Inheritance of Resistance to Phomopsis Seed Decay ...

Journal of Heredity 2008:99(6):588–592 doi:10.1093/jhered/esn037 Advance Access publication May 25, 2008

Ó The American Genetic Association. 2008. All rights reserved. For permissions, please email: [email protected].

Inheritance of Resistance to Phomopsis Seed Decay in PI 360841 Soybean SHERRIE SMITH, PATRICK FENN*, PENGYIN CHEN,

AND

ERIC JACKSON

From the Cooperative Extension Service, Department of Agriculture, University of Arkansas, Box 357, 2001 Highway 70 E., Lonoke, AR 72086 (Smith); the Department of Crop, Soil, and Environmental Sciences, 115 Plant Science Building, University of Arkansas, Fayetteville, AR 72701 (Chen); and the USDA ARS, Small Grains and Potato Germplasm Unit, 1691 S. 2700 W. Aberdeen, ID 83210 (Jackson). *Deceased author. Address correspondence to P. Chen at the address above, or e-mail: [email protected].

Phomopsis longicolla Hobbs is the primary cause of Phomopsis seed decay (PSD) in soybean. Infection may result in moldy seed and poor germination. The objective of this study was to conduct inheritance studies to characterize resistance to PSD in plant introduction (PI) 360481. Crosses were made between PI 360841 and 2 PSD-susceptible genotypes, Agripro (AP) 350 and PI 91113, to determine the number of genes for resistance. Additionally, crosses were made between PI 360841 and Phomopsis resistant parents MO/PSD-0259 and PI 80837 to test the allelism of the resistance genes. Seed infection assays were done using seed from parent plants and F2 populations. Chi-square analysis of the resistant susceptible F2 data fit to a 9R:7S model for 2 complementary dominant genes conferring PSD resistance in PI 360841. Segregation for reaction in the F2 of MO/PSD-0259 PI 360841 exhibited a good fit to a 57R:7S model for 2 complementary dominant genes from PI 360841 and a different dominant gene from MO/PSD-0259. There was no apparent segregation in the F2 population from PI 360841 PI 80837 except for one suspicious susceptible plant, suggesting one of the genes in PI 360841 is the same gene in PI 80837 for PSD resistance.

Fungi of the Diaporthe–Phomopsis complex are the pathogens causing Phomopsis seed decay (PSD) of soybean in areas where high temperatures and high humidity occur during crop maturation (Kmetz et al. 1979; Hobbs et al. 1985; Keeling 1988; Wrather et al. 2003). For example, in 1994 crop losses attributed to the Diaporthe–Phomopsis complex totaled 186 000 metric tons worldwide (Wrather et al. 1997). Phomopsis longicolla has been found to account for more than 85% of all Phomopsis seed infection (Hobbs et al. 1985). PSD can reduce yields, lower seed germination, and can lower the quality of oil and meal due to poor quality of diseased seed (Hepperly and Sinclair 1978; Rupe and Ferriss 1986; Rupe 1990; Mayhew and Caviness 1994). PSD has been exacerbated in recent years by the shift to an early season production system in the southern United States. This system uses early-maturing indeterminate cultivars, planted in early April to avoid late-season moisture deficits. Unfortunately, these cultivars mature in July or August when high temperatures and high humidity are conducive for Phomopsis seed infection (Mayhew and Caviness 1994). Resistance to PSD may be the most economical answer to the problem of poor seed quality due to the Diaporthe/

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Phomopsis complex. Different levels of resistance to PSD have been reported in some plant introductions (PIs) and cultivars. These include PI 82264, Delmar, PI 181550, PI 227687, PI 229358, PI 200510, PI 209908, Arksoy, PI 80837, PI 417479, PI 360841, and 0X615 (Yelen and Crittenden 1967; Athow 1973; Walters and Caviness 1973; Ross 1986; Athow 1987; Brown et al. 1987; Roy and Abney 1988; Zimmerman and Minor 1993; Anderson et al. 1994; Minor et al. 1995). There are several reports of breeding for resistance to PSD, including the release of 8 soybean lines derived from PI 200501 and Arksoy. These 8 lines showed significantly less seed infection than the susceptible cultivar Forrest (Ross 1986). The most detailed studies of resistance to Phomopsis seed infection have been done with PI 417479. Field studies in Missouri and Puerto Rico revealed 0.0% Phomopsis infection in PI 417479 at both locations in 1983 through 1985 (Brown et al. 1987). Genetic studies indicated that 2 complementary dominant genes control Phomopsis resistance in PI 417479 (Zimmerman and Minor 1993; Minor et al. 1995). PI 360841 also showed low levels of infection during the same field trials with 8.0% and 0.0% at the 2

