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CROP BREEDING, GENETICS & CYTOLOGY

Inheritance of Resistance to Fusarium Wilt in Two Common Bean Races

^a Dep. of Soil and Crop Sciences, Colorado State Univ., Fort Collins, CO 80523 USA
^b Dep. of Bioagricultural Sciences and Pest Management, Colorado State Univ., Fort Collins, CO 80523 USA
^c USDA-ARS Crops Research Laboratory, Fort Collins, CO 80523 USA

mbrick{at}lamar.colostate.edu

	ABSTRACT

TOP NOTES ABSTRACT INTRODUCTION Materials and methods Results and discussion Conclusions REFERENCES

 
Fusarium wilt in common bean (Phaseolus vulgaris L.) caused by Fusarium oxysporum Schlechtend. Fr. forma specialis phaseoli Kendrick and Snyder (Fop) occurs worldwide and can result in severe yield loss. Because cultural methods to control disease loss are not completely effective, cultivars with genetic resistance are needed. The objectives of this study were to determine whether genetic control of resistance to Fop race 4 differs between germplasm of races Durango and Mesoamerica of common bean and to estimate heritability of resistance found in race Mesoamerica. Resistant and susceptible lines of races Durango and Mesoamerica were crossed within races to produce F₂ and F₃ progeny. Reaction to Fop was evaluated using a root-dip inoculation method and scored using a CIAT disease severity scale from one to nine. F₂ populations derived from race Durango parents showed a 3:1 (resistant/susceptible) plant segregation ratio, and F₃ progeny tests confirmed that resistance was controlled by a single dominant gene. F₂ data from crosses between parents of race Mesoamerica had continuous distributions for reaction to Fop race 4, suggesting polygenic control of resistance. The narrow-sense heritability estimate derived from midparent–offspring regression of 10 F₂ populations derived from Mesoamerican parents was 0.85 ± 0.34, and realized heritability estimates ranged from 0.25 ± 0.19 to 0.60 ± 0.16 among five populations. The heritability estimates as well as the continuous variation in disease severity observed support the hypothesis that resistance to Fop race 4 among parents of race Mesoamerican is polygenic.

Abbreviations: DSI, disease severity index • Fop, Fusarium oxysporum forma specialis phaseoli • R, resistant • S, susceptible • SI, selection intensity

	INTRODUCTION

TOP NOTES ABSTRACT INTRODUCTION Materials and methods Results and discussion Conclusions REFERENCES

 
FUSARIUM WILT (or Fusarium yellows) in common bean occurs in the USA, South America, Europe, and Africa (Kendrick and Snyder, 1942; Armstrong and Armstrong, 1963; Abawi and Pastor-Corrales, 1990). Recent yield loss from Fusarium wilt in the High Plains region of the USA has been estimated at a minimum of 10% (Salgado et al., 1995). The first incidence of disease caused by Fop in the USA was reported by Harter (1929) in California, followed by Armstrong and Armstrong (1963) in South Carolina, and Silbernagel and Schwartz (1988) in Colorado. Following the initial observation in Colorado, an isolate of Fop was recovered by Schwartz et al. (1989) from an infected bean field in Colorado. This isolate was later found to be virulent on most bean cultivars grown in the USA (Salgado and Schwartz, 1993). The Colorado isolate was subsequently classified as Fop race 4 by Woo et al. (1996) and entered into the American Type Culture Collections as ATTC 90245. Velasquez-Valle and Schwartz (1997) found race 4 to be more virulent on many USA cultivars than isolates from Spain, Mexico, and South America.

Recommended procedures to control damage by Fop in the Central High Plains include seed treatment with fungicide, deep soil ripping, and timely application of irrigation to avoid moisture stress (Schwartz et al., 1996). Because Fop can survive in roots of several other dicot plant species such as sugar beet (Beta vulgaris L.), rotation with non-host crops such as corn (Zea mays L.), wheat (Triticum aestivum L.), and barley (Hordeum vulgare L.) is recommended to reduce inoculum carryover (Schwartz et al., 1996). In the absence of host species, chlamydospores form as thick-walled asexual spores that can survive in organic soil residues for several years (Nelson, 1981). These factors make crop rotation an incomplete control measure, and the most effective means to control economic losses from Fusarium wilt is the use of resistant cultivars (Schwartz et al., 1996).

