Acknowledgments
The authors gratefully acknowledge the cession of Argentinean varieties by DelIo Calvar (INTA Alto Valle)
utilized in this work . Likewise we are extremely grateful for the financial support provided by Instituto Nacional de
Investigaciones Agrarias by means of the Projects No SC93-183-C3-1 and SC93-184-C5-1 and to the Instituto
Valenciano de Estudios e Investigacion. S. Rosello thanks the Conselleria de Cultura, Educacio i Ciencia de is
Generalitat Valenciana for the grant of his scholarship.
Literature Cited:
Boiteux, L.S., T. Nagata and L. de B. Giordano. 1993. Field resistance of tomato Lycopersicon esculentum lines to
Tomato Spotted Wilt disease. TGC Report 43: 79.
Calvar, D.J. and A. Sansinanea. 1988. Quilquil INTA. Un cv. de tomate para la lndustria de fruto firme y con
resistencia a peste negra. EEA Alto Valle, INTA. Rio Negro, Argentina.
Gallardo, G.S. and D.J. Calvar. 1992. Tomato for industry breeding program in Argentina. Acta Horticulturae 301:
87-90.
Partial resistance loci for tomato bacterial wilt show differential race specificity
Danesh, D. and Young, N. D.
Department of Plant Pathology, Univ. Minnesota, St. Paul, MN 55108
Bacterial wilt, caused by Pseudomonas solanacearum, is one of the most devastating diseases of tomato
worldwide. While the molecular biology of pathogenicity is well-characterized in the bacterium (Boucher et al,
1992), little is known about resistance in the host. In part, this is due to the fact that resistance is multigenic and
complex (Acosta at al. 1964). Recently, we utilized DNA markers, including restriction fragment length
polymorphisms (RFLPs), to uncover major partial resistance loci for bacterial wilt in a highly resistant tomato
genotype (L285) (Danesh, et al. 1994). These results were based on the disease responses of 71 individuals in an
F2 mapping population challenged with P. solanacearum isolate UW-364 (race 1. biovar 4). Three unlinked
resistance loci of intermediate effect were identified in the mapping population. A locus on chromosome six
controlled more than 50% of total variation in resistance, while two other resistance loci were found on
chromosomes seven and ten. Notably, the locus on chromosome seven was
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