Insect reproduction can be stimulated by exposure to sublethal doses of insecticide that kill the same insects at high doses. This bi-phasic dose response to a stressor is known as hormesis and has been demonstrated with many different insect-insecticide models. The specific mechanisms of the increased reproduction in insects following sublethal pesticide exposure are unknown, but may be related to juvenile hormone (JH), which has a major role in regulation of metamorphosis and reproductive development in insects. We tested the hypothesis that exposure to sublethal concentrations of precocene, an antagonist of JH, would not result in stimulated reproductive outputs in the green peach aphid, Myzus persicae, as can be demonstrated with many neurotoxic insecticides. We also measured JH titers and the expression of various developmental (FPPS I), stress response (Hsp60), and dispersal (OSD, TOL and ANT) genes in aphids following exposure to the same precocene treatments. We found that when aphid nymphs were treated with certain sublethal concentrations of precocene, 1.5- to 2-fold increased reproductive stimulation occurred when they became adults, but this effect subsided in the following generation. Precocene treatments to nymphs resulted in no measurable effects on JH levels in subsequent reproducing adults. Although we detected major effects on gene expression following some precocene treatments (e.g. 100- to 300-fold increased expression of some genes), there were no clear relationships between gene expression and reproductive responses for a given treatment.
Keywords: Fecundity stimulation; Gene expression; Hormesis; Myzus persicae; Precocene.
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