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Abstract

Smith et al. Resistance Genes for Phomopsis in Soybean

Materials and Methods Crosses were made between PI 360841 and PSD-susceptible parents AP 350 and PI 91113, and between PI 360841 and PSD-resistant parents PI 80837 and MO/PS D-0259. F1 plants from those crosses were grown in the greenhouse. F2 populations were planted in the field at Kibler, AR in May 2005. Seed were spaced approximately 15 cm apart in 1.8m-long rows with parents planted along with the rows of F2 plants. Test rows were spaced 0.90 m apart and border rows of

Williams 82 were planted on row ends and sides around the testing block to provide uniform environmental conditions. Spores from isolate EJISO of P. longicolla tested previously for pathogenicity on soybean (Jackson 2000; Jackson et al. 2005) were streaked onto plates of potato dextrose agar (Difco, Sparks, MD) and incubated at room temperature (18–25 °C) under florescent lights with a 14-h photoperiod for 18–20 days. Sporulating cultures were flooded with sterile deionized water 3 times and agitated to dislodge conidia. Spore concentrations were adjusted to approximately 2.5 105 spores per milliliter with a hemacytometer. Inoculum was applied in the late afternoon and evening, 7:00–9:00 PM, using a backpack sprayer to inoculate parent plants and F2 populations. Overhead irrigation (2.5 cm) was applied the following morning. All F2 populations and parent plants were inoculated 3 times in 7- to 10-day intervals beginning at the R5 growth stage and finishing at R7 (Fehr et al. 1971). Seed from the bottom 60 cm of the plants from the parents and each F2 population were harvested about 7 days after the R8 growth stage. Forty seed per plant were surface disinfested with 0.5% NaOCl amended with 5 drops of Tween 20/L and rinsed twice in sterile water for 3 min. The disinfected seed were then plated on PDA amended after autoclaving with 75 lg/ml streptomycin sulfate and 1 lg/ml Danitol (fenpropathrin) and acidified to pH 4.8 with lactic acid. Phomopsis-infected seed were recorded after 10-day incubation at 21–25 °C under fluorescent lights with a 14-h photoperiod. Phomopsis colonies were identified using colony morphology, pycnidial beaks, and spore size. Seed pathogens other than Phomopsis were also recorded, but not reported as they were not relevant to the study. The percentage of seed infection of 15 parent plants randomly selected from the 4 parent rows within each population was analyzed using analysis of variance to determine differences in infection between susceptible and resistant parents (JMP 2003; SAS Institute Inc., NC). Untransformed percentage data were used in all statistical analyses because arcsine transformation did not affect statistical differences. In the (PI 360841 AP 350) F2 population in which there was an overlap in the range of Phomopsis infection of the parents, resistant F2 plants were those with percent infection below the upper value of the 95% confidence interval (CI) of the resistant parent plants, that is, 6.39% (Table 1). For the (PI 91113 PI 360841) F2 population where there was no overlap of percent seed infection between the parents, the value used to classify resistant plants was 5.0%, the highest percent seed infection of PI 360841. In the (MO/PSD-0259 PI 360841) and (PI 360841 PI 80837) F2 populations, resistant plants were those that had percent seed infection equal to or less than the highest percent seed infection of either parent. These were 5.0% and 15.0% for the (MO/PSD-0259 PI 360841) F2 and the (PI 360841 PI 80837) F2 populations, respectively. Chi-square tests were used to determine the goodness of fit of observed F2 segregation data to genetic models for 1, 2, or 3 dominant genes.

