Does diversity beget diversity? A case study of crops and weeds

Abstract. The ecological literature is ambiguous as to whether the initial diversity of a plant community facilitates or deters the diversity of colonizing species. We experimentally planted annual crop species in monoculture and polyculture, and examined the resulting weed communities. The species composition of weeds was similar among treatments, but the species richness of weeds was significantly higher in the polycultures than in the monocultures. This supports the ‘diversity begets diversity’ hypothesis. Environmental microheterogeneity, diversity promoters, and ecological equivalency do not seem able to explain the observed patterns.     

Does herbivore diversity depend on plant diversity? The case of California butterflies

It is widely believed that the diversity of plants influences the diversity of animals, and this should be particularly true of herbivores. We examine this supposition at a moderate spatial extent by comparing the richness patterns of the 217 butterfly species resident in California to those of plants, including all 5,902 vascular plant species and the 552 species known to be fed on by caterpillars. We also examine the relationships between plant/butterfly richness and 20 environmental variables. We found that although plant and butterfly diversities are positively correlated, multiple regression, path models, and spatial analysis indicate that once primary productivity (estimated by a water-energy variable, actual evapotranspiration) and topographical variability are incorporated into models, neither measure of plant richness has any relationship with butterfly richness. To examine whether butterflies with the most specialized diets follow the pattern found across all butterflies, we repeated the analyses for 37 species of strict monophages and their food plants and found that plant and butterfly richness were similarly weakly associated after incorporating the environmental variables. We condude that plant diversity does not directly influence butterfly diversity but that both are probably responding to similar environmental factors.     

Whither the diversity bargain?

In Natasha Warikoo’s account, the “diversity bargain” is widespread among white elite American college students. This bargain is tentative support for preferences for underrepresented minorities in college admissions, conditioned on the admitted minority students providing white students with multicultural experiences that signal elite cosmopolitanism. This essay reviews three possible explanations for the pervasiveness of the diversity bargain: campus experiences with the benefits of diversity; socialization into expectations that elites give lip service to the benefits of diversity; and Warikoo’s methodological and analytical choices.     

Does diversity damage corporate value? Measuring stock price reactions to a diversity award

Corporate decision-makers have increasingly adopted an approach to firm governance that places share value above other concerns, including meeting the needs of employees. Decision-makers' concerns about shareholder interests may potentially impede internal commitments to implementing diversity-friendly practices and policies. This study analyses how recognition for a company's diversity efforts impacts corporate share price. We rely on data of share price fluctuation following the receipt of Fortune Magazine's ‘Best Companies for Minorities’ Award. We find that companies recognized for their diversity efforts are penalized with a significant decline in share price, though this negative effect is mediated by the ethnic composition of the company's workforce.     

Is vascular plant species diversity a predictor of bryophyte species diversity in Mediterranean forests?

This study aimed to (i) investigate the congruence among the species composition and diversity of bryophytes and vascular plants in forests; (ii) test if site prioritization for conservation aims by the maximization of the pooled number of vascular plant species is effective to maximize the pooled number of bryophyte species. The study was performed in six forests in Tuscany, Italy. Four-hundred and twenty vascular plant species (61 of which were woody) and 128 bryophyte species were recorded in 109 plots. Despite the good predictive value of the compositional patterns of both woody plants and total vascular with respect to the compositional pattern of bryophytes, the species richness of the latter was only marginally related to the species richness of the former two. Bryophyte rare species were not spatially related to rare plant species and neither coincided with the sites of highest plant species richness. The species accumulation curves of bryophytes behaved differently with respect to those of woody plants or total vascular plants. Reserve selection analysis based on the maximization of the pooled species richness of either woody plants or total vascular plants were not effective in maximizing the pooled species richness of bryophytes. This study indicates that species diversity of vascular plants is not likely to be a good indicator of the bryophyte species diversity in Mediterranean forests.     

Is there a trade-off between species diversity and genetic diversity in forest tree communities?

