Using Independent Culling to Screen Plant Introductions for Combined Resistance to Soybean Cyst Nematode and Sudden Death Syndrome
Two infectious diseases that cause most yield losses in soybean [Glycine max (L.) Merr.] are soybean cyst nematode (SCN), caused by Heterodera glycines Ichinohe, and sudden death syndrome (SDS), caused by Fusarium solani(Mart.) Sacc. f. sp. glycines (Fsg). Because SCN and SDS have a synergistic effect on yield when they occur jointly in the field, breeders are attempting to develop varieties with dual resistance to these two diseases. Using independent culling as a selection strategy, we screened a set of 31 new soybean plant introductions (PI) that were field evaluated in 1995 at two locations in SouthernIllinois. We identified 11 elite PIs that were resistant to SCN race 3, had yellow seed coat, a relatively good field response to SDS, and a moderate seed yield. These superior genotypes can be used as potential parents in soybean breeding programs.
Abbreviations: DI, disease incidence • DS, disease severity • DX, disease index • HG, Heterodera glycines • MG, maturity group • PI, plant introductions •FI, female index, SCN, soybean cyst nematode • SDS, sudden death syndrome • SQRTDX, square root of DX
DISEASE RESISTANCE is one of the most important goals of the genetic improvement of soybean. Two diseases that cause the most yield losses in soybean are Soybean Cyst Nematode (SCN), caused by Heterodera glycines Ichinohe (Rao-Arelli et al., 1992) and Sudden Death Syndrome(SDS), caused by Fusarium solani f. sp. glycines (Fsg) (Roy, 1997). Damages are generally more severe when these two diseases occur together in the field. From a purely economic standpoint, SCN is currently the most widespread and devastating disease both in the United States and throughout the world. According to Wrather et al. (2003) of the Plant Management Network, SCN caused a yield loss estimatedat $783.8 million in the US alone during the 2002 season.
To date, 16 races of SCN have been identified with various degrees of virulence (Riggs and Schmitt, 1988). This makes it possible for resistance to be both race and cultivar specific. A major step needed for breeding SCN-resistant cultivars was the development of a classification scheme that would separate the major genetic groups ofnematodes. Initially it was proposed based on comparative development of females on four differentials. This was expanded to include 16 different races which also failed to address the variability in the nematode population and resistance characterization of soybean. The HG Type test immediately supersedes the race test for describing nematode populations (Niblack et al., 2002). The test is verysimilar to that used for race determination, but conducted according to a standardized set of rules and set of indicator lines (Plant Introductions, PI) and Female Index is calculated. For example, a nematode population that produces FI of 10 or more on ‘Peking,’ PI88788, and PI89772 is an HG Type 1.2.6. A population that produces no FI of 10 or more on all indicator lines (seven currently) is HGType zero (0) or Race 3 (Rao-Arelli, unpublished data, 2002).
The association between SCN resistance loci and yield depression has been established (Kopisch-Obuch et al., 2005), and a possible genetic linkage between the genes responsible for the plant resistance or susceptibility to SCN and SDS has also been reported (Chang et al., 1995). Although SCN is not required for SDS development in thefield, soybean infection by F. solani in the presence of SCN-3 results in SDS symptoms that were more severe and developed earlier than when SCN-3 is not present (Lawrence et al., 1988). Therefore, breeding for separate resistance may not be a successful strategy because of the synergistic effect of the two diseases in the field.
Historically, soybean breeders have used different breeding...