Published online 18 May 2006
Published in Crop Sci 46:1462-1466 (2006)
© 2006 Crop Science Society of America
677 S. Segoe Rd., Madison, WI 53711 USA
CROP BREEDING & GENETICS
Inheritance of Resistance to Purple Seed Stain Caused by Cercospora kikuchii in PI 80837 Soybean
Eric W. Jacksona,
Patrick Fennb,* and
Pengyin Chenc
a Small Grains and Potato Research Unit, USDA-ARS, Aberdeen, ID 83202
b Dep. of Plant Pathology, 217 Plant Sciences Bldg., Univ. of Arkansas, Fayetteville, AR 72701
c Dep. of Crop, Soil, and Environmental Sciences, 115 Plant Sciences Bldg., Univ. of Arkansas, Fayetteville, AR 72701
* Corresponding author (pfenn{at}uark.edu)
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ABSTRACT
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Purple seed stain (PSS) of soybean [Glycine max (L.) Merr.], caused by Cercospora kikuchii (T. Matsu. & Tomoyasu) Gardner, is favored by high moisture and warm temperatures during early pod development. PSS can significantly reduce seed and grain quality. Characterizing genetic resistance to PSS would be valuable in the development of resistant lines and varieties. PI 80837 has a high level of resistance to PSS and also good resistance to Phomopsis seed decay (PSD) caused primarily by Phomopsis longicolla Hobbs. Resistance to PSD in PI 80837 is conferred by a single dominant gene. The research reported here genetically characterizes PSS resistance in PI 80837 and examines if genes for PSS and PSD resistances are linked. Crosses were made between PI 80837 and ‘Agripro 350’ (AP 350) (susceptible to PSS and PSD), PI 91113 (susceptible to PSS and PSD), and line MO/PSD-0259 (susceptible to PSS but resistant to PSD). Populations and lines were grown in the field and C. kikuchii infection was assayed by plating seed. Cercospora seed infection of F1 plants from reciprocal crosses of AP 350 x PI 80837 was not significantly different from that of PI 80837, indicating that resistance is under nuclear control. Segregation data from each of four F2 populations fit a single dominant gene model for resistance. Data from F2:3 lines of AP 350 x PI 80837 and PI 80837 x MO/PSD-0259 fit the model for a single dominant gene for PSS resistance. A linkage test for reaction to Cercospora and Phomopsis seed infection in F2:3 lines of AP 350 x PI 80837 showed that the genes for PSS and PSD resistances in PI 80837 are not linked.
Abbreviations: AP 350, ‘Agripro 350’ • PSD, Phomopsis seed decay • PSS, purple seed stain
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INTRODUCTION
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PURPLE SEED STAIN and Cercospora blight and leaf spot of soybean are caused by C. kikuchii (Murakishi, 1951). Of these diseases, PSS occurs worldwide and causes reduced market grade, poor processing qualities, and reduced seed vigor (Wilcox and Abney, 1973; Roy and Abney, 1976; Pathan et al., 1989; Schuh, 1999). Although the effect of PSS on germination is unclear (Roy and Abney, 1977; Hepperly and Sinclair, 1981; Pathan et al., 1989), Wilcox and Abney (1973) showed that seedling emergence from purple-stained seed of six soybean cultivars was reduced by 7–15% in greenhouse and field trials.
Environmental conditions are important to the development and severity of PSS. Periods of warm temperatures and high relative humidity favor sporulation and release of conidia from overwintering soybean debris (Jones, 1968; Schuh, 1999). When these conditions persist during early pod development (R2 to R3) (Fehr et al., 1971), latent infections of pods occur (Roy and Abney, 1976; Schuh, 1993). If favorable conditions persist, the fungus can produce the phytotoxic polyketide cercosporin (Kuyama and Tamura, 1957), leading to purple discoloration of seed (Callahan et al., 1999).
