Community Dynamics

Ecological theory indicates that increasing the number of species, the number of interactions, and the strength of these interactions all tend to make communities less stable. Conversely, stability is enhanced by strong intraspecific density dependence, low connectivity, or weak trophic links. These theoretical predictions are borne out in many fish communities. Species diversity is an important metric for ecological communities. Organizing species into groups according to size, function, or diet composition can reduce the dimensionality of fish community models. Analyses of fish communities from around the world lend support to the prediction of strong compensation within functional groups, with weaker predator–prey links among groups. Size spectra describe the distribution of individuals across size classes irrespective of their species. Qualitative models can be used to assess the indirect effects of species on each other and the overall stability of the community.

Population dynamics of mutualism and intraspecific density dependence: howθ-logistic density dependence affects mutualistic positive feedback

Mutualism describes the biological phenomenon where two or more species are reciprocally beneficial, regardless of their ecological intimacy or evolutionary history. Classic theory shows that mutualistic benefit must be relatively weak, or else it overpowers the stabilizing influence of intraspecific competition and leads to unrealistic, unbounded population growth. Interestingly, the conclusion that strong positive interactions lead to runaway population growth is strongly grounded in the behavior of a single model. This model ― the Lotka-Volterra competition model with a sign change to generate mutualism rather than competition between species ― assumes logistic growth of each species plus a linear interaction term to represent the mutualism. While it is commonly held that the linear interaction term is to blame for the model’s unrealistic behavior, we show here that a linear mutualism added to aθ-logistic model of population growth can prevent unbounded growth. We find that when density dependence is decelerating, the benefit of mutualism at equilibrium is greater than when density dependence is accelerating. Although there is a greater benefit, however, decelerating density dependence tends to destabilize populations whereas accelerating density dependence is always stable. We interpret these findings tentatively, but with promise for the understanding of the population ecology of mutualism by generating several predictions relating growth rates of mutualist populations and the strength of mutualistic interaction.

Pathogens, density dependence and the coexistence of tropical trees

There is increasing interest in the role played by density-dependent mortality from natural enemies, particularly plant pathogens, in promoting the coexistence and diversity of tropical trees. Here, we review four issues in the analysis of pathogen-induced density dependence that have been overlooked or inadequately addressed. First, the methodology for detecting density dependence must be robust to potential biases. Observational studies, in particular, require a careful analysis to avoid biases generated by measurement error, and existing studies could be criticized on these grounds. Experimental studies manipulating plant density and pathogen incidence will often be preferable, or should be run in parallel. Second, the form of density dependence is not well understood and, in particular, there are no data indicating whether pathogens cause compensating or overcompensating density responses. Owing to this, we argue that the potential for pathogen-induced density dependence to generate diversity-enhancing outcomes, such as the Janzen–Connell effect, remains uncertain, as coexistence is far more probable if density dependence is overcompensating. Third, there have been few studies examining the relative importance of intra- or interspecific density dependence resulting from pathogens (or, more widely, natural enemies). This is essentially equivalent to asking to what extent pathogens are host-specific. If pathogens are generalists, then mortality rates will respond to overall plant density, irrespective of plant species identity. This will weaken the intraspecific density dependence and reduce the diversity-promoting effects of pathogens. Finally, we highlight the need for studies that integrate observations and experiments on pathogens and density dependence into the whole life cycle of trees, because as yet it is not possible to be certain of the degree to which pathogens contribute to observed dynamics.

Intraspecific density dependence in the dynamics of zooplankton under hypertrophic conditions

Intraspecific interactions may limit population growth of small cladoceran taxa under food-rich, hypertrophic conditions. Multiple-regression models significantly explained a large proportion of the variation in the body size adjusted fecundity and population growth rate of crustacean zooplankton taxa in a shallow, hypertrophic lake. The results of partial correlation analyses suggested exploitative competition to have only limited significance in determining the zooplankton dynamics. The analyses also revealed strong negative relationships between biomass and both body size adjusted fecundity and population growth rate within most taxa. Most of these relationships cannot be explained by food shortage or predation and suggest alternative mechanisms such as chemically mediated, intraspecific interference competition or life history shifts.