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locations (Brown et al. 1987). Field and greenhouse tests confirmed that PI 360841 has a high level of resistance similar to PI 417479 (Jackson et al. 2005). However, resistance in PI 360841 has not been characterized. PI 417479 was used to develop a resistant breeding line MO/PSD-0259 (Minor et al. 1993). In Arkansas, seed of MO/PSD-0259 were shown to be resistant to infection despite pod and stem blight (Jackson 2000). Jackson showed that resistance to PSD in MO/PSD-0259 was controlled by a single dominant gene (Jackson et al. 2005). It appeared that one of the resistance genes in PI 417479 was lost during the breeding process. Using simple sequence repeats (SSR) markers, Jackson et al. (2008) found that resistance in MO/ PSD-0259 was linked to Sat_317 (5.9 cM) and Sat_120 (12.7 cM) on molecular linkage group F. PI 80837 has been reported to be resistant to PSD (Athow 1987; Brown et al. 1987; Minor et al. 1995). Seed from inoculated, nonwounded pods of PI 80837 had less PSD than seed from inoculated wounded pods of PI 80837 and the susceptible cultivar Amsoy 71 (Roy and Abney 1988). This PI was found to have significantly less seed infection (,6.0%) than susceptible PI 361093 (37.0%) in field trials (Ploper et al. 1992). In addition, PI 80837 had less pod and stem blight in the field and greenhouse when inoculated with P. longicolla, than other PIs and cultivars tested (Jackson et al. 2005). Resistance to PSD in PI 80837 was shown to be conferred by one dominant gene that is different from that derived from MO/PSD-0259 (Jackson et al. 2005). In a molecular study using SSR markers, PSD resistance in PI 80837 was found linked to Sat_177 (4.3 cM) and Sat_342 (15.8 cM) on molecular linkage group B2 (Jackson et al. 2008). PI 360841 has been shown to have PSD resistance equal to or better than that found in PI 417479. It was suggested that PI 417479 and PI 360841 were the same genotype based on similar levels of PSD, morphological characteristics, and maturity dates (Brown et al. 1987). However, data from Germplasm Resources Information Network (GRIN 2007) place the 2 PIs in different maturity groups, with different shatter ratings, average seed size, and Phytophthora root rot ratings. This suggests that PI 360841 and PI 417479 are not the same. The objectives of this research were to 1) characterize resistance to PSD in PI 360841 by inheritance studies and 2) determine if the resistance genes for PSD in PI 360841 are different from that in PI 80837 and in MO/PSD-0259 by allelism test.

Journal of Heredity 2008:99(6) Table 1. Mean incidence, 95% CI, and range of Phomopsis seed infection of resistant and susceptible parents inoculated with Phomopsis longicolla in the field in 2005

Parents

a

AP 350 (S) PI 91113 (S) PI 360841 (R) MO/PSD-259 (R) PI 80837 (R)

Number of plants 15 15 15 15 15

Phomopsis seed infection (%) Mean 18.5a 25.2a 2.0c 1.5c 5.3b

b

Range 0.0–40.0 7.5–45.0 0.0–5.0 0.0–5.0 2.5–15.0

CI

c

14.1–22.9 20.7–29.6 2.4–6.4 0.3–2.7 3.8–6.9

a

S, susceptible; R, resistant.

b

Means followed by the same letters are not significantly different at P 0.05. 95% CI.

c

Table 2. Reactions to Phomopsis seed infection of PSDresistant and PSD-susceptible parents and F2 populations inoculated with Phomopsis longicolla in the field in 2005

Parents/populations AP 350 (S) PI 360841 (R) (PI 360841 AP 350) F2 PI 91113 (S) PI 360841 (R) (PI 91113 PI 360841) F2 F2 Total (df 5 2) F2 Pooled (df 5 1) Heterogeneity (df 5 1)

Number of plants

Chi square

R

S

Model

Value

Probability

1 15 56

14 0 32

9:7

1.95

0.25–0.10

0 15 50

15 0 45

9:7

0.51

0.50–0.25

106

77

2.46 0.21 2.25

0.75–0.50 0.25–0.10

Results

Figure 1. Susceptible parent PI 91113 (left) showing 57% Phomopsis seed infection and resistant parent PI 360841 (right) showing no Phomopsis seed infection.

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S, susceptible; R, resistant; df, degrees of freedom.

model for 2 complementary dominant genes plus a third dominant gene (Tables 3 and 4). The Chi-square tests for (PI 360841 PI 80837) F2 population data fit a 63R:1S for 3 different dominant genes (Table 3). The one susceptible plant in this population had 30% seed infection, whereas resistant plants ranged from 0.0% to15.0%.

Discussion PSD is very sensitive to environment and field conditions, which make it difficult to screen for resistance in the field unless steps are taken to optimize disease development (Zimmerman and Minor 1993). We tried to optimize conditions for Phomopsis seed infection by planting in a field having a history of soybean production; artificially inoculating the plants 3 times from R5 to R7 and having the test plots overhead irrigated the day following evening inoculations. It appeared that the artificial inoculation was effective and the field infection was adequate to separate the susceptible and resistant parents (Table 1). One plant in the resistant PI 80837 parent had a seed infection of 15%. This was possibly due to cracks in the pod wall and the heavy inoculum amounts used for the artificial inoculations. Additionally, there was one plant of the susceptible parent AP 350 which had 0.0% infection. This may have resulted from a seed mix or an escape from the infection. Where there was an overlap in the range of Phomopsis infection of the parents, resistant F2 plants were those with percent infection below the upper value of the 95% CI of the resistant parent plants. Although reciprocal crosses of the susceptible parents with resistant PI 360841 were unsuccessful, the frequency distributions of plants in all the F2 populations were skewed toward the distribution of PI 360841 with a good fit to a ratio of 9R:7S, providing evidence that resistance to PSD is qualitatively inherited with dominance. Reciprocal crosses would have revealed any evidence of maternal inheritance;


