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Published online 27 October 2005
Published in Crop Sci 45:2400-2404 (2005)
© 2005 Crop Science Society of America
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CROP BREEDING, GENETICS & CYTOLOGY

Inheritance of Resistance to Phomopsis Seed Decay in Soybean PI 80837 and MO/PSD-0259 (PI 562694)

Eric W. Jacksona, Patrick Fennb,* and Pengyin Chenc

a Small Grains and Potato Research Unit, U.S. Dep. of Agriculture, Agricultural Research Service, 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)


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 
Phomopsis seed decay [PSD; caused by Diaporthe phaseolorum var. sojae (Lehman) Wehmeyer, Diaporthe phaseolorum (Cooke & Ellis) Sacc. var. caulivora Athow & Caldwell, and Phomopsis longicolla Hobbs) reduces quality of soybean [Glycine max (L.) Merr.] seed when moist conditions and warm temperatures occur during seed development and maturation. Control of PSD by genetic resistance has not been well explored. Of the genotypes reported with PSD resistance, PI 417479 and PI 80837 have received the most study. The PSD-resistant line MO/PSD-0259 derives its resistance from PI 417479. Objectives of this research were to characterize the inheritance of PSD resistance in PI 80837 and to determine if it differs from resistance in MO/PSD-0259. PI 80837 was crossed with PSD-susceptible ‘Agripro 350’ (AP 350); PSD-susceptible PI 91113; and with MO/PSD-0259. Populations and lines were screened in the field, and Phomopsis infection was assayed by plating seed. Seed infection of reciprocal F1 plants of AP 350 x PI 80837 was not different from that of PI 80837. Data from F2 populations of AP 350 x PI 80837 and PI 91113 x PI 80837; and F2:3 lines from AP 350 x PI 80837 fit models for a single dominant gene in PI 80837 that confers PSD resistance. F2 population data from AP 350 x MO/PSD-0259 also fit a model for single dominant gene resistance in MO/PSD-0259, and data from an F2 population and F2:3 lines of PI 80837 x MO/PSD-0259 fit a model for two different dominant genes. These results show that PSD resistance in PI 80837 is conferred by a single dominant gene under nuclear control that is different from the gene in MO/PSD-0259.

Abbreviations: AP 350, ‘Agripro 350’ • DPC, Diaporthe/Phomopsis complex • PI, plant introduction • PSB, pod and stem blight • PSD, Phomopsis seed decay • RFLP, restriction fragment length polymorphism


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 
FUNGI of the Diaporthe/Phomopsis complex (DPC) cause several important diseases of soybean including seed decay, pod and stem blight, and stem canker (Kulik and Sinclair, 1999a; Kulik and Sinclair, 1999b). Of these, Phomopsis seed decay (PSD) can affect the production of seed and grain, and affect the qualities of oil and meal (Hepperly and Sinclair, 1978; Kulik and Sinclair, 1999a; Sinclair, 1993). Of the fungi that cause PSD, Phomopsis longicolla is the most aggressive seed pathogen and is endemic in soybean production areas worldwide (Brown et al., 1987; Hobbs et al., 1985; Kulik and Sinclair, 1999a).

Environmental factors are important in the development and severity of PSD (McGee, 1983; Zimmerman and Minor, 1993). Periods of high humidity, free moisture, and warm temperatures during pod development favor latent infection of pods by the DPC (Kmetz et al., 1978; TeKrony et al., 1996). When these conditions persist during seed development and maturation, pod infection leads to seed infection and decay (McGee, 1983). Increased incidences of PSD in the southern United States are associated with earlier plantings of soybean when pod and seed development occur during conditions favorable for disease (Mayhew and Caviness, 1994; TeKrony et al., 1996; Wrather et al., 2003). Therefore, approaches to control PSD will become more important with the continuing shift of soybean production to earlier planting systems.

