transgenic rotated maize or a 3-year rotation with unattractive wheat were the most effective management strategies for slowing the evolution of resistance. Each of these strategies kept the resistance allele frequency at low values (≤0.02) over 15 years with each type of gene expression (Fig.
8.6). Only the repellent soybean and transgenic maize were economically valuable as well and, of these two technologies, only transgenic maize is close to commercialization. This model did not consider resistance to transgenic maize during the 15-year time horizon.
sition in non-transgenic maize fields to published literature. Dispersal rates produced adult female WCR populations in first-year maize fields comparable to observations of Godfrey and Turpin (1983). The period of oviposition in the model matched observations by Hein and Tollefson (1985).
Expression of the allele for resistance to the transgenic toxin and toxin dose in the maize plant were the two most important factors affect- ing resistance development. A dominant resistance allele allowed rapid evolution of resistance to transgenic maize, whereas a recessive resistance allele delayed resistance more than 99 years. With high dosages of toxin and additive expression of resistance, the time required to reach 3%
resistance allele frequency ranged from 13 to more than 99 years.
Table 8.1 shows how refuge size, configuration and dose of toxin affect the length of time it takes for the resistant allele frequency to reach 3% when gene expression is additive. Without a refuge in continuous transgenic maize, the length of time to reach 3% resistant allele frequency increases as toxicity decreases. In the block configuration, with toxin doses that allowed 0.001 or fewer susceptibles to survive, the resistant allele frequency did not exceed 3% in 99 years. The number of years nec- essary to reach 3% resistant allele frequency ranged from 5 at 5% refuge with 5% of susceptibles surviving, to 9 for 30% refuge and 20% of sus- ceptibles surviving in transgenic maize (Table 8.1).
Heterogeneous Landscapes and Variable Behaviour 163
Fig. 8.6. Resistance allele frequency in year 15 for four management strategies: 2-year rota- tion (2-year), repellent soybeans (Rsoy), transgenic-rotated maize (Trans) and a 3-year rota- tion with unattractive wheat (3-year UE), with the allele for rotation resistance as recessive (X> y), additive (x= y) or dominant (Y> x).
1.0 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0.0
Y allele frequency
x= y
2-year Rsoy Trans 3-year UE
Y> x X> y
chap08.qxd 15/11/04 2:51 PM Page 163
A row-strip configuration resulted in much shorter times to reach 3%
resistant allele frequency compared with the block configuration (Table 8.1). If the concentration of toxin in the crop corresponds to a survival rate for susceptible larvae of 0.001, the allele frequency for resistance to transgenic maize never reached 3% resistant allele frequency with the block refuge configuration. However, with a row-strip configuration, the time to reach 3% resistant allele frequency ranged from 13 years at 5%
refuge to 34 years at 30% refuge.
Submodels of the probability of females finding a mate (Kuno, 1978) were incorporated to address the possibility of genetic isolation in block refuge configurations. WCR are protandrous, with males emerging about 1 week prior to the first females. The sex ratio of beetles observed in first- year maize and soybeans suggested that the male dispersal rate was one- quarter the dispersal rate of adult females. Given the additional week, even the lowest levels of male dispersal were enough to mate all teneral females in all maize fields. Consequently, the dispersal rate for adult beetles did not significantly affect the time to 3% allele frequency with a block configuration.
When sublethal effects of transgenic maize cause susceptible pheno- types to emerge later than normal in a block configuration, resistance can develop much faster when expression of resistance is recessive. When resistance to transgenic maize is recessive and only homozygous suscep- tibles are delayed 6 days, the time to 3% allele frequency was shortened in the two lowest toxin doses. For 10% survival of susceptibles, the time to 3% allele frequency ranged from 51 to 95 years, respectively, for 5 to 30% refuge. For 20% survival of susceptibles, the time to 3% allele fre- quency ranged from 22 to 46 years, respectively. These time periods should be compared to the standard 99 plus years. With recessive expres-
164 D.W. Onstad et al.
Table 8.1.Year in which the allele frequency for resistance to the transgenic toxin reached 0.03 in a region of continuous maize (no rotated maize), additive expression of resistance and an initial allele frequency of 0.0001. Survival of susceptibles is a function of the dose of toxin.
Survival of susceptibles
Proportion in refuge 0.0 0.001 0.05 0.2
No refuge
0.0 1 3 3 6
Refuge as adjacent block
0.3 > 99 > 99 7 9
0.2 > 99 > 99 6 8
0.05 > 99 > 99 5 6
Refuge as row strips
0.3 > 99 34 4 6
0.2 > 99 29 3 5
0.05 52 13 2 4
sion where both susceptible phenotypes are delayed 6 days, the allele frequency did not change in the 99 years of using transgenic maize. When the homozygous susceptibles were delayed by 3 to 9 days with additive allele expression, resistance developed more quickly relative to the stan- dard, but the number of years required to reach 3% allele frequency did not change by more than 1 year (and then only for the lowest dose).
Storer (2003) created a stochastic, spatially explicit computer model that simulates the adaptation by WCR to transgenic maize. The model reflects the ecology of the rootworm in much of the Corn Belt of the USA.
It includes functions for crop development, egg and larval mortality, adult emergence, mating, egg laying, mortality and dispersal to simulate the population dynamics of WCR and compares alternative methods of rootworm control. The allele for resistance to transgenic maize varies from incompletely recessive to incompletely dominant, depending on the efficacy of the toxin in the crop. Validation was achieved by comparing populations from the model with field data on population dynamics, and with field data documenting WCR adaptation to cyclodienes and organophosphates. The model was used to compare the rate at which the resistance allele spread through the population under different refuge deployment scenarios, and with crops of different efficacy.
For a given refuge size, the model indicated that placing the refuge in a block within a transgenic maize field would be likely to delay WCR resistance longer than planting the refuge in separate fields in varying locations. If a portion of the refuge were planted in the same fields or the same in-field blocks each year, WCR adaptation would be substantially delayed.
Storer (2003) conducted a brief analysis of the need for insecticide use in refuges because results suggested that resistance to transgenic maize would be unaffected by soil insecticide treatment in the refuge. In this analysis, refuge insecticide treatments were warranted for the first few years of transgenic deployment until the regionwide population was reduced. The smaller the proportion of fields planted to non-transgenic maize, the smaller the proportion of them that require treatment.