似Allee效应对2-物种集合种群竞争动态的影响

集合种群具有与局域种群Allee效应相似的现象被称为似Allee效应.将似Allee效应引入2-竞争物种集合种群系统,建立了具有似Allee效应的2-物种集合种群演化动态模型.大量的数值模拟表明:(1)似Allee效应导致集合种群水平上两竞争物种构成的系统具有多个平衡态;(2)似Allee效应使竞争共存物种无法续存甚至全部灭绝,即使种群具有很高的初始斑块占有率,并且最终平衡态随初始斑块占有率变化而改变;(3)似Allee效应可能使竞争排斥物种共同灭绝,且效应越强,物种存活时间越短;但似Allee效应不会增强强物种对弱物种的排斥强度,反而可能使强物种变为弱物种,弱物种变为强物种,其具有与栖息地毁坏类似的影响种群竞争等级排序的作用;(4)似Allee效应对竞争集合种群续存是一个不稳定的干扰因素,微小的变化都将引起系统平衡态的剧变.但对于已经达到平衡态的集合种群系统,似Allee效应对强弱种群多度起到调节与制约的作用,有助于平衡态集合种群的稳定与共存,这一结论更完整的揭示了似Allee效应在竞争集合种群系统发展的不同阶段所起的不同作用.以上这些结论对物种保护及集合群落的管理具有重要的指导意义.     

生境破坏的模式对集合种群动态和续存的影响

构建了空间关联的集合种群模型,该模型不但包含了种群的空间结构信息,而且引入了破坏生境的全局密度和局部密度两个指标,它们描述了破坏生境的模式.模型揭示了破坏生境的空间分布格局复杂地影响了集合种群的动态和续存,破坏和未破坏生境斑块的均匀混合不利于集合种群的增长和续存,而生境类型聚集分布可以促进集合种群的快速增长和长期续存;对于两种斑块类型相对均匀混合的生境来说,均匀场假设可能会高估集合种群的续存,对于相对斑块类型高度聚集的生境,均匀场假设可能会低估集合种群的续存;物种的迁移范围也会影响集合种群的续存,迁移范围越大的物种越容易抵御生境的破坏而免遭灭绝.这意味着在生物保护中不能仅仅考虑生境的恢复和斑块质量的改善,生境结构的构建也是很重要的,加强生境斑块之间的连通性也有利于物种的长期续存.     

局域种群的Allee效应和集合种群的同步性

从包含Allee效应的局域种群出发,建立了耦合映像格子模型,即集合种群模型.通过分析和计算机模拟表明:(1)当局域种群受到Allee效应强度较大时,集合种群同步灭绝;(2)而当Allee效应强度相对较弱时,通过稳定局域种群动态(减少混沌)使得集合种群发生同步波动,而这种同步波动能够增加集合种群的灭绝风险;(3)斑块间的连接程度对集合种群同步波动的发生有很大的影响,适当的破碎化有利于集合种群的续存.全局迁移和Allee效应结合起来增加了集合种群同步波动的可能,从而增加集合种群的灭绝风险.这些结果对理解同步性的机理、利用同步机理来制定物种保护策略和害虫防治都有重要的意义.     

生境丧失对具有似Allee效应集合种群的影响及对策——以江苏盐城为例

似Allee效应对物种续存是潜在的扰动因素,稀有物种更易受其影响,可能增加生存于破碎化栖息地中的珍稀物种的死亡风险;但似Allee效应对多物种集合种群续存的影响及其在珍稀物种保护中的应用未能引起足够重视。将似Allee效应引入集合种群动力模式,建立了生境丧失下具有似Allee效应的n-珍稀物种的集合种群模式,并以江苏盐城滩涂湿地中的29种珍稀物种为研究实例。研究结果表明:(1)似Allee效应导致n-物种集合种群多度作长期变周期振荡,原本竞争共存物种可能无法继续共存,甚至灭绝。(2)似Allee效应增强对次强种及劣势种的生存极为不利,导致次强物种由强至弱灭绝,劣势物种由弱至强依次灭绝。(3)盐城天然湿地丧失29%后,11种劣势物种的集合种群由弱到强将最终依次灭绝,灭绝迟豫时间为304～890a,这些物种即Hanski所指的"活死者"。(4)适度增加栖息地面积是保护珍稀物种多样性的有效方法之一,在盐城现存3200km2的天然湿地基础上适度增加1801～2064km2左右栖息地面积,可以有效保护29种濒危物种的多样性,同时应注意结合针对具体物种的保护措施来提高濒危物种多度。研究结果对物种多样性保护及自然保护区建设具有重要的理论指导意义。     