The two most important components of biodiversity, species diversity and genetic diversity, have generally been treated as separate topics, although a coordination between both components is believed to be critical for ecosystem stability and resilience. Based on a new trait concept that allows for the assessment of genetic diversity across species, the relationship between species diversity and genetic diversity was examined in eight forest tree communities composed of different tree genera including both climax and pioneer species. It was intended to check whether a trade-off exists between the two diversity components as was found in a few studies on animal species.Using several isozyme-gene systems as genetic markers, the genetic diversity across species within each of the tree communities was determined by two measures, the commonly used intraspecific genetic diversity averaged over species and the recently developed transspecific genetic diversity per species. Both data sets were compared with the corresponding community-specific species diversity resulting in a positive relationship between the two diversity components. A statistically significant positive correlation was established between the transspecific genetic diversity per species and the species diversity for three isozyme-gene systems. Beyond that, consistent results were obtained using different parameters of the diversity measure which characterize the total, the effective and the number of prevalent variants. The number of prevalent variants reflected most significantly the non-randomness of the observed diversity patterns.These findings can be explained by the observation that the pioneer tree species reveal a by far higher genetic diversity than the climax tree species, which means that an increase in species diversity, due to the addition of several pioneer species at the expense of one or two climax species, goes along with an increase in the level of genetic diversity. Forest tree communities with the highest degree of species diversity exhibit therefore the highest transspecific genetic diversity per species. This result was discussed with regard to the particular composition and stability of forest tree communities.     

Does predation contribute to tree diversity?

Seed and seedling predation may differentially affect competitively superior tree species to increase the relative recruitment success of poor competitors and contribute to the coexistence of tree species. We examined the effect of seed and seedling predation on the seedling recruitment of three tree species, Acer rubrum (red maple), Liriodendron tulipifera (yellow poplar), and Quercus rubra (northern red oak), over three years by manipulating seed and seedling exposure to predators under contrasting microsite conditions of shrub cover, leaf litter, and overstory canopy. Species rankings of seedling emergence were constant across microsites, regardless of exposure to seed predators, but varied across years. A. rubrum had the highest emergence probabilities across microsites in 1997, but Q. rubra had the highest emergence probabilities in 1999. Predators decreased seedling survival uniformly across species, but did not affect relative growth rates (RGRs). Q. rubra had the highest seedling survivorship across microsites, while L. tulipifera had the highest RGRs. Our results suggest that annual variability in recruitment success contributes more to seedling diversity than differential predation across microsites. We synthesized our results from separate seedling emergence and survival experiments to project seedling bank composition. With equal fecundity assumed across species, Q. rubra dominated the seedling bank, capturing 90% of the regeneration sites on average, followed by A. rubrum (8% of sites) and L. tulipifera (2% of sites). When seed abundance was weighted by species-specific fecundity, seedling bank composition was more diverse; L. tulipifera captured 62% of the regeneration sites, followed by A. rubrum (21% of sites) and Q. rubra (17% of sites). Tradeoffs between seedling performance and fecundity may promote the diversity of seedling regeneration by increasing the probability of inferior competitors capturing regeneration sites.     

Are protected areas maintaining bird diversity?

Evaluating the effectiveness of protected areas for sustaining biodiversity is crucial to achieving conservation outcomes. While studies of effectiveness have improved our understanding of protected‐area design and management, few investigations (< 5%) have quantified the ecological performance of reserves for conserving species. Here, we present an empirical evaluation of protected‐area effectiveness using long‐term measures of a vulnerable assemblage of species. We compare forest and woodland bird diversity in the Australian Capital Territory over 11 yr on protected and unprotected areas located in temperate eucalypt woodland and matched by key habitat attributes. We examine separately the response of birds to protected areas established prior to 1995 and after 1995 when fundamental changes were made to regional conservation policy. Bird diversity was measured in richness, occurrence of vulnerable species, individual species trajectories and functional trait groups. We found that protected areas were effective in maintaining woody vegetation cover in the study region, but were less effective in the protection of the target bird species assemblage. Protected areas were less species rich than unprotected areas, with significant declines in richness across sites protected prior to 1995. Small, specialised and vulnerable species showed stronger associations with unprotected areas than protected areas. Our findings indicate that recently established reserves (post‐1995) are performing similarly to unprotected woodland areas in terms of maintaining woodland bird diversity, and that both of these areas are more effective in the conservation of woodland bird populations than reserves established prior to 1995. We demonstrate that the conservation value of protected areas is strongly influenced by the physical characteristics, as well as the landscape context, of a given reserve and can diminish with changes in surrounding land use over time. Both protected areas and off‐reserve conservation schemes have important roles to play in securing species populations.     

