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2019 ASHS Annual Conference

Allelism of Resistance to Cucurbit Yellow Stunting Disorder Virusin Melon Accessions PI 313970 and TGR 1551

Thursday, July 25, 2019: 11:30 AM
Partagas 1 (Tropicana Las Vegas)
James D. McCreight, USDA-ARS, Salinas, CA
Eric T. Natwick, University of California ANR, Cooperative Extension Imperial County, Holtville, CA
William M. Wintermantel, USDA-ARS, Salinas, CA
Ana I. Lopez-Sese, IHSM-La Mayora, UMA-CSIC, Algarrobo, Malaga, Spain
MarĂ­a L. Gomez-Guillamon, IHSM-La Mayora, UMA-CSIC, Malaga, Spain
Cucurbit yellow stunting disorder virus(CYSDV) is a whitefly-transmitted closterovirus that reduces melon (Cucumis melo) fruit yield and quality in greenhouse and open-field production systems in the Middle East, the Mediterranean Basin, the Americas, and Asia. Resistance to CYSDV was first reported in melon accession TGR 1551 (PI 482420) and then in PI 313970, both members of the C. meloAcidulus Group from Zimbabwe and India, respectively. Neither accession is immune to CYSDV infection. Resistance in TGR 1551 was initially reported to be dominant to susceptibility in controlled-inoculation greenhouse tests in Spain. Recessive resistance was observed in PI 313970 in naturally-infected field tests in Imperial Valley, California. This presented an opportunity for combining two potentially different genes to achieve a higher level of resistance than exhibited by either source alone. We thus crossed the two accessions with the goal of combining their resistances to CYSDV and initiated a selection program for CYSDV resistance and crossed their offspring with western U.S. shipper type muskmelon and honeydew, but higher levels of resistance were not observed in field selections. Resistance in TGR 1551 was subsequently found to be recessive. Analysis of disease reaction data from the two resistance sources, their two F1, F2, and testcross progenies in two naturally-infected field tests in Imperial Valley and a controlled greenhouse test in Málaga suggest resistance to CYSDV exhibited by these two lines may be allelic. PI 313970 and TGR 1551 exhibited high-level resistance in one test, where both accessions showed some variation in symptom expression, but their F1was very uniform. In the second test, PI 313970 and the F1 PI 313970 x TGR 1551 exhibited greater variation in symptom expression than TGR 1551. A significant difference between the parents in the second test indicates an effect on their different genetic background or quantitative trait loci (QTL) on expression resistance to CYSDV in the two lines. Research is underway to map their respective QTL for resistance to CYSDV in order to increase resistance to this virus.
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