Abstract
BackgroundIn many insect species, fitness trade-offs exist between maximizing body size and developmental speed. Understanding how various species evolve different life history strategies requires knowledge of the physiological mechanisms underlying the regulation of body size and developmental timing. Here the roles of juvenile hormone (JH) and insulin/target of rapamycin (TOR) signaling in the regulation of the final body size were examined in the tobacco hornworm, Manduca sexta.ResultsFeeding rapamycin to wild-type larvae decreased the growth rate but did not alter the peak size of the larvae. In contrast, feeding rapamycin to the JH-deficient black mutant larvae caused the larvae to significantly increase the peak size relative to the DMSO-fed control animals by lengthening the terminal growth period. Furthermore, the critical weight was unaltered by feeding rapamycin, indicating that in Manduca, the critical weight is not influenced by insulin/TOR signaling. In addition, post-critical weight starved black mutant Manduca given rapamycin underwent metamorphosis sooner than those that were fed, mimicking the “bail-out mechanism”.ConclusionsOur study demonstrates that JH masks the effects of insulin/TOR signaling in the determination of the final body size and that the critical weights in Drosophila and Manduca rely on distinct mechanisms that reflect different life history strategies. Our study also suggests that TOR signaling lengthens the terminal growth period in Manduca as it does in Drosophila, and that JH levels determine the relative contributions of nutrient- and body size-sensing pathways to metamorphic timing.
Highlights
In many insect species, fitness trade-offs exist between maximizing body size and developmental speed
Our findings suggest that both a body size-sensing pathway mediated by juvenile hormone (JH) and a nutrition-sensitive pathway mediated by insulin/target of rapamycin (TOR) signaling exist in Manduca and that JH normally masks the nutrition-sensitive pathway to determine the timing of metamorphosis
Rapamycin increases the peak body size of black mutant larvae but not wild-type larvae In order to determine the effect of inhibiting insulin/ TOR signaling in the wild-type and the JH-deficient black mutant larvae, fifth instar larvae were fed either a diet treated with rapamycin or dimethyl sulfoxide (DMSO)
Summary
Fitness trade-offs exist between maximizing body size and developmental speed. Understanding how various species evolve different life history strategies requires knowledge of the physiological mechanisms underlying the regulation of body size and developmental timing. Growth control has important consequences for an organism’s fitness [1]. Developmental time has important consequences for an organism’s fitness, especially in geographic locations with seasonality. These two aspects of growth, exhibit fitness trade-offs: maximizing body size tends to lengthen the developmental time, whereas accelerating developmental time necessitates the truncation of the growth period, resulting in smaller adult forms. Selection molds body size control and developmental time regulation in a taxon-specific manner [2]. The degree of conservation in the underlying mechanisms remains unclear
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