具有Allee效应的合作进化

Allee效应对物种的续存是潜在的干扰因素,在很大程度上将增加种群局部甚至全局灭绝的可能性。对许多物种,尤其是濒临物种更容易受其影响。将Allee效应引入囚徒困境博弈模型,通过理论分析与数值模拟相结合的方法分析讨论了Allee效应对合作进化的影响。研究结果表明:在恶劣的环境条件下,Allee效应极易使物种灭绝,不利于合作进化;在相对优越的环境条件下(死亡率较低),Allee效应促进合作进化,且Allee效应强度越强,更有利于合作进化,不过种群的空间斑块占有率也会随着Allee效应强度的增强而降低,使物种最终灭绝。     

集合种群空间混沌的模拟研究以及Allee效应、拥挤效应与捕食效应对空间模式的影响

集合种群的空间模式研究是当今生态学的核心问题之一。本研究利用常微分动力系统以及基于网格模型的元胞自动机模型对Allee效应、拥挤效应以及捕食作用集合种群的空间分布模式做了全面的模拟研究。Allee效应描述当种群水平低于某一阈值时会发生由生殖成功几率下降造成的种群负增长率,而拥挤效应是指当种群密度过高时引起的个体性为异常从而达到调节种群增长率的作用。文章组建了3个空间确定性模型：局部作用模型(CIM)、距离敏感模型(DSM)和集合种群捕食模型(MMP)。局部作用模型显示在一维生境中空斑块形成金字塔状,二维模型显示出明显的动态拟周期性以及由空间混沌所形成的异质性。距离敏感模型可导致由迁移个体中密度制约强度决定的集合种群大小复杂动态与种群密度的双峰分布。这些结果说明动态行为的复杂性,不仅可用于表征研究物种的特性,而且可以表明该物种的续存能力与灭绝风险。集合种群捕食模型是概率转换空间模型,利用该模型得出了依赖于模型参数和生境尺度的白组织种群概率空间分布模式。模拟的结果表明,系统的内在机制和这种白组织模式导致捕食者形成集团型不明显的“捕食小组”或“杀手小组”,并具有较高扩散力．但却包括侵占率低、灭绝率高的特点。而使猎物种群形成高集团性、高侵占率、低灭绝率、低扩散力的种群集团。这种特点又使捕食者种群在生境中处于中心地带,而使猎物种群形成在捕食者和生境边缘间的环状分布。这些结果还说明了尺度对于生态学的研究是至关重要的,不同的尺度将产生不同的系统模式。     

集合种群的理论框架与应用研究进展

集合种群的研究是当今国际生态学的重要前沿与热点。随着全球范围的生境破坏和破碎化,集合种群的研究方法已成为数学生态学、理论生态学和保护生物学的重要手段。由于其迅速的发展,集合种群的概念与理论得到迅速扩展与丰富。为了能总观集合种群进展的全局并开展进一步的工作．首先对集合种群的已有概念、理论和模型做了全面的分析和总结;其次对集合种群的发展和概念进行了探讨,以集合种群模型的中心框架：Levins的斑块占据模型为基础,展开对其它原理、效应和机制的探讨;主要包括了Levins原理．即当生境遭到破坏时,空斑块比例在集合种群灭绝前保持不变,然后还分析了Allee效应(集合种群的Allee效应主要是由于建群困难和扩散损失造成的);第三,分析了援救效应：迁入个体可以降低斑块中现有局域种群的灭绝风险。援救效应会增强集合种群的生存力,使空斑块比例下降。第四,探讨了两竞争集合种群的共存机制,即竞争,侵占妥协,其共存机制为空间生境中物种共存提供了有力的理论解释。最后,对集合种群群落中的灭绝债务进行了讨论。并给出了2种最为主要的集合种群空间模拟方法。     

集合种群竞争机制在庐山森林演替模拟中的应用

通过对森林植被群落的动态模拟,可以揭示森林植被的恢复过程和演替规律。本文将动物集合种群竞争模型引入森林演替模拟中,以庐山为研究区域选取10个优势乔木种进行了森林演替模拟。在MATLAB中分别对当前生境条件、生境破坏条件和生境恢复条件进行模拟,结合庐山森林演替动态曲线和各优势种对外界条件响应规律,总结了对不同物种续存的保护机制。结果表明:(1)庐山森林种群整体向常绿阔叶林方向演替,混生林中阔叶树占优势;(2)森林群落中的优势物种可分为3个等级:第一等级优势种对恶劣生态环境适应性强,但在生态环境得到保护时容易被低优势度物种侵占,应防止人工引进的外来物种对原有优势种造成过度侵占;第二等级优势种对生境变化敏感,生境严重破坏会造成这类物种灭绝,生境恢复能使之续存;第三等级优势种在生境恢复条件下也难以续存,应采取人工育林等措施进行保护。     