How adaptive is parasite species diversity?

Has species diversity in parasites evolved as a by-product of adaptive diversification driven by competition for limited resources? Or is it a result of gradual genetic drift in isolation? One can move closer to answering these questions by evaluating the ubiquity of host switching, the key stage of adaptive diversification. Studies dealing with evolutionary role of host switching suggest that this process is extremely common in the wild, thus pointing at adaptive nature of parasite species diversity. However, most of these studies are focused on the evidence that may or may not have emerged as a consequence of host switching, – an approach potentially associated with a degree of uncertainty. After an overview of the data I am making an attempt to get a clearer view on host switching by focusing on factors that cause this phenomenon. In particular, I review theoretical work and field observations in order to identify the type of genetic host-use variance and the type of dispersal that underpin host switching. I show that host switching is likely to require generalist modifier alleles which increase the host range of individual genotypes and is likely to be promoted by wave-like patterns of dispersal. Both factors appear to be common in parasites. I conclude by outlining key areas for future research, including: (i) direct testing for divergence with gene flow, the main “footprint” of adaptive speciation; (ii) investigating the association between demography, dispersal potential and the potential to colonise novel habitats; and (iii) determining the genetic mechanisms underpinning host range variance in parasites.     

Are local patterns of anthropoid primate diversity related to patterns of diversity at a larger scale?

Aims (1) To determine the relationship between local and regional anthropoid primate species richness. (2) To establish the spatial and temporal scale at which the ultimate processes influencing patterns of primate species coexistence operate. Location Continental landmasses of Africa, South America and Asia (India to China, and all islands as far south as New Guinea). Methods The local–regional species richness relationship for anthropoid primates is estimated by regressing local richness against regional richness (independent variable). Local richness is estimated in small, replicate local assemblages sampled in regions that vary in total species richness. A strong linear relationship is taken as evidence that local assemblages are unsaturated and local richness results from proportional sampling of the regional pool. An asymptotic curvilinear relationship is interpreted to reflect saturated communities, where strong biotic interactions limit local richness and local processes structure the species assemblage. As a further test of the assumption of local assemblage saturation, we looked for density compensation in high‐density local primate assemblages. Results The local–regional species richness relationship was linear for Africa and South America, and the slope of the relationship did not differ between the two continents. For Asia, curvilinearity best described the relationship between local and regional richness. Asian primate assemblages appear to be saturated and this is confirmed by density compensation among Asian primates. However, density compensation was also observed among African primates. The apparent assemblage saturation in Asia is not a species–area phenomenon related to the small size of the isolated islands and their forest blocks, since similar low local species richness occurs in large forests on mainland and/or peninsular Asia. Main conclusions In Africa and South America local primate assemblage composition appears to reflect the influence of biogeographic processes operating on regional spatial scales and historical time scales. In Asia the composition of primate assemblages are by‐and‐large subject to ecological constraint operating over a relatively small spatial and temporal scale. The possible local influence of the El Niño Southern Oscillations on the evolution and selection of life‐history characteristics among Asian primates, and in determining local patterns of primate species coexistence, warrants closer inspection.     

What hope for African primate diversity?