Control strategies for PSD, including deep tillage, crop rotation, and fungicide use, have given inconsistent results (Kmetz et al., 1979; Jeffers et al., 1982; McGee et al., 1980; Slater et al., 1991). Reports have indicated that good resistance exists in some plant introductions (PI) and some cultivars. PI 82264 (Walters and Caviness, 1973) and PI 181550 (Athow, 1987) have resistance to Phomopsis seed infection, while ‘Delmar’ (Crittenden and Cole, 1967) has resistance to pod and stem blight caused by Phomopsis sojae Lehman, [teleomoph; D. phaseolorum var. sojae (Lehman) Wehm.]. Ross (1986) reported the release of lines derived from PI 200501 and ‘Arksoy’ with resistance to PSD. Field tests by Brown et al. (1987) showed that PI 181550 and ‘Delmar’ had less Phomopsis seed infection than did susceptible controls, whereas PI 80837, PI 417479, and PI 360841 consistently had the lowest seed infection.

Data from inheritance studies of PSD resistance in PI 417479 fit models for qualitative inheritance of one or two dominant genes (Zimmerman and Minor, 1993). The resistant phenotype was found to be associated with RFLP marker A708 located on the F linkage group and RFLP marker A162 on the H linkage group (Berger and Minor, 1999). Pedigree selection from PI 417479 x ‘Merschman Dallas’ for low incidence of Phomopsis seed infection led to the release of MO/PSD-0259, an F5 line having no PSD (Minor et al., 1993). In Missouri and Nebraska field trials, both MO/PSD-0259 and PI 417479 had low levels (0 to 6%) of PSD (Elmore et al., 1998 and Minor et al., 1993). MO/PSD-0259 has been used recently to develop two lines, SS 93–6012 and SS 93–6181, with good PSD resistance (Wrather et al., 2003).

PI 80837 has been estimated to contribute about 2.3% to southern soybean germplasm (Gizlice et al., 1994). Useful traits from PI 80837 include resistances to Mexican bean beetle, soybean mosaic virus, purple seed stain, and PSD (Buss et al., 1979; Ploper et al., 1992; Roy and Abney, 1988; Wilcox et al., 1975; Yelen and Crittenden, 1967). Field tests by Ploper et al. (1992) showed that PI 80837 had low levels of PSD. Yelen and Crittenden (1967) and Roy and Abney (1988) suggested that tissue layers in the pod control resistance to PSD. In addition, the severity of pod and stem blight on PI 80837 was less than that of MO/PSD-0259, PI 91113, and AP 350 in field and greenhouse tests (Jackson, 2000).

Since PI 80837 has good resistance to PSD, our objectives were to study the inheritance of resistance to Phomopsis seed infection in PI 80837 and to determine if this resistance is different from that found in MO/PSD-0259 (Minor et al., 1993).


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS AND DISCUSSION
 REFERENCES
 
PI 80837 was crossed with the PSD-susceptible cultivar Agripro 350 (AP 350) (Zimmerman and Minor, 1993) and the PSD-resistant line MO/PSD-0259 in the greenhouse in 2001. F2 populations were produced from two F1 seeds from the same pod for each cross. One hundred and twenty (AP350 x PI 80837) and 110 (PI 80837 x MO/PSD-0259) F2 seed were sown in the greenhouse and, at the V2–3 stage (Fehr et al., 1971), seedlings were transplanted into the field at Kibler, AR. The site was regularly used for cowpea trials and cover-cropped with winter wheat. Seedlings were planted in two tests based on population. Individual plants were spaced approximately 25 cm apart in rows with both parents planted throughout the plot every 4 to 6 F2 seedlings. Rows were spaced 0.91 m apart, and border rows were planted on row ends and sides to maintain uniform environmental conditions.

To ensure disease pressure, two spray applications of P. longicolla conidial suspensions were made 16 d apart beginning at R5. Inoculum was prepared from an isolate with consistent sporulation and was tested previously for virulence on soybean in the field and greenhouse (Jackson, 2000). Cultures were grown on potato dextrose agar (Difco, Detroit, MI) under a 14-h photoperiod for 18 to 20 d. Sporulating cultures were flooded with sterile deionized water and agitated to disperse conidia. Conidial suspensions were adjusted to approximately 105 conidia/mL determined by hemacytometer counts. Plants were sprayed with a backpack sprayer until pods were covered with drops of suspension. Inoculum was applied at dusk before dew or scheduled overhead irrigation to provide conditions favorable for infection.

