Biological Reviews最新文献

Trait-based approaches have emerged as a general framework that translates species-specific knowledge to understand the processes driving patterns of diversity and distributions. Morphological traits are relatively easy to measure and can provide information on organism–environment interactions and community structure due to their close linkage to ecological function and habitat partitioning. Freshwater mussels (Family: Unionidae) are a diverse (~360 North American species) and endangered group of organisms. Mussels display great interspecific morphological variation potentially yielding broad ecological implications. We aimed to modify quantitively an existing shell morphological classification system by combining size, shape, and sculpturing data using a robust data set of 1362 individuals representing 64 species spanning a broad cross section of the diverse North American freshwater mussel fauna. Using multivariate techniques, we classified species into morphological classes based on trait similarities hypothesized to explain species distributions and habitat associations. We then tested how well the classification system predicted trait–environment relationships using quantitative mussel survey data with paired environmental data collected at three spatial scales [river (km), reach (40–150 m), patch (0.25 m²)]. Mussel species clustered into six different morphological classes based on sculpturing, shape, and body size traits. We found associations between morphological classes and environmental parameters at each spatial scale. The modified classification explained more variation in community distribution as predicted by abiotic variables than previous frameworks. Our study underscores the value of morphological traits in predicting species distributions and understanding mechanisms of community assembly and we provide a foundation for fellow researchers to expand our morphological classification. This knowledge has significant implications for mussel conservation and management, as it helps identify suitable habitats that can guide reintroduction strategies through incorporating multiple spatial scales, a broad representation of species and geographical distribution and a wide suite of morphological traits.

Amazonia contains Earth's largest freshwater basin, largest contiguous stretch of tropical forest, and most species-rich terrestrial biota on Earth. Rivers are key geographic features that drive diversification of the Amazonian biota, but they are also dynamic, which challenges their role as long-term barriers to dispersal and gene flow. The impacts of such river dynamics on organismal evolution have only recently been explored in detail. Here I examine biodiversity patterns and processes in Amazonia to elucidate how taxa diversify in the context of river network dynamics. I borrow the River Capture Hypothesis from ichthyology, and draw on evidence from speciation genomics, hybrid zones, and community assembly to demonstrate the effects of river network evolution on biodiversification. The idea is simple: populations of organisms whose dispersal is restricted by rivers become semi-isolated by rivers. Drift and selection against introgression drive divergence, but as rivers move, previously isolated populations come into secondary contact, facilitating lineage fusions or the migration of hybrid zones to other rivers. The basin's unique macroecological patterns and rich biota thus may have resulted from repeated divergences, lineage fusions, and range expansions around a network of non-stationary extrinsic barriers with variable results depending on the degree of intrinsic reproductive isolation that accumulates during this process. The evolutionary consequences of dynamic landscapes extend beyond Amazonia as “fission–fusion–fission” cycles modulate the diversification and spatial patterning of life on Earth in general.

Studies of symbiosis employ the term “parasitism” to connote different sorts of relationships. Within the context of mutualistic symbioses, parasites are otherwise cooperative individuals or strains that appropriate a disproportionate amount of the synergistic products. In the context of antagonistic symbioses, there is no pretence of cooperation, and instead parasites are defined as individuals or strains that derive fitness benefits at a fitness cost to their hosts. In both cases, parasitism is selected for at the lower level (that of the individual symbiont) but selected against at the higher level (the group of symbionts in a single host). Despite these similarities, these different sorts of parasitism likely evolve by different pathways. Once a host–symbiont relationship initiates, if functional synergy is lacking, the relationship will remain exploitative, although parasites may differ in their detrimental effects on the host and the higher-level unit. If functional synergy is present, however, cooperation may develop with benefits for both host and symbionts (i.e. mutualism). Nevertheless, parasites may still evolve from within these incipient relationships when individuals or strains of symbionts act parasitically by defecting from the common good to further their selfish replication. Levels-of-selection dynamics thus underlie both forms of parasitism, but only in the case of latent functional synergy can true symbiotic complexity at the higher level emerge.

A large proportion of arthropod species are infected with endosymbionts, some of which selfishly alter host reproduction. The currently known forms of parasitic reproductive manipulations are male-killing, feminization, cytoplasmic incompatibility, parthenogenesis induction and distortion of sex allocation. While all of these phenomena represent adaptations that enhance parasite spread, they differ in the mechanisms involved and the consequent infection dynamics. We focus here on the latter aspect, summarizing existing theoretical literature on infection dynamics of all known reproductive manipulation types, and completing the remaining knowledge gaps where dynamics have not been modelled yet. Our unified framework includes the minimal model components required to describe the effects of each manipulation. We establish invasion criteria for all potential combinations of manipulative endosymbionts, yielding predictions for an endosymbiont's increase from rarity within a host population that is initially either uninfected or infected with a different symbiont strain. We consider diplodiploid and haplodiploid hosts, as the mechanisms as well as the infection dynamics of reproductive manipulations can differ between them. Our framework reveals that endosymbionts that a priori have the best invasion prospects are not necessarily the most commonly found ones in nature; priority effects play a role too, and cytoplasmic incompatibility excels in this regard. As a whole, considerations of the ease with which a symbiont spreads have to be complemented with knowledge of how easy it is to achieve a particular manipulation, and with factors influencing the probability that interspecific host switching occurs and succeeds.

How diseases are transmitted within a multi-host community is a complex biological process with important ecological and societal consequences. The intricacies of interspecific disease transmission determine when a disease can spread to a novel host, including humans (zoonosis), and the severity of emerging epidemics. Interspecific disease transmission also mediates long-term disease prevalence within a multi-host community which is at the core of the disease–diversity relationship. Mathematical models play a central role in formulating predictions about spillover, prevalence, and the disease–diversity relationship. Yet, how the complexity of transmission is captured (or not) by the assumptions of these models is often unclear. Here, we decompose the transmission process into five biological stages using bovine tuberculosis (bTB) as an illustrative example of transmission in a multi-host system. We then examine the often-implicit assumptions that classic compartmental models make about this process. We use the intuition gained from this decomposition to formulate hypotheses for how transmission can mediate outbreak potential, infection prevalence, and the amplifying or diluting effects of host diversity on disease prevalence. We further illustrate the key principles and implications of transmission with a diverse array of examples of multi-host pathogens. Throughout we emphasise the role of evolution in shaping interspecific transmission, from the evolutionary relatedness of the hosts themselves to the adaptation of the pathogen to novel hosts.