Keystone and Intraguild Predation, Intraspecific Density Dependence, and a Guild of Coexisting Consumers

2014 ◽  
Vol 183 (1) ◽  
pp. E1-E16 ◽  
Author(s):  
Mark A. McPeek
2006 ◽  
Vol 273 (1604) ◽  
pp. 2909-2916 ◽  
Author(s):  
Robert P Freckleton ◽  
Owen T Lewis

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.


2014 ◽  
Vol 60 ◽  
pp. 1-6 ◽  
Author(s):  
Javier Fernandez-de-Simon ◽  
Francisco Díaz-Ruiz ◽  
Francesca Cirilli ◽  
Francisco S. Tortosa ◽  
Rafael Villafuerte ◽  
...  

2017 ◽  
Author(s):  
Christopher M. Moore ◽  
Samantha A. Catella ◽  
Karen C. Abbott

AbstractMutualism 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.


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