Seeds were threshed by hand from each F2 and parent plant about 10 d after maturity at R8 (Fehr et al., 1971; Zimmerman and Minor, 1993). Seeds from the lower 0.4 m of the plants were collected for assays, while seed from the upper nodes were harvested for F2:3 lines. For seed assay, a random sample of 30 seeds was surface disinfested in 0.5% (w/v) NaOCl amended with five drops of Tween 20/L for 5 min and rinsed twice in sterile water for 3 min (Brown et al., 1987). Seeds were plated onto potato dextrose agar amended after autoclaving with 1µg/mL fenpropathrin [(RS)-{alpha}-cyano-3-phenoxybenzyl 2,2,3,3-tetramethylcyclopropanecarboxylate] to control mites, 75 µg/mL streptomycin sulfate, and acidified to pH 4.8 with lactic acid to prevent growth of bacteria. The percentage of seed infected with Phomopsis was recorded after incubation under fluorescent light with a 14-h photoperiod for 10 d.

In 2003, six tests were planted at Kibler, AR. These were (i) F2:3 lines from seeds collected from F2 plants (AP 350 x PI 80837 and PI 80837 x MO/PSD-0259) grown in 2002; (ii) reciprocal F1 hybrids from AP 350 x PI 80837; (iii) a new F2 population from AP 350 x PI 80837; (iv) a new F2 population from PI 80837 x MO/PSD-0259; (v) an F2 population from PI 91113 x PI 80837; and (vi) an F2 population from AP 350 x MO/PSD-0259. About 25 seeds of each F2:3 line (80 to 104 lines) were planted in 1.8 m long rows. Parent rows (1.8 m long) were randomly planted among the lines. Seed of F2 populations were planted in rows, with 1.8 m long rows of parents distributed every 25 to 30 F2 seed. Row spacing and border rows were used as described in 2002.

Supplemental inoculum was applied in 2003 as in 2002, except that the final concentration was adjusted to approximately 2.5 x 105 conidia/mL before spraying. Three applications were made 11 d apart, beginning at R5. The lower 65 cm of each plant was threshed by machine about 10 d after R8. The tops of the plants were discarded. Eleven or 12 plants were threshed from each F2:3 line. Forty random seeds from each plant were bioassayed as described above and percent seed infection recorded.

ANOVA (analysis of variance) was done on the percent seed infection data from parent plants randomly selected from the 1.8 m parent rows within each population to determine differences in infection between resistant and susceptible parents (P = 0.05; JMP, SAS Institute Inc., Cary, NC). Arc-sine transformation of percentage data was compared to untransformed data. Since transformation did not affect statistical differences, untransformed percentage data was used in all statistical analyses. Plants were considered resistant to Phomopsis seed infection if the percent infection was below the upper 95% confidence interval of the resistant parent plants within each population. Percentage seed infection which determined resistant individuals in populations were, in 2002, F2 (AP 350 x PI 80837) <15.7% and F2 (PI 80837 x MO/PSD-0259) <8.6%; and in 2003, F2 (AP 350 x PI 80837) <29.0%, F2 (PI 80837 x MO/PSD-0259) <35.5%, F2 (PI 91113 x PI 80837) <44.6%, F2 (AP 350 x MO/PSD-0259) <29.6%, F2:3 (AP 350 x PI 80837) <15.0%, and F2:3 (PI 80837 x MO/PSD-0259) <22.5%. Seed infection data from the resistant parent PI 80837, and reciprocal F1 plants were analyzed by ANOVA (P = 0.05) and means were separated by students t test (JMP, SAS Institute Inc., Cary, NC). Chi-square ({chi}2) tests were used to determine the goodness-of-fit of observed F2 and F2:3 segregation data to the expected ratios for segregation of single dominant gene(s).


