Figure 1.

Responses of split broods of F₁ progeny to four toxins. The first letter of each family name denotes the strain of the female parent (Q = NO-QA, L = LAB-P). Families are arranged from lowest (left) to highest mortality caused by Cry1Aa. Two or three groups of 10 or 11 larvae from each family were tested against each toxin (n = 80–121 larvae per family). Concentrations were 100 mg of Cry1A toxin per liter and 10 ml of formulated Cry1F per liter. Bars show mean mortality plus one standard error. Mortality was genetically correlated between all six pairs of toxins as determined by analysis of arcsine-transformed data (Cry1Aa/Cry1Ab: r = 0.80, P = 0.016; Cry1Aa/Cry1Ac: r = 0.71, P = 0.047; Cry1Aa/Cry1F: r = 0.79, P = 0.021; Cry1Ab/Cry1Ac: r = 0.89, P = 0.0032; Cry1Ab/Cry1F: r = 0.99, P = 5 × 10⁻⁶; Cry1Ac/Cry1F: r = 0.86, P = 0.0056; df = 6 for each correlation). Two-way ANOVA of the arcsine-transformed data revealed significant effects of family (df = 7, 88, F = 46.4, P < 0.0001), toxin (df = 3, 88, F = 9.3, P < 0.0001), and family by toxin interaction (df = 21, 88, F = 2.15, P = 0.012).