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The 2010 ASHS Annual Conference

4421:
Resistance in Melon PI 313970 to Cucurbit Yellow Stunting Disorder Virus

Thursday, August 5, 2010: 2:00 PM
Springs K & L
James D. McCreight, USDA ARS, Salinas, CA
William M. Wintermantel, U.S. Agricultural Research Station, U.S. Department of Agriculture, Agricultural Research Service, Salinas, CA

Cucurbit yellow stunting disorder virus (CYSDV; genus Crinivirus, family Closteroviridae), causes a devastating of disease of melon (Cucumis melo L.), and is readily transmitted by the sweetpotato whitefly (Bemisia tabaci biotype B) resulting in reduced fruit quality and yield. CYSDV was first identified on melons in the 1980s in the United Arab Emirates and has since spread throughout many melon-producing regions in the Middle East and the Mediterranean. CYSDV emerged in the lower Rio Grande Valley of Texas and the adjacent area of Mexico in 1999 and was identified for the first time in the desert melon production regions of southwestern U.S. (Arizona, and California) and western Mexico (Sonora) in Fall 2006. It has since been found on melons in Florida in the U.S (2008) and near Shanghai, China (2008), illustrating that CYSDV is a rapidly emerging virus worldwide. CYSDV has impacted virtually the entire Fall-planted melon crop in Arizona and California through 2009, but incidence and impact in Spring-planted melons remained low until 2009. Genetic resistance to CYSDV in the African melon accession TGR-1551 (= PI 482420; (subsp. melo) was expressed as a dominant trait in Spain (monogenic) and Texas (polygenic). We observed PI 313970, a non-sweet melon (subsp. agrestis var. acidulus) from India, to express high-level resistance to CYSDV in Arizona and California in 2006 when the virus first appeared in these areas. Neither TGR-1551 nor PI313970 was immune to CYSDV as determined by RT-qPCR, and both expressed yellowing symptoms under heavy whitefly feeding pressure typical of the U.S. desert southwest. Inheritance of resistance to CYSDV in PI 313970 was studied in a cross with ‘Top Mark’ in naturally infected field tests in Fall 2008 and Spring 2009. Total plants per entry in seven replications ranged from 30 for ‘Top Mark’ (TM) to 163 for the F2 family. Reaction to CYSDV infection was evaluated as percent symptomatic leaves per plant. The F1 and backcross to ‘Top Mark’ were susceptible, indicating resistance in PI 313970 to be recessive. The F2 and backcross to PI 313970 segregated in accordance with a recessive character and indicated two or more genes were involved. These data suggest TGR-1551 and PI 313970 possess unique, possibly complementary, resistance genes that if combined could provide a higher level of genetic resistance against CYSDV.