Available empirical evidence suggests that many primate populations are increasingly threatened by anthropogenic actions and we present evidence to indicate that Africa is a continent of particular concern in terms of global primate conservation. We review the causes and consequences of decline in primate diversity in Africa and argue that the major causes of decline fall into four interrelated categories: deforestation, bushmeat harvest, disease and climate change. We go on to evaluate the rarity and distribution of species to identify those species that may be particularly vulnerable to threats and examine whether these species share any characteristic traits. Two factors are identified that suggest that our current evaluation of extinction risk may be overly optimistic; evidence suggests that the value of existing forest fragments may have been credited with greater conservation value in supporting primate populations than they actually have and it is clear that the extinction debt from historical deforestation has not being adequately considered. We use this evaluation to suggest what future actions will be advantageous to advance primate conservation in Africa and evaluate some very positive conservation gains that are currently occurring.     

Commentary: Do we have a consistent terminology for species diversity? The fallacy of true diversity

There is no single best index that can be used to answer all questions about species diversity. Entropy-based diversity indices, including Hill’s indices, cannot account for geographical and phylogenetic structure. While a single diversity index arises if we impose several constraints—most notably that gamma diversity be completely decomposed into alpha and beta diversity—there are many ecological questions regarding species diversity for which it is counterproductive, requiring decomposability. Non-decomposable components of gamma diversity may quantify important intrinsic ecological properties, such as resilience or nestedness.     

Understanding extracellular vesicle diversity – current status

ABSTRACT

Introduction: Extracellular vesicles (EVs) represent an important mode of intercellular communication. There is now a growing awareness that predominant EV subtypes; exosomes from endosomal origin, and shed microvesicles from plasma membrane budding, can be further stratified into distinct subtypes, however specific approaches in their isolation and markers that allow them to be discriminated are lacking.

Areas covered: Knowledge about these distinct EV subpopulations is important including the regulation of composition, release, targeting/localization, uptake, and function. This review discusses the mechanisms of distinct EV biogenesis and release, defining select EV classes (and subpopulations), which will be crucial for development of EV-based functions and clinical applications. We review the dynamics of cargo sorting leading to the mechanisms of EV heterogeneity, their mechanisms of formation, intracellular trafficking pathways, and provide an uptake about biochemical/functional differences. With advances in purification strategies and proteomic-based quantitation, allows significant benefit in accurately describing differences in EV protein cargo composition and modification.

Expert commentary: The advent of quantitative mass spectrometry-based proteomics, in conjunction with advances in molecular cell biology, and EV purification strategies, has contributed significantly to our improved characterization and understanding of the molecular composition and functionality of these distinct EV subpopulations.     

Do infectious diseases drive MHC diversity?

The primary function of the major histocompatibility complex (MHC) is to allow the immune system to identify infectious pathogens and eliminate them. Infectious diseases are now thought to be the main selection force that drives and maintains the extraordinary diversity of the MHC.     

Does predation maintain tit community diversity?

European tits of the genus Parus constitute a complex group of coexisting boreal birds. Here we present a survey of the distribution of three coniferous-living Parus species and one of their main predators, the pygmy owl ( Glaucidium passerinum ), on nine isolated islands in Scandinavia. On all islands the coal tit ( Parus ater ) is the sole tit species when the pygmy owl is absent. The two larger species, the willow tit ( P. montanus ) and the crested tit ( P. cristatus ), only coexist with the coal tit when pygmy owls are present. We suggest that the coexistence of willow tits, crested tits and coal tits is the result of a combination of competition for food and predator-safe foraging sites. The smaller coal tit is superior in exploitation competition for food, while the two larger species have an advantage in interference competition for predator-safe foraging sites. The association between the distribution of the pygmy owl and the two larger tit species on isolated islands in Scandinavia is consistent with the idea that the pygmy owl is a keystone predator.     

