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Early blight (EB), caused by the fungus Alternaria solani, is a destructive disease of tomato (Lycopersicon esculentum) worldwide. Sources of genetic resistance have been identified within related wild species, including green-fruited L. hirsutum and red-fruited L. pimpinellifolium. We have employed traditional protocols of plant breeding and contemporary molecular markers technology to discern the genetic basis of EB resistance and develop tomatoes with improved resistance. Backcross breeding has resulted in the development of germplasm with improved resistance; however, linkage drag has been a major obstacle when using L. hirsutum as a donor parent. To identify and map QTLs for EB resistance, we used several filial and backcross populations derived from interspecific crosses between L. esculentum and either L. hirsutum or L. pimpinellifolium. In each population, an average of seven resistance QTLs were detected. While similar QTLs were detected in different generations of the same cross, generally different QTLs were identified in populations derived from different crosses. The results suggested stability of QTLs across environments and generations but variation in QTLs in different interspecific populations. It is expected that marker-assisted pyramiding of QTLs from different sources results in development of germplasm with strong and durable resistance. Further inspection of the results led to the identification and selection of six QTLs with stable and independent effects for use in marker–assisted selection (MAS). However, to facilitate “clean” transfer and pyramiding of these QTLs, near-isogenic lines (NILs) containing individual QTLs in a L. esculentum background should be developed.

Most cultivars of tomato (Lycopersiconesculentum) are susceptible to early blight (EB), a devastating fungal (Alternariasolani) disease of tomato in the northeast and eastern part of the U.S. The most economic and durable measure of disease control is by using genetic resistance. There is limited EB resistance within the cultivated tomato. However, genetic sources of resistance exist within the tomato-related wild species L. hirsutum and L. pimpinellifolium. Early blight resistance does not follow the gene-for-gene model of host–pathogen interaction. Mapping QTLs conferring horizontal resistance is an effective approach for studying complex resistance traits such as EB. We have developed F₂, F₃, F₄, and an F_2:7 derived RIL population of a L. esculentum× L. pimpinellifolium cross and evaluated them for EB resistance under field conditions. Genetic maps were constructed based on the F₂ (including 256 RFLP, EST and RGA markers) as well as the RIL population (including over 220 RFLP and EST markers). In each of the F₂, F₃, and F₄ population, an average of seven QTLs were identified for resistance, which were highly consistent across populations. Mapping of EB resistance QTLs in the RILs is underway. Co-localizations of QTLs with several ESTs and RGAs were observed, suggesting potential involvement of the latter markers with EB resistance. Furthermore, co-localizations were observed among QTLs, ESTs, and RGAs and several known tomato vertical disease resistance genes. Possible occurrence of such co-localization in the RIL population will be reported. It is speculated that candidate-gene approach is an effective way of identifying and mapping new R genes in tomato. This study may lead to the identification of genes underlying EB resistance in tomato.