Environmental conditions and inoculum levels were favorable for Phomopsis seed infection at the Kibler site in 2005. The susceptible parents, AP 350 and PI 91113, had significantly greater levels of Phomopsis seed infection than the resistant PI 360841 (Figure 1). The mean infection for AP 350 and PI 91113 was 18.5% and 25.2%, respectively. There was no significant difference in seed infection between PI 360841 (2.0%) and PSD-resistant MO/PSD0259 (1.5%). However, PI 360841 and MO/PSD-0259 had significantly less seed infection than PSD-resistant PI 80837 (5.3%) (Table 1). Chi-square test for segregation of the (PI 360841 AP 350) F2 population showed a good fit a 9 resistant:7 susceptible (9R:7S) model for 2 complementary dominant genes in PI 360841. Similarly, the (PI 91113 PI 360841) F2 population exhibited a segregation ratio of 9R:7S as expected for 2 complementary dominant genes for resistance in PI 360841. A heterogeneity test for a 9R:7S model done on the 2 resistant susceptible F2 populations showed that resistance in PI 360841 behaved the same in both crosses (Table 2). The Chi-square tests for the (MO/PSD-0259 PI 360841) F2 population data showed a good fit to a 57R:7S

Smith et al. Resistance Genes for Phomopsis in Soybean Table 3. Reactions to Phomopsis seed infection of resistant parents and F2 populations inoculated with Phomopsis longicolla in the field in 2005 Number of plantsa

Chi square

Parents/populations

R

S

Model

Value

Probability

MO/PSD-0259 (R) PI 360841 (R) (MO/PSD-0259 PI 360841) F2 PI 360841 (R) PI 80837 (R) (PI 360841 PI 80837) F2

15 15 101

0 0 14

57:7

0.18

0.75–0.50

15 15 89

0 0 1

63:1

0.12

0.75–0.50

R, resistant; S, susceptible.

Table 4. A proposed genetic model for resistance to Phomopsis seed decay in F2 population from PI 360841 (R1R1 R2R2 r3r3) MO/PSD-0129 (r1r1 r2r2 R3R3) F2 genotypes

Frequency

F2 reaction

R1R 1R2R2 R3R3 R1R 1R2R2 R3r3 R1R1 R2R2 r3r3 R1R 1R2r2 R3R3 R1R 1R2r2 R3r3 R1R1 R2r2 r3r3 R1R1 r2r2 R3R3 R1R1 r2r2 R3r3 R1R1 r2r2 r3r3 R1r1 R2R2 R3R3 R1r1 R2R2 R3r3 R1r1 R2R2 r3r3 R1r1 R2r2 R3R3 R1r1 R2r2 R3r3 R1r1 R2r2 r3r3 R1r 1r2r2 R3R3 R1r1 r2r2 R3r3 R1r1 r2r2 r3r3 r1r1 R2R2 R3R3 r1r1 R2R2 R3r3 r1r1 R2R2 r3r3 r1r1 R2r 2R3R3 r1r1 R2r2 R3r3 r1r 1R2r2r 3r3 r1r1 r2r2 R3R3 r1r1 r2r2 R3r3 r1r1 r2r2 r3r3 Total

1 2 1 2 4 2 1 2 1 2 4 2 4 8 4 2 4 2 1 2 1 2 4 2 1 2 1 64

R R R R R R R R S R R R R R R R R S R R S R R S R R S 57R:7S

R, resistant to Phomopsis seed decay; S, susceptible to Phomopsis seed decay.

