Powdery mildew in watermelon [Citrullus lanatus (Thumb.) Matsum. and Nakai] caused by the fungus Podosphaera xanthii race 2W has in recent years become a concern among growers as well as plant breeders in United States (Davis et al., 2001; McGrath, 2001), China (Feng, 1996; Zhang et al., 2011), and other parts of the world (McGrath, 2001; Tomason and Gibson, 2006). The disease causes significant yield loss as well as decreased fruit quality (McGrath and Thomas, 1996) through mycelial coverage of the leaves, leaf necrosis, and premature death of the plant (Davis et al., 2001). Powdery mildew of watermelon occurs throughout the southeastern United States, extending north to New York as well as into western states (Davis et al., 2005).
Development of genetic resistance is an important objective in watermelon breeding programs. Screening of the U.S. watermelon germplasm collection identified high resistance in several wild accessions of C. lanatus var. citroides (Davis et al., 2007; Tetteh et al., 2010), but none of the accessions in the primary gene pool. However, one accession of C. lanatus var. lanatus, PI 270545, originating from Sudan was found to have intermediate resistance (Tetteh et al., 2010). Resistance in this accession was characterized by few mycelium on leaf and stem, and affected plants survived to fruit production stage (Tetteh et al., 2010).
To help breed cultivars resistant to powdery mildew, it is important to understand the inheritance and gene action. Tetteh et al. (2013) evaluated the gene action of leaf and stem resistance in the watermelon accession, PI 189225, and established that mainly additive gene action controlled leaf resistance, whereas for stem resistance, additive, dominance, and epistasic gene actions were significant. There are several reports on inheritance of resistance to P. xanthii in melon (Cucumis melo L.). Most agree that there are several genes controlling resistance (Epinat et al., 1993; Kenigsbuch and Cohen, 1992; McCreight, 2003; McCreight et al., 1987; Pitrat et al., 1998). Perchepied et al. (2005) working with quantitative trait loci (QTL) revealed that powdery mildew resistance in melon was under the control of major gene effects and digenic epistasis. Inheritance of powdery mildew resistance in watermelon was investigated by generation means analysis by Tetteh et al. (2013). Studies have demonstrated a close correspondence between generation mean analysis and QTL mapping (Jung et al., 1994; Perchepied et al., 2005).
Estimation of genetic effects in different crosses should inform the breeding strategy for development of resistant cultivars. Although additive and dominance models can be determined with the scaling tests in generation means analysis, the identification of non-allelic interactions requires more powerful tests such as the joint scaling test (Mather, 1949) or QTL analysis (Perchepied et al., 2005). In most cases, the variation unaccounted for by a major gene is provided by digenic epistasis.
A major deficiency of generation means is in nondetection of additive effects resulting from dispersion of alleles with similar effects between parents and internal cancellation of dominance effects exhibited in opposite directions at different loci (Crow and Kimura, 1970). Saudhu and Nittal (1988) studied two Gossypium arboreum crosses and reported the absence of nonallelic interaction in the six-parameter model, whereas the joint scaling test predicted the presence of epistasis for yield of seed cotton per plant (Iqbal and Nadeem, 2003).
Given the lack of genetic information on powdery mildew resistance in the primary gene pool of watermelon, a generation means analysis was carried out to determine inheritance, gene action, and heritability of resistance in PI 270545. Information on these parameters would be useful for designing an efficient breeding strategy for watermelon powdery mildew resistance.
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