Management of PSS is particularly important where pod development and seed maturation occur under warm humid conditions (Grau et al., 2004) and where early maturing varieties which may have high susceptibility to Cercsospora leaf blight (Walters, 1980) are frequently grown. Such conditions often occur with the early planting systems that are popular in the southern United States. Suggested control strategies for PSS include fungicide applications during pod development (Grau et al., 2004), crop rotation, tillage (Jones, 1968; Almeida et al., 2001), planting less-susceptible cultivars (Schuh, 1999), and use of genetic resistance (Wilcox et al., 1975; Srisombun and Supapornhemin, 1993). Little research has been done to identify PSS-resistant genotypes (Orth and Schuh, 1994), and only PI 80837 (Wilcox et al., 1975) and cultivar SJ.2 (Srisombun and Supapornhemin, 1993) have been studied in some detail. The PSS resistance in SJ.2 was reported as controlled by a single dominant gene (Srisombun and Supapornhemin, 1993). Wilcox et al. (1975) investigated the heritability of PSS resistance in PI 80837 using ‘Amsoy’ x PI 80837. Broad-sense heritabilities were 0.91 in the F2 and 0.51 in the F3, suggesting that resistance in PI 80837 was under strong genetic control. Other studies (Roy and Abney, 1976; Ploper et al., 1992) confirm that PI 80837 has good resistance to PSS.
PI 80837 is known to have resistance to PSD (Brown et al., 1987; Roy and Abney, 1988; Ploper et al., 1992; Jackson, 2000), and a recent study showed that resistance to Phomopsis seed infection in PI 80837 is conferred by a single dominant gene (Jackson et al., 2005). Since PSS and PSD are most often responsible for poor seed and grain quality, PI 80837 should be a useful source of resistance to both diseases. During recent research by Jackson et al. (2005) to characterize the inheritance of PSD resistance in PI 80837 and in MO/PSD-0259 (Minor et al., 1993) in field plots, all seed lots from parents, F2 plants, and from plants in F2:3 lines were assayed for infection by C. kikuchii in addition to Phomopsis spp. Analyses of the Cercospora seed infection data indicated the mode of inheritance of PSS resistance in PI 80837. This paper presents results indicating that resistance to Cercospora seed infection in PI 80837 is conferred by a single dominant gene, and that the genes for resistances to Phomopsis and Cercospora seed infection in PI 80837 are not linked.
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MATERIALS AND METHODS
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All crosses were made and F2 seed raised in the greenhouse at Fayetteville, AR. All field tests were done at the University of Arkansas Vegetable Substation at Kibler, AR. The field site (Dardanelle silt loam out wash, fine-silty, mixed, superactive, thermic Typic Argiudolls) was regularly used for cowpea trials and cover cropped with winter wheat. Soybean variety trials are rotated at the site, and both Phomopsis spp. and C. kikuchii were recovered from soybean grown on the site (Jackson, 2000). All field tests received 2.00–2.54 cm of water each week by overhead irrigation.
In 2002, F2 seed of AP 350 x PI 80837 and of PI 80837 x MO/PSD-0259 were sown in the greenhouse and at the V2–3 stage (Fehr et al., 1971) the seedlings were transplanted to the field. Seedlings were planted approximately 25 cm apart in rows with seedlings of the parents transplanted every four to six F2 seedlings. There were 108 F2 plants of AP 350 x PI 80837, 102 F2 plants of PI 80837 x MO/PSD-0259, and 15 plants of each parent. The test had 12, 6-m-long rows with 0.91-m row spacing. Border rows were planted on the ends and sides to ensure consistent environmental conditions. In 2003, six tests were planted at the Kibler site: (i) F2:3 lines from seed collected from the upper nodes of F2 plants of AP 350 x PI 80837 grown in 2002; (ii) F2:3 lines from seed of F2 plants of PI 80837 x MO/PSD-0259 grown in 2002; (iii) F1 and reciprocal F1 seed from AP 350 x PI 80837; (iv) a new F2 population from AP 350 x PI 80837; (v) an F2 population from PI 80837 x MO/PSD-0259; and (vi) an F2 population from PI 91113 x PI 80837. Seeds were sown about 10 cm apart in rows with 1.8-m-long row segments (about 20–25 seed) of parents planted every 25 to 30 F2 seed. Three row segments of each parent accompanied each F2 population. Each F2:3 line (104 lines of AP 350 x PI 80837 and 80 lines of PI 80837 x MO/PSD-0259) was planted (about 25 seed line–1) in a 1.8-m-long row. Parents were planted in 1.8-m row segments randomly located among each family of F2:3 lines. Five- to seven-row segments of each parent were planted with each F2:3 line test. Row spacing was 0.91 m and border rows were used as in 2002.
