DO DYNAMICS OF CROP MATURATION AND HERBIVOROUS INSECT LIFE-CYCLE INFLUENCE THE RISK OF ADAPTATION TO TOXINS IN TRANSGENIC HOST PLANTS

Because host-plant chemistry is dynamic, chemical defenses are dynamic , and senescence in plants causes many proteins to decompose after flo wering, laboratory and field studies on transgenic crops performed ove r only part of a plant generation or part of a season may not provide sufficient data to evaluate strategies for resistance management. As a n example, we focused on the recent introduction of transgenic corn to control European corn borer, Ostrinia nubilalis (Hubner) (Lepidoptera : Pyralidae). We gathered data from literature on the life cycle of Eu ropean corn borer and con, crop maturation to study the role that phen ological relationships may play in resistance evolution. In addition, we simulated hypothetical titer declines resulting in increased surviv al in European corn borer populations infesting transgenic corn using a model of population dynamics and genetics. The relationship between European corn borer hatching period and corn maturation varies greatly from site to site and year to year. The peak of the hatching period i n the late summer generation of the European corn borer occurs at or a fter the average midpoint of the dough stage of corn. The last larvae tend to hatch after the dough stage is past and after the midpoint of the dent stage. In simulations where 5% of a region is planted with no ntransgenic corn in separate refuge plots and 95% is planted with tran sgenic corn, complete loss of titer as a result of senescence produces resistance at the 3% resistance-allele level after 5-42 yr, which is less than the 83 yr predicted by the standard model for resistance dev elopment when the transgenic corn loses no titer as a result of senesc ence. We hypothesize that genetically engineered toxins will often dec rease in leaf and stem titer as crops reach maturation. The insects fe eding and surviving on a crop during its senescence may have important consequences for the population genetics of the breakdown of host pla nt resistance.