively. Differences in segregation distortion of markers were also compared between parents, and three clusters of skewed markers were observed on linkage groups 6, 7 and 14.
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Acknowledgments
Research funding from the California Department of Food and Agriculture’s Pierce’s Disease Board, the California Grape Rootstock Improvement Commission and the Louis P. Martini Endowed Chair funds is gratefully acknowledged. The authors are also grateful to Eileen Sweeney, Rong Hu, Rita Zhou, Jasmine Roberts, Juliana Chow, Nick Roncoroni, and Dan Ng for their various roles in facilitating this study.
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Riaz, S., Krivanek, A.F., Xu, K. et al. Refined mapping of the Pierce’s disease resistance locus, PdR1, and Sex on an extended genetic map of Vitis rupestris × V. arizonica . Theor Appl Genet 113, 1317–1329 (2006). https://doi.org/10.1007/s00122-006-0385-0
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DOI: https://doi.org/10.1007/s00122-006-0385-0