Freckleton Robert P, Lewis Owen T
Department of Animal & Plant Sciences, University of Sheffield, Sheffield S10 2TN, UK.
Proc Biol Sci. 2006 Dec 7;273(1604):2909-16. doi: 10.1098/rspb.2006.3660.
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.
天敌尤其是植物病原体引起的密度依赖死亡率在促进热带树木共存和多样性方面所起的作用，正受到越来越多的关注。在此，我们回顾了病原体诱导的密度依赖分析中四个被忽视或未得到充分解决的问题。首先，检测密度依赖的方法必须对潜在偏差具有稳健性。特别是观察性研究，需要仔细分析以避免测量误差产生的偏差，现有研究可能因此受到批评。操纵植物密度和病原体发生率的实验性研究通常更可取，或者应该并行进行。其次，密度依赖的形式尚未得到很好的理解，特别是没有数据表明病原体是否会引起补偿性或超补偿性密度反应。因此，我们认为病原体诱导的密度依赖产生多样性增强结果（如简森 - 康奈尔效应）的可能性仍然不确定，因为如果密度依赖是超补偿性的，共存的可能性要大得多。第三，很少有研究考察病原体（或更广泛地说，天敌）引起的种内或种间密度依赖的相对重要性。这本质上等同于询问病原体在多大程度上具有宿主特异性。如果病原体是泛化种，那么死亡率将对总体植物密度做出反应，而与植物物种身份无关。这将削弱种内密度依赖并降低病原体促进多样性的效果。最后，我们强调需要将对病原体和密度依赖的观察与实验整合到树木整个生命周期的研究，因为目前尚无法确定病原体对观察到的动态的贡献程度。