   RESULTS AND DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
REFERENCES
 
Environmental conditions and inoculum levels were favorable for seed infection at the Kibler site in 2002 and 2003. In both years the susceptible cultivar AP 350 had significantly greater Phomopsis seed infection than did the resistant PI 80837 (Table 1). In 2003, disease pressure was higher than in 2002, as indicated by higher seed infection in both parents. The increased concentration of inoculum and three rather than two applications may have accounted for this difference. In addition, we tried to implement some of the recommendations of Zimmerman and Minor (1993) with regard to inoculation, plant sampling, and harvest time to minimize escapes that can affect the results and interpretation of seed infection studies.


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  		Table 1. Incidence of Phomopsis seed infection from parents AP 350 and PI 80837 and reciprocal F1 plants inoculated with Phomopsis longicolla in the field over 2 yr.

 
Phomopsis seed infection in reciprocal F1 hybrids of AP 350 x PI 80837 and the resistant parent PI 80837 were not significantly different (Table 1). These data suggest that resistance to Phomopsis seed infection is under nuclear genetic control and not controlled by a cytoplasmic component. Furthermore, the lack of differences between both hybrids and PI 80837 indicate that resistance is a dominant trait. Similarly, inheritance of resistance in PI 417479 to Phomopsis seed infection was shown previously to be a dominant trait under nuclear control (Zimmerman and Minor, 1993).

In categorizing resistant versus susceptible F2 and F3 plants, the upper 95% confidence interval for the resistant parent was used. Even using this selection criterion, some resistant parent plants were classified as susceptible (Tables 2, 3, 4, and 5). Seed from these plants may have become infected through disruptions in the pod, insect damage, or seed coat cracking during or after maturity (Athow and Laviolette, 1973). The pod appears to be very important in conferring resistance in PI 80837 (Roy and Abney, 1988). Moreover, the high percent seed infection of PI 80837 (28.2%) and MO/PSD-0259 (27.1%) in our 2003 tests, which normally ranges from 3.0 to 6.0% for these resistant genotypes (Brown et al., 1987; Elmore et al., 1998; Jackson, 2000; Minor et al., 1993; Ploper et al., 1992), indicated that disease pressure was high. Because only one susceptible parent plant (AP 350) in these studies was classed as resistant (Table 4), disease escapes were few, if any, and did not affect the results.


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  		Table 2. Reactions to Phomopsis seed infection of parents and F2 populations from resistant x susceptible crosses inoculated with Phomopsis longicolla in the field over 2 yr.

 

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  		Table 3. Reactions to Phomopsis seed infection of parents and F2:3 lines from AP 350 x PI 80837 inoculated with Phomopsis longicolla in the field in 2003.

 

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  		Table 4. Reactions to Phomopsis seed infection of parents and an F2 population from AP 350 x MO/PSD-0259 after inoculation with Phomopsis longicolla in the field in 2003.

 

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  		Table 5. Reactions to Phomopsis seed infection of parents and F2 populations from PI 80837 x MO/PSD-0259 after inoculation with Phomopsis longicolla in the field over 2 yr.

 
Segregation ratios for the F2 populations screened in 2 yr (AP 350 x PI 80837 and PI 91113 x PI 80837) were not significantly different from a 3R:1S model for a single dominant gene (Table 2). Combined results from all F2 populations over 2 yr were a satisfactory fit to a one-dominant-gene model. All populations were homogeneous, suggesting that inheritance of resistance from PI 80837 responded the same over 2 yr and when combined with two different susceptible backgrounds (Table 2).

Data from F2:3 lines showed a close fit to a 1 (all resistant): 2 (segregating): 1 (all susceptible) model expected from the segregation of a single dominant gene (Table 3). These results provide strong evidence that a single dominant gene controls resistance to Phomopsis seed infection in PI 80837.

Segregation for the AP 350 x MO/PSD-0259 F2 population was not different from a 3R:1S model for a single dominant gene (Table 4). Furthermore, segregation ratios for PI 80837 x MO/PSD-0259 F2 populations were not significantly different from a 15R:1S model for segregation of two different dominant genes in both years (Table 5). Combined results over 2 yr were a good fit to this model and were homogenous (Table 5). F2:3 line data from PI 80837 x MO/PSD-0259 closely fit a 7:8:1 (all resistant:segregating:all susceptible) model for two different dominant genes (Table 6). Together, these data show that in MO/PSD-0259 and in PI 80837 resistance to PSD is controlled by a single dominant gene, and that these genes are different.