集合种群的似Allee效应

从局域种群出发,建立了一个既包括局域种群动态,又包含集合种群侵占率的整合模型,并在这两个层次上进行了计算机模拟,结果表明：（1）同局域种群的Allee效应相类似,集合种群的斑块（适宜生境）侵占比例也存在一个临界值,即使有足够的适宜生境,当斑块的侵占比例低于这个临界值时,集合种群优将趋于灭绝。（2）这个临界值与局域种各的Allee效应密切相关,这将给自然保护,尤其稀有生物的保护以很大的启示。     

集合种群的Allee效应研究进展

随着全球环境破坏的加剧,物种丧失的速度加快,人们日益关注生物多样性的保护。种群生物学和自然保护生物学的一些研究表明,如果一个局域种群受到Allee效应的影响,最终可能走向灭绝。从物种保护的角度考虑,分别介绍了集合种群水平上的Allee效应的和似Allee效应,比较了集合种群的Allee效应和似Allee效应产生的原因,以及集合种群的Allee效应和局域种群的Allee效应之间的关系、集合种群的似Allee效应和局域种群的Allee效应之间的关系,并提出集合种群的Allee效应还需要进一步的研究。     

Habitat selection reduces extinction of populations subject to Allee effects

Theoretical studies indicate that a single population under an Allee effect will decline to extinction if reduced below a particular threshold, but the existence of multiple local populations connected by random dispersal improves persistence of the global population. An additional process that can facilitate persistence is the existence of habitat selection by dispersers. Using analytic and simulation models of population change, I found that when habitat patches exhibiting Allee effects are connected by dispersing individuals, habitat selection by these dispersers increases the likelihood that patches persist at high densities, relative to results expected by random settlement. Populations exhibiting habitat selection also attain equilibrium more quickly than randomly dispersing populations. These effects are particularly important when Allee effects are large and more than two patches exist. Integrating habitat selection into population dynamics may help address why some studies have failed to find extinction thresholds in populations, despite well-known Allee effects in many species.     

滨海湿地植物种群Allee效应驱动机制研究进展

Allee效应是指生物个体适应度与种群规模或密度之间呈正向关联的现象,因与植物种群动态和种群灭绝密切相关而受到生态学家的普遍重视。阐释多重胁迫下滨海湿地植物种群响应机制,从保护生物多样性和维持生态系统稳定性层面发展系统性生态修复措施成为相关研究关注的重点。本研究分别从遗传过程、花粉扩散过程和生物互作关系不同层面,总结分析了植物种群Allee效应驱动机制的研究进展。一方面,植物因遗传过程中近交衰退、遗传变异丧失、有害突变累积等遗传结构改变造成繁殖失败而引发Allee效应;另一方面,植物花粉扩散过程和动植物互作关系影响下的花粉限制也通过影响植物种群繁殖力成为驱动Allee效应的关键因素。滨海湿地水盐梯度变异及格局破碎化影响下,植物种群遭受Allee效应的风险需引起关注,维持滨海湿地植物种群适宜分布格局和生物连通过程成为缓解Allee效应的重要手段。结合生理学与化学生态学研究手段和长时间尺度动态监测技术,有助于进一步阐释环境及生物等多重胁迫下Allee效应的非线性驱动机制。     

Metapopulation models for extinction threshold in spatially correlated landscapes

Simple analytical models assuming homogeneous space have been used to examine the effects of habitat loss and fragmentation on metapopulation size. The models predict an extinction threshold, a critical amount of suitable habitat below which the metapopulation goes deterministically extinct. The consequences of non-random loss of habitat for species with localized dispersal have been studied mainly numerically. In this paper, we present two analytical approaches to the study of habitat loss and its metapopulation dynamic consequences incorporating spatial correlation in both metapopulation dynamics as well as in the pattern of habitat destruction. One approach is based on a measure called metapopulation capacity, given by the dominant eigenvalue of a "landscape" matrix, which encapsulates the effects of landscape structure on population extinctions and colonizations. The other approach is based on pair approximation. These models allow us to examine analytically the effects of spatial structure in habitat loss on the equilibrium metapopulation size and the threshold condition for persistence. In contrast to the pair approximation based approaches, the metapopulation capacity based approach allows us to consider species with long as well as short dispersal range and landscapes with spatial correlation at different scales. The two methods make dissimilar assumptions, but the broad conclusions concerning the consequences of spatial correlation in the landscape structure are the same. Our results show that increasing correlation in the spatial arrangement of the remaining habitat increases patch occupancy, that this increase is more evident for species with short-range than long-range dispersal, and that to be most beneficial for metapopulation size, the range of spatial correlation in landscape structure should be at least a few times greater than the dispersal range of the species.     

