Although transgenic crops have been grown commercially since 1992, most cultivars were released with only cursory ecological risk assessments. One ecological risk is that transgenes could move into wild populations following transgenic crop-wild hybridization. Crop-wild hybridization and subsequent introgression provides wild plants with novel traits, and these traits could potentially alter the size and dynamics of wild plant populations. Crop-wild hybridization is common, indicating that transgene introgression from transgenic crops into wild populations is likely when the crop and wild relative co-occur. Wild squash, Cucurbita pepo, is native to south-central US and northern Mexico, and this range overlaps with commercial squash production. Cultivated squash readily interbreeds with its wild progenitor, and non-transgenic cultivated alleles have been identified in wild squash populations. Wild and cultivated squash are susceptible to several mosaic viruses. Because virus infection can drastically reduce yield, virus-resistant transgenic squash was developed, deregulated in the US, and was first available for commercial use in 1994. Though virus-resistant transgenic squash has been planted for close to fifteen years, little is known about the effects of virus and transgenic virus resistance on wild squash population dynamics.
Results/Conclusions
To better understand the potential effects of transgenic resistance on wild squash population dynamics we developed a stochastic population dynamics model. In this model we assume that transgenic resistance has already moved into and increased in frequency in wild populations; thus, we are interested in the consequences, rather than the risk of, introgression. To parameterize our model we conducted field surveys to estimate the prevalence of virus infection in wild populations and we performed common garden experiments in which we evaluated the effect of virus infection and transgenic resistance on plant fitness. In addition, we obtained additional estimates of these parameters from the literature. Results from our common garden experiments indicate that the timing of virus infection relative to flower and fruit production has a large effect on the fitness consequences of virus infection; thus, the fitness effects of infection may be more variable in the wild than is apparent from many common garden studies. Model output will include estimates of virus prevalence and fitness consequences of infection and transgenic virus resistance that would greatly alter either the size or dynamics of wild squash populations.
