How can mortality increase population size? A test of two mechanistic hypotheses

Abstract

Overcompensation occurs when added mortality increases survival to the next life-cycle stage. Overcompensation can contribute to the Hydra effect, wherein added mortality increases equilibrium population size. One hypothesis for overcompensation is that added mortality eases density dependence, increasing survival to adulthood ("temporal separation of mortality and density dependence"). Mortality early in the life cycle is therefore predicted to cause overcompensation, whereas mortality later in the life cycle is not. Another hypothesis for overcompensation is that threat of mortality (e.g., from predation) causes behavioral changes that reduce overexploitation of resources, allowing resource recovery, and increasing production of adults ("prudent resource exploitation"). Behaviorally active predation cues alone are therefore predicted to cause overcompensation. We tested these predictions in two experiments with larvae of two species of Aedes. As predicted, early mortality yielded greater production of adults, and of adult females, and greater estimated rate of population increase than did later mortality. Addition of water-borne predation cues usually reduced browsing on surfaces in late-stage larvae, but contrary to prediction, resulted in neither significantly greater production of adult mosquitoes nor significantly greater estimated rate of increase. Thus we have strong evidence that timing of mortality contributes to overcompensation and the Hydra effect in mosquitoes. Evidence that predation cues alone can result in overcompensation via prudent resource exploitation is lacking. We expect the overcompensation in response to early mortality will be common in organisms with complex life cycles, density dependence among juveniles, and developmental control of populations.

Finding the sweet spot: What levels of larval mortality lead to compensation or overcompensation in adult production?

“…, Abrams , Zipkin et al. , Hilker and Liz , McIntire and Juliano ). Mortality occurring before the onset of density dependence is predicted to lead to overcompensation (Jonzen and Lundberg , Abrams ), and this prediction has been supported in controlled laboratory experiments (McIntire and Juliano ).…”

“…). There is evidence for (Maciá and Bradshaw , McIntire and Juliano ) and against (Ower and Juliano ) overcompensation in container mosquitoes. None of the cited studies have tested the model of Sandercock et al.…”

“…Overcompensation has been demonstrated in response to harvest (Nicholson , Cameron and Benton , Zipkin et al. , McIntire and Juliano ), parasitism (Washburn et al. ), and real or simulated toxin exposure (Agudelo‐Silva and Spielman , Moe et al.…”

“…), but feeding preferences for the three Aedes species are unknown. Past empirical studies on overcompensation in mosquitoes have used random harvesting (McIntire and Juliano ) or predation (Nannini and Juliano ) as sources of mortality, but none have compared the two. Differences in the effects of the two mortality sources (e.g., selectivity of mortality by predators, biomass remaining as partially consumed victims, or anti‐predator behavior modifications in prey) may result in differences among these species in likelihoods or levels of overcompensation.…”

“…a–d). We further postulate that if mortality imposed by real predators and random harvest are equally unselective with respect to prey traits, they will yield similar levels of overcompensation in adult production for similar levels of mortality; alternatively, if real predators selectively remove individuals with a greater or lesser chance of dying due to density‐dependent intrinsic mortality, or if real predators have non‐consumptive effects, such as inducing reduced foraging (Abrams , McIntire and Juliano ), then we expect the two mortality sources to yield different levels of overcompensation.…”