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This article in CS

  1. Vol. 40 No. 4, p. 954-958
    Received: July 28, 1999

    * Corresponding author(s): mbrick@lamar.colostate.edu
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Inheritance of Resistance to Fusarium Wilt in Two Common Bean Races

  1. Hugh Crossa,
  2. Mark A. Brick *a,
  3. Howard F. Schwartzb,
  4. Lee W. Panellac and
  5. Patrick F. Byrnea
  1. 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


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.

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