Because this research was designed to study the inheritance of resistance to Phomopsis seed infection in PI 80837, efforts were made to optimize conditions and sampling for Phomopsis infection following criteria proposed by Zimmerman and Minor (1993). These included supplying supplemental inoculum, sampling from the lower portion of the stems since the incidence of Phomopsis seed infection can decrease with plant height, and prompt harvesting of seed at a uniform time after R8 (Zimmerman and Minor, 1993). For inoculum, conidial suspensions of an isolate of P. longicolla Hobbs were produced from 18- to 20-d-old cultures on potato dextrose agar. Concentrations were adjusted by hemocytometer and dilutions made in deionized water. Plants were sprayed with a backpack sprayer until pods were covered with drops of conidial suspension. In 2002, two spray applications (approximately 105 conidia mL–1) were made 16 d apart starting at approximately R5 (Jackson et al., 2005). In 2003, three applications (approximately 2.5 x 105 conidia mL–1) were made 11 d apart starting at approximately R5. No supplemental inoculum of C. kikuchii was used in either year.
In 2002, seed were harvested about 10 d after maturity at R8 (Fehr et al., 1971). Seed from three or four randomly selected parent plants from each parent row segment within each test and all F2 plants were harvested. Seeds from the lower 40 cm of each plant were hand harvested for seed assays, and seed from the upper nodes were collected for F2:3 lines. In 2003, plants were larger because of better growing conditions, so seed were harvested from the lower 65 cm of each plant using a single-plant thresher about 10 d after R8. Eleven or 12 randomly selected plants were harvested individually from each F2:3 line; a number deemed adequate to determine if a line was homogeneous or was segregating for disease reaction. Five or six randomly selected parent plants were harvested from each parent row segment planted with each F2 population or family of F2:3 lines. Because of wet soils, damping-off and poor seedling vigor, a number of lines were lost or contained fewer than 15 plants at maturity. Plants were harvested only from the F2:3 lines with 15 or more plants. Of the 104 F2:3 lines of AP 350 x PI 80837 and 80 F2:3 lines of PI 80837 x MO/PSD-0259 planted, 89 and 50 were harvested, respectively.
In 2002, a random sample of 30 seeds from each F2 and parent plant was assayed for seed infection. Seeds were disinfested in 0.5% w/v NaOCl amended with five drops of polyoxyethylene (20) sorbitan monolaurate (Tween 20) L–1 for 5 min and rinsed twice in sterile water for 3 min (Brown et al., 1987). Seeds were plated on potato dextrose agar amended after autoclaving with 1 µg mL–1 fenpropathrin, 75 µg mL–1 streptomycin sulfate, and acidified to pH 4.8 with lactic acid to control mites and bacteria. In 2003, 40 random seeds from each F2, F3, and parent plant were bioassayed as more seed were available than in 2002. After incubation under fluorescent light with a 14-hr photoperiod for 10 d, the number of seeds from which typical colonies of C. kikuchii or Phomopsis spp. grew was recorded. The percentage Cercospora seed infection was calculated as (no. seeds with colonies of C. kikuchii/no. seeds plated x 100). The percentage of Phomopsis seed infection was calculated similarly.
Percentage seed infection of the randomly selected parent plants within each test was analyzed by ANOVA (P = 0.05; JMP, SAS Institute Inc., Cary, NC). Arcsine transformation of percentage data to equalize the variances did not affect statistical differences, so percentage data were used in all analyses. In all tests except one, the range of values for Cercospora seed infection of the resistant parent did not overlap the range of seed infection of the susceptible parent. In 2002, a susceptible parent plant (AP 350) had no Cercospora seed infection, that is, not different from infection of PI 80837 at 0.0%. This was the only test in which the ranges of the parents overlapped for the populations in both years. Therefore, plants in F2 populations and F2:3 lines were classified as resistant if their percentage seed infection was equal to or less than the highest value of the resistant parent plants grown with that population. Percentages of Cercospora seed infection used to classify resistant plants were in 2002, F2 (AP 350 x PI 80837) = 0.0%; in 2003, F2 (AP 350 x PI 80837) 
17.5%, F2 (PI 80837 x MO/PSD-0259) 20.0%, F2 (PI 91113 x PI 80837) 12.5%, F2:3 (AP 350 x PI 80837) 10.0%, F2:3 (PI 80837 x MO/PSD-0259) 15.0% infection. All F2 plants and plants from F2:3 lines with higher percentages of seed infection were classified as susceptible. Correlation of Phomopsis seed infection with Cercospora seed infection for the combined F2 (AP 350 x PI 80837) and F2 (PI 91113 x PI 80837) populations from 2003 was done by the JMP statistical package (SAS Institute Inc., Cary, NC). Plants were classified as susceptible to Phomopsis seed infection if their mean percentage infection was above the highest value of the 95% confidence interval of PI 80837 (Jackson et al., 2005). Chi-square tests were used to determine the goodness of fit of observed F2 and F2:3 segregation data to the expected ratios for a single dominant gene(s). Phomopsis and Cercospora seed infection data for 89 F2:3 lines of AP 350 x PI 80837 were used to determine if PSD and PSS resistance genes in PI 80837 are linked.