Genetic mechanisms that control resistance to Fusarium wilt have been shown to differ between races of common bean, which are based on geographical origin (Singh et al., 1991). Sources of resistance have been found in germplasm from races Durango and Mesoamerica (Salgado et al., 1990, 1995; Velasquez-Valle et al., 1997; Velasquez-Valle and Schwartz, 1997). Salgado et al. (1995) reported that resistant lines and cultivars from race Durango possessed a single dominant gene that controls resistance to Fop race 4. In contrast, lines from race Mesoamerica appeared to possess polygenic control of resistance. However, evidence to prove inheritance was polygenic was inconclusive and they did not estimate heritability in lines or cultivars from race Mesoamerica. Because lines from races Durango and Mesoamerica appeared to differ in their inheritance patterns, Salgado et al. (1995) suggested that genes that control resistance may have evolved differently in their respective regions of origin.

The objectives of this study were to determine whether the genetics of resistance to Fop race 4 differ between common bean germplasm from races Durango and Mesoamerica and to estimate narrow-sense heritability of resistance found in race Mesoamerica.

	Materials and methods

TOP NOTES ABSTRACT INTRODUCTION Materials and methods Results and discussion Conclusions REFERENCES

 
Plant Material
To evaluate genetic control of resistance, crosses were made within parents representative of races Durango and Mesoamerica (Table 1) . Parents were selected as resistant (R) or susceptible (S) based on their reaction to Colorado isolate B-13 of Fop (ATTC 90245), originally recovered from an infected plant of pinto cultivar UI 114 in northeast Colorado and later classified as Fop race 4 by Woo et al. (1996).

Susceptible lines and cultivars representative of race Mesoamerica used as parents included, BAT 477 and HF 465 supplied by CIAT, and the navy cultivar Crestwood. Black-seeded cultivars UI 911, Jamapa, and Rio Tibagi were used as resistant parents. Ten F₂ populations derived from R x S and R x R parental crosses (Table 2) were developed.

Plant Inoculation
Plant reactions to Fop were based on a root-dip inoculation procedure developed by Pastor-Corrales and Abawi (1987) and later modified by Salgado and Schwartz (1993) and Velasquez-Valle and Schwartz (1997) to reduce the frequency of escapes. The isolate used to inoculate all plants was the Colorado isolate B-13 classified as Fop race 4 by Woo et al. (1996). Stocks of this isolate have been maintained at -4°C in culture tubes containing autoclaved, finely sieved sandy soil mixed with 2% powdered oat meal and 15% distilled water. Fifteen to 20 d before inoculation, 2 to 4 mg of stock were plated onto potato-dextrose agar, pH 5.6 ± 0.2, in petri dishes and allowed to grow at room temperature (22–25°C) to produce conidia. The day of inoculation, conidia from the cultures were suspended in distilled water, vortexed for 30 s, then filtered through cheesecloth into an erhlenmeyer flask. The filtered inoculum concentration was adjusted to 10⁶ conidia mL^-1 with a hemacytometer and poured into a 1-L beaker and stirred immediately prior to each use as a root-dip inoculum. The inoculum concentration was the same used by Salgado and Schwartz (1993) to closely represent the degree of infection observed under field conditions

Seedlings were removed from pots and excess soil removed from the root system by gentle shaking. The roots were washed with tap water to further remove soil and plants were maintained with their root systems immersed in cool tap water for 5 to 10 min. Sixteen to twenty plants were taken out of the water bath and the distal one-half to one-third of each root system was clipped with scissors. The clipped plants were placed in the inoculum solution for 5 min to allow conidia to enter wounds in the root system. Control plants for each experiment were clipped and placed in sterile, distilled water.