The structural diversity in α1-antitrypsin misfolding

The structure of α1-antitrypsin polymers, which cause a devastating disease, is vigorously debated. Here, the state of the field is discussed in view of a paradigm-changing structure published in this issue of EMBO reports.EMBO Rep (2011) advance online publication. doi:10.1038/embor.2011.171We were all taught that proteins have to fold correctly to be active and that the primary sequence of amino acids acts as the ‘blueprint'' for successful, productive folding. In recent years, we have also learnt how sensitive that blueprint is to change. For example, a single amino-acid change in the protein sequence, or a subtle change in temperature at which folding takes place, can lead to the formation and accumulation of non-native species, which have a tendency to self-associate and deposit in and around tissues, thereby triggering disease. To understand protein misfolding and its links with disease, we need information about the structures of all the key players and their relationships with each other. This has proven exceptionally challenging due to the transient nature of many of the species involved and the heterogeneity of the final misfolded product.For one misfolding disorder, α₁-antitrypsin deficiency—a devastating disease that affects approximately 1 in 2,500 individuals—we are a step closer to characterizing all of the main culprits. In this issue of EMBO reports, Huntington and colleagues present the X-ray crystal structure of an α₁-antitrypsin trimer that sheds light on the structure of a potentially pathogenic form of α₁-antitrypsin and provides new insights into the molecular mechanism of α₁-antitrypsin deficiency (Yamasaki et al, 2011).Attempts to understand the molecular basis for α₁-antitrypsin deficiency began in 1963 when Laurell & Eriksson noticed its absence from the serum of a cohort of patients with obstructive lung disease (Laurell & Eriksson, 1963). Sharp and co-workers subsequently described periodic acid Schiff-positive inclusions of α₁-antitrypsin within hepatocytes of α₁-antitrypsin-deficient patients (Sharp et al, 1969). These two findings linked the major clinical outcomes of the disease. α₁-Antitrypsin inhibits elastase in the lower respiratory tract and, therefore, a plasma deficiency leads to early onset emphysema due to uncontrolled elastase activity. The aggregation of α₁-antitrypsin at its site of production—the hepatocyte—leads to liver damage and cirrhosis. In the early 1990s, elegant work by Lomas and colleagues revealed that the key molecular event leading to the deficiency was the misfolding and formation of α₁-antitrypsin polymers within the endoplasmic reticulum of hepatocytes (Lomas et al, 1992).α₁-Antitrypsin, like all members of the serpin superfamily, is a large single-domain protein consisting of 394 amino acids that fold into three β-sheets surrounded by nine α-helices (Fig 1; Elliott et al, 2000). Protruding from the core structure is the flexible reactive centre loop, containing the scissile bond that dictates the inhibitory specificity of a serpin. Similar to all serpins, α₁-antitrypsin undergoes a marked conformational change to inhibit proteinases, which involves the insertion of the reactive centre loop into the middle of β-sheet A. This conformational change is possible because the native state of the serpin superfamily is metastable. However, the instability of the native state of α₁-antitrypsin makes it extremely susceptible to misfolding and polymerization, which results in the formation of more thermodynamically stable conformations. The most common mutation that causes polymerization in α₁-antitrypsin is the Z mutation (Glu342Lys), which is present in approximately 4% of northern Europeans. This mutation does not alter the stability of the native molecule but slows down its folding rate such that a polymerization-prone intermediate state persists longer, favouring polymerization (Knaupp et al, 2010). In addition, the native state of Z α₁-antitrypsin is more easily polymerized than its wild-type counterpart (Lomas et al, 1992). Although we have known the structure of native wild-type α₁-antitrypsin for more than 10 years (Elliott et al, 2000), and despite a wealth of biochemical and biophysical studies, we do not know the structure of the final polymeric form.Open in a separate windowFigure 1Structures of native α₁-antitrypsin and the known three types of polymer. The reactive centre loop region is highlighted in blue. Antitrypsin is deposited in the Protein Data Bank, ID no. 1QLP. Models of the s4A/s5A swap polymer and carboxy-terminal swap polymer were kindly provided by Professor J. Huntington; the model of the s4A swap polymer was kindly provided by Professor J. Whisstock.Over the past 20 years, various linkages between α₁-antitrypsin monomers have been reported and/or suggested, which involve different sheets and extents of interaction. Until recently, the most widely accepted model for α₁-antitrypsin polymerization involved the reactive centre loop of one molecule entering the β-sheet A of another in the strand 4 position (s4A