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RESULTS AND DISCUSSION
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Although Cercospora seed infection was low in 2002, susceptible AP 350 had significantly more seed infection than PI 80837 (Table 1), and the F2 plants of AP 350 x PI80837 suggested a 3:1 segregation for resistant–susceptible plants (Table 2). Cercospora seed infection of MO/PSD-0259 was very low in 2002 (0.0–2.0%), and F2 plants of PI 80837 x MO/PSD-0259 showed no evidence of segregation for seed infection. In 2003, disease pressure was greater as indicated by higher Cercospora seed infection in both AP 350 and PI 80837 (Table 1). As in 2002, no Cercospora inoculum was applied in 2003. Environmental variables at specific growth stages were not recorded, so the reason(s) for differences in Cercospora seed infection between years is unknown.
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Table 1. Incidence of Cercospora seed infection in parents AP 350 and PI 80837 and reciprocal F1 plants grown in the field during 2 yr.
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Table 2. Reactions to Cercospora seed infection of parents and F2 populations from resistant x susceptible crosses grown in the field across 2 yr.
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Cercospora infection of seed from F1 and reciprocal F1 plants of AP 350 x PI 80837 were not significantly different in 2003 (Table 1). This suggests that resistance to Cercospora is a dominant trait under nuclear control. Segregation ratios for the F2 population (AP 350 x PI 80837) screened in 2002 and the F2 populations (one of AP350 x PI80837, one of PI 80837 x MO/PSD-0259, and one of PI 91113 x PI 80837) screened in 2003 were not significantly different from a 3:1 resistant–susceptible model for a single dominant gene (Table 2); however, pooled data for all four populations from both years did not fit a single dominant gene model (Table 2). A test for heterogeneity, however, indicated that inheritance of PSS resistance from PI 80837 responded the same in three different susceptible backgrounds across 2 yr (Table 2).
The discrepancy between the individual F2 population data and pooled data can be traced to a greater-than-expected number of susceptible than resistant plants in all four F2 populations (Table 2). One interpretation for these results is that there is more than one gene for resistance to Cercospora seed infection in PI 80837, and these are segregating in the F2 populations. However, this explanation is not supported by the F2:3 line data (see below). The most reasonable explanation derives from the method used to classify F2 plants as resistant or susceptible. Because the ranges of seed infection of resistant and susceptible parent plants did not overlap in the F2 populations, all F2 plants with Cercospora seed infection above the highest value of the resistant parent, including those with percentage infection between the resistant and susceptible ranges, were classed as susceptible. Thus, any F2 plants with a percentage infection between the ranges in all four populations were classified as susceptible. This accounts for the excess of susceptible plants in each F2 population and the fact that the pooled data for the F2 populations does not agree with the model for a single dominant gene (Table 2).
Data from F2:3 lines of both AP 350 x PI 80837 and PI 80837 x MO/PSD-0259 showed a close fit to a 1:2:1 resistant–heterogeneous–susceptible model for a single dominant gene (Table 3). Combined data from the two crosses fit a one-gene model, and showed that resistance to Cercospora seed infection from PI 80837 responded the same when combined with two susceptible backgrounds (Table 3). These results provide strong evidence that a single dominant gene controls resistance in PI 80837 and supports the conclusion from heritability studies by Wilcox et al. (1975) that resistance to PSS in PI 80837 is under strong genetic control.
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Table 3. Reactions to Cercospora seed infection of parents and F2:3 lines from AP 350 x PI 80837 and PI 80837 x MO/PSD-0259 grown in the field, 2003.