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however, data from previous studies of PSD suggest that resistance is under nuclear genetic control and not controlled by a cytoplasmic component (Zimmerman and Minor 1993; Jackson et al. 2005). Segregation ratios for both the (PI 360841 AP 350) and (PI 91113 PI 360841) F2 populations were not different from 9R:7S as expected for 2 complementary dominant genes for resistance in PI 360841. In addition, the

(PI 91113 PI 360841) F2 data also fit a 1R:1S ratio (Table 2) which is not expected for any meaningful genetic model. However, it is unlikely that PI 360841 would be heterozygous for one dominant gene for PSD resistance. PI 360841 is a pure line, and if heterozygous, there would have been susceptible plants in the parent population. A heterogeneity test for the (PI 360841 AP 350) and (PI 91113 PI 360841) F2 populations fit the 9R:7S model, indicating that resistance from PI 360841 behaved similarly in both susceptible backgrounds. Brown et al. (1987) suggested that PI 360841 and PI 417479 are the same or closely related genotypes based on their similar agronomic characteristics and PSD resistance. Both PIs originated from Japan. Brown et al. (1987) suggested that the 2 are the same genotype but were given different PI numbers because they were submitted to the Germplasm Collection at separate times; PI 360841 in 1971 and PI 417479 in 1977. However, the GRIN showed that PI 417479 and PI 360841 belong to different maturity groups and have different shatter and Phytophthora resistance ratings. It is important to note that PSD resistance in PI 417479 was also found to fit a 9R:7S model for inheritance conferred by 2 complementary dominant genes in a previous study (Zimmerman and Minor 1993), again raising the question of whether PI 360841 and PI 417479 are the same genotype. Nevertheless, this PI identity controversy is not conflicting with our research finding but supportive of our conclusion that PI 360841 carries 2 complementary genes for PSD resistance. MO/PSD-0259 is a highly PSD-resistant line derived from PI 417479 and was shown to have a single dominant gene for PSD resistance (Jackson et al. 2005). The F2 population of (MO/PSD-0259 PI 360841) fit a 57R:7S model (Tables 3 and 4) for 2 complementary dominant genes plus a third different dominant gene conferring PSD resistance. This is additional evidence that resistance in PI 360841 is conferred by 2 complementary dominant genes and that the gene in MO/PSD-0259 is different from those in PI 360841. The 57R:7S segregation would not be expected if the resistance gene in MO/PSD-0259 were the same as either of the 2 complementary genes in PI 360841, in which case there would be no segregation for susceptibility. Because MO/PSD-0259 was derived from PI 417479 and presumed to have inherited its resistance from PI 417479, the results from this study, along with evidence from GRIN, seem to indicate that PI 417479 and PI 360841 are not the same. Crossing PI 360841 with PI 417479 and screening the F2 population for resistance should reveal whether they have the same resistance genes. If they do, there should be no segregation in the F2 population for susceptibility to PSD. Alternatively, screening both PI with a set of molecular markers would show if they are genetically the same. PI 360841 was also crossed with PI 80837 to determine whether they have the same or different genes for resistance to PSD. Resistance in PI 80837 was shown previously to be conferred by a single dominant gene that is different from the dominant gene for PSD resistance in MO/PSD-0259

Journal of Heredity 2008:99(6)

Funding This research was supported by the Arkansas Soybean Promotion Board and Arkansas Agricultural Experiment Station.

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Received February 8, 2008 Accepted April 14, 2008 Corresponding Editor: Lisa J. Rowland


(Jackson et al. 2005). In this study, segregation in the (PI 360841 PI 80837) F2 population closely fit a 63R:1S ratio as expected for a 3 dominant gene model. However, we believe that the one susceptible plant in the population was a mixture or possibly a volunteer and that there was virtually no segregation for susceptibility to PSD. That would be consistent with the results obtained with the other crosses, showing that 2 dominant genes are involved and that the dominant gene for PSD resistance in PI 80837 is the same as one of the dominant genes in PI 360841. The results of this study show that PI 360841 carries 2 complementary dominant genes that confer strong resistance to Phomopsis seed infection. Furthermore, these 2 genes in PI 360841 are different from the single dominant gene for resistance in MO/PSD-0259; PI 360841 has one resistance gene in common with PI 80837. Screening of F2:3 lines should help confirm the mode of inheritance and expression of these genes for PSD resistance. This was attempted during the 2006 growing season, but because of adverse field conditions due to flooding, the F2:3 populations were lost. These results reveal one new gene for PSD resistance. This gene along with the different genes conferring resistance to PSD in MO/PSD-0259 and PI 80837 offers new opportunities for breeders to develop lines with strong PSD resistance and good agronomic qualities. Because of the multiple genes, the development of molecular markers linked to these genes for resistance would clarify the mode of inheritance and expression of these genes (Jackson et. al. forthcoming). Molecular markers would also help in incorporating these genes in a breeding program for resistance to PSD. Research is currently underway to confirm these results and to identify genetic markers.