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  		Table 6. Reactions to Phomopsis seed infection of parents and F2:3 lines from PI 80837 x MO/PSD-0259 inoculated with Phomopsis longicolla in the field in 2003.

 
Zimmerman and Minor (1993) concluded that resistance to PSD in PI 417479 (parent of MO/PSD-0259) is conferred by two complementary dominant genes. Whether MO/PSD-0259 contains two genes for PSD resistance is not known. While our F2 populations from AP 350 x MO/PSD-0259 and PI 80837 x MO/PSD-0259 fit 3R:1S; and 15R:1S models, respectively, the ratios of resistant to susceptible plants tended to be lower than expected (Tables 4 and 5). This could indicate that a second gene in MO/PSD-0259 affects resistance in this line. Screening the F2:3 lines of AP 350 x MO/PSD-0259 could have provided evidence of a second gene, but this was not done in our study. However, the strongest support for concluding that MO/PSD-0259 contains one major gene for PSD resistance is revealed in the F2:3 lines of PI 80837 x MO/PSD-0259 (Table 6). If a second gene for PSD resistance occurs in MO/PSD-0259, it would have a very small effect on resistance.

The ability to easily characterize the mode of inheritance of resistance to seed decay in PI 80837 and in MO/PSD-0259 was attributed to the high disease pressure generated by inoculating field plots and by implementing the screening criteria proposed by Zimmerman and Minor (1993) to optimize conditions for disease and to standardize seed harvest.

These results support previous reports that PI 80837 is a good source of resistance to PSD (Athow, 1973; Roy and Abney, 1988; Ploper et al., 1992). Because resistance in PI 80837 is simply inherited, it could be easily manipulated in programs aimed at breeding for resistance to PSD. Combining resistance from PI 80837 with other sources; for example, PI 417479 or MO/PSD-0259, in which resistance to seed decay is dominant, controlled by different gene(s), and simply inherited, is possible and should increase the durability of resistance. However, assaying seed for Phomopsis seed infection alone would not reliably distinguish plants with multiple resistance genes from those with only one. Molecular markers linked to the different genes for PSD resistance would facilitate such a breeding program.

Further research will help to clarify the nature of and inheritance of resistance in soybean to diseases caused by fungi of the DPC. Resistance to stem canker has been shown to be controlled by several single dominant genes (Tyler, 1996). Although resistance to pod and stem blight (PSB) has been reported from several plant introductions and cultivars (Athow, 1987; Kulik and Sinclair, 1999b), several of which derived their resistance from PI 80837 (Gizlice et al., 1994; Buss et al., 1979), little is known about inheritance of PSB resistance from PI 80837 and its relationship, if any, to PSD resistance. Data from Elmore et al. (1998) indicated that resistance to PSD from PI 417479, found in MO/PSD-0259, does not appear to control PSB. We have observed severe PSB on MO/PSD-0259 in the field (Jackson and Fenn, unpublished). Whether the gene controlling seed decay resistance in PI 80837 also controls resistance to PSB is not known. PSB occurred on the susceptible genotypes, PI 91113, MO/PSD-0259, and AP 350, but rarely on PI 80837 in our plots in both years (Jackson and Fenn, unpublished). However we did not closely evaluate whether F2 populations or lines from PI 80837 were segregating for PSB reaction. Further research could determine whether a single gene is associated with reaction to PSB and PSD in PI 80837, and its usefulness in breeding for disease resistance to improve yield and seed quality.


   ACKNOWLEDGMENTS
 
This research was supported by the Arkansas Soybean Promotion Board and the Arkansas Agricultural Experiment Station. The authors thank Pamela Miller and Sherrie Smith for their technical expertise. We also thank the staff of the Univ. of Arkansas Vegetable Substation at Kibler, AR, for field maintenance; Dr. H.C. Minor, Univ. of Missouri, Columbia, MO, for seed of MO/PSD-0259; and Keith Bilyeu from Agripro Seeds, Inc., Ames, IA, for seed of ‘Agripro 350.’

Received for publication September 8, 2004.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 




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This Article
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