Transgenic technologies are a promising tool for species-specific, environmentally friendly pest management. Conditionally lethal transgenes have been developed that make males functionally sterile, and males carrying these genes can be released for autocidal control. While laboratory and field trials indicate these transgenic lethality systems are promising, comprehensive tests of efficacy and risk assessment are needed for these technologies to be widely adopted. Here, we assess the extent to which environmental conditions can cause transgene failure for a conditionally lethal transgene that generates early embryonic lethality. The transgene is an engineered pro-apoptotic protein, and we hypothesized that sub-optimal environmental conditions that activate stress responses will make the transgene less effective. To test this hypothesis, we measured lethality and gene expression of the conditionally lethal transgene across a range of temperature and nutritional conditions in Drosophila melanogaster. When embryos harboring the transgene were exposed to high or low temperatures, there was a slight but significant reduction in lethality. Further, cross-generation effects were observed, as the offspring of adults that experienced sub-optimal temperature or nutrition were also more likely to escape lethality. These reductions in lethality were not explained by transgene expression, as transcript abundance of the lethal transgene was not correlated with lethality. Thus, the mechanism explaining environmentally mediated variation in transgene efficacy is downstream of transcription. Together, our results indicate that environmental factors can influence the efficacy of conditionally lethal transgenes, and thus phenotypic plasticity in transgene susceptibility should be considered when designing and testing constructs.
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