swap polymer; Fig 1; Sivasothy et al, 2000), which was supported by extensive biochemical and biophysical analyses. This model was recently challenged when Yamasaki and colleagues described a new polymeric linkage in which monomers were linked by the insertion of two strands (strands 4 and 5) into β-sheet A of another serpin (s4A/s5A swap polymer; Fig 1; Yamasaki et al, 2008). Notably, these polymers were formed in the presence of the denaturant guanidine hydrochloride and so their physiological relevance was unclear. Extensive experimental work by the Lomas group has shown that heat-induced polymerization of α₁-antitrypsin produces polymers with a structure similar to those formed in hepatocellular inclusions (Ekeowa et al, 2010). The key to their studies was the identification and characterization of the antibody 2C1, which recognizes only polymerized α₁-antitrypsin formed both in vitro and in vivo (Miranda et al, 2010).“One of the most striking results of this work is the heterogeneity of polymer formation, which has important implications…”In this current paper, Yamasaki and colleagues set out to determine the structure of these heat-induced polymers. The authors initially compare heat- and denaturant-induced polymers by using native PAGE. They find that the s4A/s5A swap polymers dominate when denaturant is used to induce polymerization, whereas the heat-induced polymers are made up of a mixture of s4A/s5A swap polymers and another polymer morphology that binds to the 2C1 antibody. By using this information, they construct a recombinant α₁-antitrypsin molecule that cannot undergo the s4A/s5A swap reaction. By heating this α₁-antitrypsin variant at 60 °C, they form and subsequently purify short polymers that bind to the 2C1 antibody, indicating that they contain the pathological structure. The resultant polymer is a trimer that cannot be extended. Structural analysis showed that the monomers are linked through a swap of secondary structure involving the carboxyl terminus of the protein, specifically the first strand from the β-sheet C and strands 4 and 5 from β-sheet B were swapped from one serpin to another (C-terminal swap polymer; Fig 1).“…more than one polymer structure might be formed simultaneously during polymerization […] toxic and non-toxic polymers might coexist”The C-terminal swap polymer was obtained by heating recombinant protein at 60 °C, raising questions about its biological relevance, which the authors tried to answer by using protein engineering. For the C-terminal swap polymer to form, the C-terminus must move. Thus, the authors engineered a disulphide bond between the third strand of β-sheet C and the C-terminus, effectively preventing the conformational change. Notably, when this disulphide-bonded protein was polymerized by using heat, only s4A/s5A swap polymers—which cannot bind to the 2C1 antibody—were formed. In further experiments, they used a protein engineering approach to examine what happens in two cell models—the yeast Pichia pastoris and monkey COS-7 cells—of Z α₁-antitrypsin production. Both models produce Z α₁-antitrypsin polymers that react with the 2C1 antibody. By using the introduced cysteine residues to probe for the polymeric linkage, they were able to show that the C-terminal swap mechanism dominated in both cell models.The study by Yamasaki and colleagues provides another important piece of the puzzle in identifying, characterizing and linking all the players involved in α₁-antitrypsin deficiency. One of the most striking results of this work is the heterogeneity of polymer formation, which has important implications for understanding this disease and the development of therapeutic strategies. α₁-Antitrypsin is a flexible molecule capable of extreme conformational change and this inherent ‘desire'' for a more stable conformation makes it susceptible to polymerization. Numerous parallel pathways of polymer production probably occur, but the structural and/or environmental factors involved in deciding which pathway is followed remain unknown. In addition, does this ability to form different polymers affect which type of polymer is cleared from the cell? The kinetics of these polymerization reactions need to be elucidated and previous studies by several groups might need to be re-evaluated, as it is possible that heterogeneous populations of polymers were being formed, which would confuse the data analysis.From a biomedical perspective, identifying the pathological species and determining how it damages the liver is critical. The C-terminal swap polymer is probably found in hepatocytes, but this does not mean that it is the toxic agent. The results of the Yamasaki study suggest that more than one polymer structure might be formed simultaneously during polymerization, which raises the possibility that toxic and non-toxic polymers might coexist. Therefore, another polymer form—such as the s4A/s5A swap polymer or one not yet identified—could be damaging to cells. Answers to these questions will come in time and hopefully will lead to successful therapeutic approaches to prevent α₁-antitrypsin deficiency.