JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. Ecological Society of America is collaborating with JSTOR to digitize, preserve and extend access to Ecology.Abstract. Phenotypic plasticity is a widespread and often adaptive feature of organisms living in heterogeneous environments. The advantages of plasticity seem particularly clear in organisms that show environmentally cued switches between alternative morphs. Information concerning the presence and nature of variation underlying the induction of these morphs, especially under field conditions, would be valuable. Here we examined the basis for variation underlying a predator-induced defense in an intertidal barnacle (Chthamalus anisopoma). In a previous experiment, juvenile barnacles were exposed to a predatory gastropod (Acanthina angelica). Some of these individuals were induced to develop as a predation-resistant form, but other individuals developed as the default, undefended morph. Here we tested two alternative explanations for this observation. One, the "continuoussensitivity" model, holds that there is normally distributed genetic variation for sensitivity to the cue. This model predicts that, given sufficient exposure to the predator, all individuals would develop as the induced form; it suggests that the previous findings resulted from an insufficient dose of the cue. The second model, the "discontinuous-sensitivity" model, asserts that there is a genetic polymorphism for inducibility such that some individuals are not able to respond to the cue. This model suggests that, with repeated exposures to the predator, the resulting dose-response curve would reach an asymptote at <100%. We conducted a dose-response experiment in order to contrast these two alternatives, and to examine an expectation generated by life-history theory, namely, that repeated exposure to the predator would induce maturity at a younger age. With respect to the life-history prediction, we found no evidence to suggest that repeated exposure of juvenile barnacles to Acanthina affected the age at maturity, even though we found strong evidence for sizeselective attack by this predator. With respect to variation underlying induction to the defended morph, we obtained a dose-response curve showing a significant asymptote at about 22% induction, which is inconsistent with the continuous-sensitivity model. Hence the results indicate the possibility of a developmental polymorphism in the barnacle, but no indication of life-history shifts in response to the predator.
Phenotypic plasticity is a widespread and often adaptive feature of organisms living in heterogeneous environments. The advantages of plasticity seem particularly clear in organisms that show environmentally cued switches between alternative morphs. Information concerning the presence and nature of variation underlying the induction of these morphs, especially under field conditions, would be valuable. Here we examined the basis for variation underlying a predator‐induced defense in an intertidal barnacle (Chthamalus anisopoma). In a previous experiment, juvenile barnacles were exposed to a predatory gastropod (Acanthina angelica). Some of these individuals were induced to develop as a predation‐resistant form, but other individuals developed as the default, undefended morph. Here we tested two alternative explanations for this observation. One, the “continuous‐sensitivity” model, holds that there is normally distributed genetic variation for sensitivity to the cue. This model predicts that, given sufficient exposure to the predator, all individuals would develop as the induced form; it suggests that the previous findings resulted from an insufficient dose of the cue. The second model, the “discontinuous‐sensitivity” model, asserts that there is a genetic polymorphism for inducibility such that some individuals are not able to respond to the cue. This model suggests that, with repeated exposures to the predator, the resulting dose–response curve would reach an asymptote at <100%. We conducted a dose–response experiment in order to contrast these two alternatives, and to examine an expectation generated by life‐history theory, namely, that repeated exposure to the predator would induce maturity at a younger age. With respect to the life‐history prediction, we found no evidence to suggest that repeated exposure of juvenile barnacles to Acanthina affected the age at maturity, even though we found strong evidence for size‐selective attack by this predator. With respect to variation underlying induction to the defended morph, we obtained a dose–response curve showing a significant asymptote at about 22% induction, which is inconsistent with the continuous‐sensitivity model. Hence the results indicate the possibility of a developmental polymorphism in the barnacle, but no indication of life‐history shifts in response to the predator.
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