After inoculation, two plants were transplanted into each pot filled with sterilized fresh potting mix. Plants were grown in a greenhouse maintained at 16 and 32°C night and day temperatures, respectively. Supplemental lighting was provided to give the plants 12 h of light per day. Photosynthetically active radiation measured at the bench level inside the greenhouse with artificial light was 400 to 600 µmol m^-2 s^-1. Plants were watered immediately after transplanting and every 3 d thereafter. Three days after inoculation, the plants were fertilized with a 100-mL solution of commercial 5-10-5 liquid fertilizer with micronutrients at a concentration of 6 g 20 L^-1. Inoculated resistant and susceptible parental checks were used in each experiment to evaluate uniformity of inoculation and to confirm their disease classification.

Disease Evaluation
Plants were evaluated for reaction to Fop race 4 21 d after inoculation using the CIAT disease severity scale (Pastor-Corrales and Abawi, 1987). The CIAT scale rates plants according to percentage of leaf tissue with wilting or chlorosis as follows: 1 = no disease symptoms and completely healthy, 3 = 10% leaf surface area showing disease symptoms, 5 = 25% of leaf surface exhibiting disease symptoms as well as whole plant stunting, 7 = disease symptoms on 50% of leaves and severely stunted, and 9 = plant death. Plants classified 2, 4, 6, and 8 were intermediate to the next higher and lower classifications. A plant was considered resistant if it scored 1, 2, or 3; intermediate if it scored 4, 5, or 6; and susceptible if it scored 7, 8, or 9 in the CIAT scale. The disease severity index (DSI) was calculated as the mean score of 40 plants for parents, 30 to 50 plants for F₂ populations, and 20 to 35 plants for each F₃ family.

Methods Used to Estimate Heritability in Race Mesoamerica
Two methods were used to estimate narrow-sense heritability, midparent–offspring regression, and realized heritability. Midparent–offspring regression utilized the DSI from each of the 10 F₂ populations regressed on the calculated midparent value (Falconer and Mackay, 1996). The slope (b) of the fitted regression line is a direct estimate of narrow-sense heritability (h²) with this method. The standard error was calculated according to Hallauer and Miranda (1988). Midparent–offspring regression was considered significantly different from zero based on the F test (P < 0.05) for the slope (b) of the fitted regression equation.

Realized heritability was calculated by computing the ratio of selection gain to selection differential in the F₂ and F₃ from five of the 10 populations. F₂ plants were selfed to produce F₃ families to calculate F₃ family means. The F₃ families were evaluated twice for reaction to Fusarium wilt and an estimate of heritability was calculated for each evaluation. The formula used to estimate realized heritability was as follows:

(1)

where _F3selected is the mean disease severity rating of F₃ families derived from selected F₂ plants, _F3population is the mean disease severity rating of F₃ families derived from random F₂ plants, _F2selected is the mean disease severity rating of selected F₂ plants, and _F2population is the mean disease severity rating of F₂ population.

Selection intensity among populations varied from 0.20 to 0.06 because F₂ populations that contained few resistant individuals also had relaxed selection intensity. The standard error of each realized heritability estimate was calculated according to Prout (1962). Estimates were considered significant when the interval for the standard error did not include zero.

	Results and discussion

TOP NOTES ABSTRACT INTRODUCTION Materials and methods Results and discussion Conclusions REFERENCES