Spatial variation in branch size promotes metapopulation persistence in dendritic river networks

1. Despite years of attention, the dynamics of species constrained to disperse within riverine networks are not well captured by existing metapopulation models, which often ignore local dynamics within branches.
2. We develop a modelling framework, based on traditional metapopulation theory, for patch occupancy dynamics subject to local colonisation–extinction dynamics within branches and regional dispersal between branches in size-structured, bifurcating riverine networks. Using this framework, we investigate whether and how spatial variation in branch size affects species persistence for dendritic systems with directional dispersal, including one-way (up- or downstream only) and two-way (both up- and downstream) dispersal.
3. Variation in branch size generally promotes species persistence more obviously at higher relative extinction rate, suggesting that previous studies ignoring differences in branch size in real riverine systems might overestimate species extinction risk.
4. Two-way dispersal is not always superior to one-way dispersal as a strategy for metapopulation persistence especially at high relative extinction rate. The type of dispersal that maximises species persistence is determined by the hierarchical level of the largest, and hence most influential, branch within the network. When considering the interactive effects of up- and downstream dispersal, we find that moderate upstream-biased dispersal maximises metapopulation viability, mediated by spatial branch arrangement.
5. Overall, these results suggest that both branch-size variation and species traits interact to determine species persistence, theoretically demonstrating the ecological significance of their interplay.

     

Temporal autocorrelation can enhance the persistence and abundance of metapopulations comprised of coupled sinks

In spatially heterogeneous landscapes, some habitats may be persistent sources, providing immigrants to sustain populations in unfavorable sink habitats (where extinction is inevitable without immigration). Recent theoretical and empirical studies of source-sink systems demonstrate that temporally variable local growth rates in sinks can substantially increase average abundance of a persisting population, provided that the variation is positively autocorrelated--in effect, temporal variation inflates average abundance. Here we extend these results to a metapopulation in which all habitat patches are sinks. Using numerical studies of a population with discrete generations (buttressed by analytic results), we show that temporal variation and moderate dispersal can jointly permit indefinite persistence of the metapopulation and that positive autocorrelation both lowers the magnitude of variation required for persistence and increases the average abundance of persisting metapopulations. These effects are weakened--but not destroyed--if variation in local growth rates is spatially synchronized and dispersal is localized. We show that the inflationary effect is robust to a number of extensions of the basic model, including demographic stochasticity and density dependence. Because ecological and environmental processes contributing to temporally variable growth rates in natural populations are typically autocorrelated, these observations may have important implications for species persistence.     

How does intraspecific density regulation influence metapopulation synchrony and persistence?

Intraspecific density regulation influences the synchronization of local population dynamics through dispersal. Spatial synchrony in turn may jeopardize metapopulation persistence. Joining results from previous studies suggests that spatial synchrony is highest at moderate over-compensation and is low at compensating and at very strong over-compensating density regulation. We scrutinize this supposition of a unimodal relationship using a process-based metapopulation model with explicit local population dynamics. We extend the usually studied range of density regulation to under-compensation and analyse resulting metapopulation persistence. We find peaks of spatial synchrony not only at over-compensatory but also under-compensatory density regulation and show that effects of local density compensation on synchrony follow a bimodal rather than unimodal relationship. Persistence of metapopulations however, shows a unimodal relationship with a broad plateau of high persistence from compensatory to over-compensatory density regulation. This range of high persistence comprises both levels of low and high spatial synchrony. Thus, not synchrony alone jeopardizes metapopulation persistence, but only in interplay with high local extinction risk. The functional forms of the relations of density compensation with spatial synchrony and persistence are robust to increases in dispersal mortality, landscape dynamics, or density dependence of dispersal. However, with each of these increases the maxima of spatial synchrony and persistence shift to higher over-compensation and levels of synchrony are reduced. Overall, for over-compensation high landscape connectivity has negative effects while for under-compensation connectivity affects persistence positively. This emphasizes the importance of species life-history traits for management decisions with regard to landscape connectivity: while dispersal corridors are essential for species with under-compensatory density regulation, they may have detrimental effects for endangered species with over-compensation.     

Anthropogenic, ecological and genetic factors in extinction and conservation

Anthropogenic factors constitute the primary deterministic causes of species declines, endangerment and extinction: land development, overexploitation, species translocations and introductions, and pollution. The primary anthropogenic factors produce ecological and genetic effects contributing to extinction risk. Ecological factors include environmental stochasticity, random catastrophes, and metapopulation dynamics (local extinction and colonization) that are intensified by habitat destruction and fragmentation. Genetic factors include hybridization with nonadapted gene pools, and selective breeding and harvesting. In small populations stochastic factors are especially important, including the ecological factors of Allee effect, edge effects, and demographic stochasticity, and the genetic factors of inbreeding depression, loss of genetic variability, and fixation of new deleterious mutations. All factors affecting extinction risk are expressed, and can be evaluated, through their operation on population dynamics.