Submitted to: Legume Viruses Working Group Proceedings
Publication Type: Abstract only
Publication Acceptance Date: 1/10/2005
Publication Date: 4/30/2005
Citation: Wintermantel, W.M., Grube, R.C., Anchieta, A.A. 2005. Mapping of tombusvirus resistance in lettuce and the influence of soil salinity on lettuce dieback disease development. Joint Conference of the International Working Groups on Legume and Vegetable Viruses Proceedings. p. 43. Interpretive Summary:
Technical Abstract: Lettuce dieback is responsible for losses in Romaine and leaf lettuce production in California and Arizona. Losses vary, ranging from severe in some years to mild in others, and the disease is tightly linked to fields with poorly drained soils. Characteristic symptoms include severe stunting, necrosis and death of lettuce plants. Field isolates from lettuce have been identified and characterized as the tombusviruses, Lettuce necrotic stunt virus (LNSV), and Tomato bushy stunt virus (TBSV). To identify factors contributing to variability in infection, soil analyses were conducted on adjacent lettuce fields with similar soil type, but differing in the presence or absence of LNSV infected lettuce. These studies, coupled with subsequent greenhouse and growth chamber studies, demonstrated that high salt, as measured by elevated electrical conductivity levels in soil, rather than soil moisture, lead to increased LNSV infection and increased incidence of lettuce dieback in two different soils. The inheritance of tombusvirus resistance was studied for Salinas, a modern iceberg cultivar, and PI491224, the progenitor of recently released romaine germplasm with resistance to lettuce dieback. Resistance was conferred by a dominant allele at a single locus in both genotypes. The tombusvirus resistance locus from Salinas, Tvrl, was mapped in an intraspecific Lactuca sativa population to a location that corresponds to linkage group 2 on the consensus map of Lactuca. To our knowledge, Tvrl is the first tombusvirus resistance gene identified for any plant host. Although this gene is highly effective in preventing symptom development, the mechanism of resistance is not known, and ELISA results suggest that not all symptom-free plants are completely immune to viral infection.