 
Race Durango
The DSI ratings among race Durango parents (Table 1) confirmed that Fisher and CO33142 were resistant and Viva was susceptible to Fop race 4. These DSI ratings were similar to previous reports (Salgado et al., 1995). A bimodal distribution of resistant and susceptible reactions among F₂ plants was observed in both populations of R x S crosses, and no intermediate reactions were observed. Segregation for resistance in the two F₂ Durango populations fit a 3:1 (R/S) ratio (P > 0.25) (Table 3) . This ratio suggested that one dominant gene controls resistance to Fop race 4. Progeny testing was conducted in the Viva x Fisher cross to detect escapes and to confirm the proposed hypothesis. Segregation within 34 F₃ families derived from resistant F₂ plants fit a 1:2 (nonsegregating/segregating) family ratio. This segregation pattern confirmed the dominant single gene hypothesis reported by Salgado et al. (1995). Disease reactions within the F₃ families were also dichotomous in that every plant exhibited either a resistant or susceptible reaction. The dichotomous reactions seen in both the F₂ and F₃ further support the hypothesis that one gene controls resistance to Fop race 4 among these parents representative of race Durango. Ribeiro and Hagedorn (1979) designated the gene controlling resistance to the Brazilian and South Carolina races of Fop as Fop1 and Fop2, respectively. Because Woo et al. (1996) concluded that isolates of Fop from Colorado (race 4) and South Carolina (race 1) were distinct races, genes controlling resistance to the Colorado and South Carolina race require different designations. We propose to designate the gene controlling resistance to Fop race 4 in the cultivar Fisher as Fop4.

View this table: [in this window] [in a new window]   Table 3 Segregation ratios, expected ratios, 2, and probability (P) within two F2 common bean populations derived from resistant by susceptible crosses between parents of race Durango, and family segregation among F3 families derived from resistant F2 plants

Race Mesoamerica
In contrast to the dichotomous reactions observed among plants in populations derived from race Durango, the distributions of disease ratings for F₂ plants from populations derived from crosses between parents from race Mesoamerica were continuous on the CIAT disease severity scale. F₂ distributions were near normal, but some were slightly skewed to the susceptible end of the scale. Parental lines used in this study (Table 1) were also evaluated by Salgado et al. (1995) and found to have similar DSI scores. Segregation patterns derived from crosses between parents in the Mesoamerican race did not fit any simple genetic models that could be confirmed in the F₃. The continuous distributions among plants in the F₂ populations suggested that inheritance of resistance to Fop in race Mesoamerica differs from race Durango and led to the following analyses using a polygenic model.

Midparent–offspring regression analysis using 10 F₂ populations provided a narrow-sense heritability (h²) estimate of 0.85 ± 0.34 (Fig. 1) . The estimate suggests that resistance to Fop among the parents used in this study was heritable. The normal continuous distribution of individuals within each of the F₂ populations and h² results suggest that inheritance of resistance is controlled in an additive manner. Because this experiment was not replicated across environments, environmental effects and genotype x environment interactions were not measured. Regression estimates have been found to overestimate heritability by confounding effects of environment and genotype x environment interaction (Chiyembekeza et al., 1993).

View larger version (10K): [in this window] [in a new window]   Fig. 1 Midparent–offspring regression for F2 population means regressed on the midparent value from crosses between common bean parents of race Mesoamerica

Significant heritability estimates in these studies ranged from 0.25 ± 0.19 to 0.85 ± 0.34. The standard error interval for estimates obtained from midparent–offspring regression overlapped with the standard error intervals for all but one significant h²_R estimate. The observations from two methods to estimate heritability, as well as the wide range of variation observed in disease severity, support the hypothesis that resistance to Fop among parents of race Mesoamerica used in this study is polygenic and moderately heritable.

	Conclusions

TOP NOTES ABSTRACT INTRODUCTION Materials and methods Results and discussion Conclusions REFERENCES

 
The results of these studies confirm that germplasm from races Durango and Mesoamerica possess different genetic mechanisms for resistance to Fusarium wilt caused by Fop race 4. The results are in agreement with earlier studies conducted by Salgado et al. (1995) that concluded that genes that control resistance in germplasm from race Durango is controlled by a single dominant gene and present new evidence that confirms resistance in germplasm representative of race Mesoamerica is polygenic and moderately heritable.

	NOTES

TOP NOTES ABSTRACT INTRODUCTION Materials and methods Results and discussion Conclusions REFERENCES

 
Research supported in part by the Colorado Agriculture Experiment Station.

Received for publication July 28, 1999.

	REFERENCES

TOP NOTES ABSTRACT INTRODUCTION Materials and methods Results and discussion Conclusions REFERENCES

 

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