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Since resistances to Cercospora and Phomopsis seed infection in PI 80837 were found to be controlled by single dominant genes, a linkage test for these genes was done with the data from the AP 350 x PI 80837 F2:3 lines. These lines were shown previously to segregate 19:50:20 resistant–heterogeneous–susceptible (
2 = 1.382 for a 1:2:1 ratio, P = 0.50–0.25) for reaction to Phomopsis seed infection (Jackson et al., 2005). Comparing the disease reaction of these lines to both seed pathogens clearly showed that the data fit a model for two dominant genes that are not linked (Table 4).
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Table 4. Test of genetic linkage of resistances to Phomopsis seed infection and Cercospora seed infection in F2:3 lines from AP 350 x PI 80837 screened in the field, 2003.
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Numerous reports of statistically significant negative correlations between incidences of seed infection by C. kikuchii and Phomopsis spp. have indicated an antagonistic interaction in which early Cercospora infection inhibits infection or colonization by Phomopsis spp. This is found especially with soybean genotypes that are very susceptible to Cercospora seed infection (Roy and Abney, 1977; Hepperly and Sinclair, 1981; Pathan et al., 1989). Since we used the same plants and seed lots to investigate inheritance of resistance to both pathogens, the data on inheritance of Phomopsis resistance may have been affected by Cercospora infection. To examine this possibility, a correlation analysis was done of Phomopsis (dependent variable) with Cercospora seed infection (independent variable) for the combined 2003 F2 populations from AP 350 x PI 80837 and PI 91113 x PI 80837 (N = 222 plants). The correlation was not significant (r = –0.00058, P = 0.9931), indicating no evidence of antagonism. The PI 80837 plants grown with these F2 populations had <17 and <12.5% Cercospora seed infection, respectively. In working with PI 80837, Roy and Abney (1977) showed no evidence of antagonism when infection was 14.2% or less in both Cercospora-inoculated and uninoculated field plots. In addition, Hepperly and Sinclair (1981) found no antagonism in PI 80837 when Cercospora seed infection was <10%. In our studies, the overall mean Cercospora infection increased more than threefold from 4.9% in 2002 to 15.4% in 2003, while the overall mean Phomopsis seed infection remain nearly the same at 16.9% in 2002 and 18.3% in 2003. At these levels of natural Cercospora seed infection, antagonism by C. kikuchii was not an important factor in our studies of inheritance of resistance to Phomopsis in PI 80837 in these plant populations and lines.
Purple seed stain and PSD can severely lower seed quality where and when conditions are conducive for these diseases. This study has shown that resistance to PSS in PI 80837 is conferred by a single dominant gene that is not linked to the gene for resistance to Phomopsis seed infection in this line (Jackson et al., 2005). Breeding to combine PSS and PSD resistances from PI 80837 into lines and varieties would be a valuable approach to controlling these major seed diseases. In screening for resistances from PI 80837 in inoculated field plots, one would need to consider the stages in reproductive development when the soybean is most susceptible to subsequent seed infection; R2–R3 for Cercospora (Roy and Abney, 1977) and R6–R7 for Phomopsis. It would seem feasible to inoculate the same F2 populations with both pathogens at the most susceptible stages since the strong resistance to PSS from PI 80837 should keep Cercospora infection low enough to prevent any antagonism to Phomopsis infection, thus permitting accurate identification of Phomopsis-resistant plants. Alternatively, screening could be delayed to later generations when sufficient progeny are available to screen lines to determine which carry resistance to both seed diseases.
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ACKNOWLEDGMENTS
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This research was supported by the Arkansas Soybean Promotion Board and the Arkansas Agricultural Experiment Station. The authors thank Pamela Miller for her expertise and help with this project, and the staff of the Univ. of Arkansas Vegetable Substation at Kibler, AR, for their help with field management. We also thank K. Bilyeu from Agripro Seeds Inc., Ames, IA, for seed of Agripro 350, and Dr. H.C. Minor of Univ. of Missouri, Columbia, MO, for seed of MO/PSD-0259.
Received for publication October 22, 2005.
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E. W. Jackson, C. Feng, P. Fenn, and P. Chen
Genetic Mapping of Resistance to Purple Seed Stain in PI 80837 Soybean
J. Hered.,
May 1, 2008;
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ABSTRACT
INTRODUCTION
