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We develop a quantitative genetic model for conditional strategies that incorporates the ecological realism of previous strategic models. Similar to strategic models, the results show that environmental heterogeneity, cue reliability, and environment-dependent fitness trade-offs for the alternative tactics of the conditional strategy interact to determine when conditional strategies will be favored and that conditional strategies should be a common form of adaptive variation in nature. The results also show that conditional and unconditional development can be maintained in one of two ways: by frequency-dependent selection or by the maintenance of genetic variation that exceeds the threshold for induction. We then modified the model to take into account variance in exposures to the environmental cue as well as variance in response to the cue, which allows a derivation of a dose-response curve. Here the results showed that increasing the genetic variance for response both flattens and shifts the dose-response curve. Finally, we modify the model to derive the dose-response curve for a population polymorphic for a gene that blocks expression of the conditional strategy. We illustrate the utility of the model by application to predator-induced defense in an intertidal barnacle and compare the results with phenotypic models of selection.

The conditional expression of alternative phenotypes underlies the production of almost all life history decisions and many dichotomous traits, including male alternative reproductive morphs and behavioral tactics. Changes in tactic fitness should lead to evolutionary shifts in developmental switch points that underlie tactic expression. We used experimental evolution to directly test this hypothesis by rearing ten generations of the male-dimorphic mite Rhizoglyphus echinopus in either simple or three-dimensionally complex habitats that differed in their effects on morph fitness. In R. echinopus, fighter males develop weapons used for killing rivals, whereas scrambler males do not. Populations evolving in complex 3D habitats, where fighters had reduced fitness, produced fewer fighters because the switch point for fighter development evolved to a larger critical body size. Both the reduced mobility of fighter males and the altered spatial distribution of potential mates and rivals in the complex habitat were implicated in the evolutionary divergence of switch point between the habitats. Our results demonstrate how abiotic factors like habitat complexity can have a profound effect on evolution through sexual selection.

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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.