Density and diversity - Nature

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Jun 13, 2002 - Astronomy, University of Maryland at College Park,. College Park, Maryland 20742, USA. e-mail: dcr@astro.umd.edu. 1. Nesvorný, D., Bottke ...
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Derek C. Richardson is in the Department of Astronomy, University of Maryland at College Park, College Park, Maryland 20742, USA. e-mail: [email protected]

1. Nesvorny´, D., Bottke, W. F. Jr, Dones, L. & Levison, H. F. Nature 417, 720–722 (2002). 2. Housen, K. R., Holsapple, K. A. & Voss, M. E. Nature 402, 155–157 (1999). 3. Asphaug, E., Ostro, S. J., Hudson, R. S., Scheeres, D. J. & Benz, W. Nature 393, 437–440 (1998). 4. Zappalà, V., Bendjoya, Ph., Cellino, A., Farinella, P. & Froeschle, C. Icarus 116, 291–314 (1995). 5. Michel, P., Benz, W., Tanga, P. & Richardson, D. C. Science 294, 1696–1700 (2001). 6. Bottke, W. F. Jr, Vokrouhlicky´, D., Broz, M., Nesvorny´, D. & Morbidelli, A. Science 294, 1693–1696 (2001). 7. Farinella, P., Vokrouhlicky´, D. & Hartmann, W. K. Icarus 132, 378–387 (1998). 8. Durda, D. D., Greenberg, R. & Jedicke, R. Icarus 135, 431–440 (1998). 9. Clark, B. E. et al. Meteor. Planet. Sci. 36, 1617–1637 (2001). ›

erase the tell-tale signatures of the break-up. So it might be possible to determine whether the family members are intact fragments or gravitational re-accumulations of smaller pieces. This new cluster will no doubt be the focus of attention for the asteroid community for some time. Meanwhile, the search for ever younger families will continue, in the hope of taking us closer to understanding the origins of our Solar System. ■

Ecology

Density and diversity Hans ter Steege and Roderick Zagt One explanation for the especially rich diversity of trees in the tropics is that a process called ‘density-dependent mortality’ operates there. It turns out, however, that this process occurs in temperate forests too. he latitudinal gradient in species diversity is arguably the most universal pattern in global biodiversity: the lower the latitude, the higher the number of species in a given area. This pattern, with biodiversity peaking in the tropics (Fig. 1), is found in most taxonomic groups and may be as old as life itself 1–3. For plants, one explanation centres on a phenomenon called ‘densitydependent mortality’, in which the survival rates of species decrease as they become more common, leaving space for rarer species. It has been suggested4,5 that densitydependent mortality is more intense at lower latitudes, so, at least in part, accounting for the gradient in diversity. As they describe on page 732 of this issue, however, Hille Ris Lambers and colleagues6 have tested this hypothesis and found it wanting. It is not surprising that many researchers ROINE MAGNUSSON/THE IMAGE BANK

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have sought to find an explanation for the latitudinal pattern in species diversity. Biologists study diversity at different scales and it is becoming clear that scale is an important bridging element between the various theories that have been developed for regional and local levels. As far as trees are concerned, local processes such as the rate and extent at which gaps for seedling colonization occur, as well as density-dependent mortality, may limit the extent to which one species excludes another, and thus promote local diversity. Densitydependent mortality, however, will maintain high diversity only if it is species specific — that is, if it decreases the density of a species as a function of the density of that species alone, rather than of the density of all species. If species-specific, density-dependent mortality contributes to the latitudinal gradient in species diversity, the effect should be

Figure 1 Trees in the tropics — the height of diversity. 698

© 2002 Nature Publishing Group

stronger in the tropics than in temperate areas. The rationale for this is that much seed and seedling destruction stems from attack by insects and fungi, which reach higher densities in tropical regions because the tropics do not experience seasonal variations and tend to remain hot and humid4,5. Hille Ris Lambers et al.6, however, show that density-dependent mortality acts in temperate as well as in tropical forests. Their results come from a forest in North Carolina, where they found that six out of seven tree species experience density-dependent mortality at one or more transitions in their early stages: from seed to seedbank; from seed or seedbank to seedling; and in seedling survival (the seedbank phase is a latent period in which seeds lie dormant in the soil before germination). The results clearly show not just the effect of general density-dependent mortality, but also species-specific, densitydependent mortality. This suggests that rather than the driving factors being resource competition for light or nutrients alone, predators or pathogens are responsible. Hille Ris Lambers et al. also compared previous studies carried out in temperate and tropical areas, in which several species were tested for density-dependent mortality, and conclude that the proportion of species affected is not greater in the tropics. All in all, this study6 adds support to those who claim that general ecological mechanisms, such as the creation of gaps in vegetation that allow colonization by seedlings, and density-dependent regulation, operate similarly in the tropics and temperate zones. So theories invoking these processes fail to explain the higher diversity in the tropics compared with temperate zones. Still, further investigations are required. As Hille Ris Lambers et al. point out, many different protocols have been used in this kind of research, producing varying and sometimes confusing results. By re-analysing their own data with the approaches used in other studies, the authors show that these approaches have invariably underestimated the effects of density dependence. They propose a framework for simultaneously assessing the impact of seedling and adult density on seed and seedling fate. This framework should now be applied in future work at various latitudes. The authors’ main message, then, is that the proportion of species subject to densitydependent regulation is not lower in temperate areas than in the tropics. But the ecologically more significant question may be to what extent species are actually regulated by the process. Are the effects strong or weak? And is there a latitudinal component? Addressing these questions will require identifying and quantifying latitudinal trends in the relevant factors. Earlier work demonstrated that density-dependent patterns of seed loss tend to be associated with predation by NATURE | VOL 417 | 13 JUNE 2002 | www.nature.com/nature

news and views Random extinction

Immigration

Speciation

Regional diversity

Environmental filters Dispersal limitation

Local diversity

Interspecies competition

Predation

Extinction

Figure 2 Determinants of biodiversity. Impacts on diversity occur at both regional and local scales8,9: here, green arrows indicate processes that increase diversity (species are added) and red arrows those that decrease it (species are lost). Regionally, diversity is mainly influenced by speciation and extinction and, to a certain extent, by immigration. These processes determine the number of regional species from which communities can ‘draw’ particular species. Of course not all species can occur everywhere, either because the habitat is unsuitable (environmental filters) or because of constraints on their movement (dispersal limitation). Locally, processes such as interspecies competition, random extinction and predation affect diversity. Predation can have a double effect. It can remove species. But in the case of density-dependent mortality of seeds and seedlings discussed by Hille Ris Lambers et al.6, it can increase diversity if it favours rarer species by selectively reducing the population density of the most common species.

insects rather than by vertebrates, and that if spatial and temporal availability of seeds is predictable it can have an effect on seed loss7. So which predators determined the outcomes of the studies by Hille Ris Lambers et al.? And is there a latitudinal difference in the relative prevalence of insect and vertebrate predation, and of fungal attack? There is likely to be a difference in the fruiting time of particular plant communities, and in the occurrence of irregular heavy fruiting that swamps consumers and means a higher proportion of seeds escapes predation. If indeed the small-scale processes observed in temperate and tropical areas are much the same, how can the latitudinal gradient in biodiversity be explained? Diversity is influenced by regional as well as local processes2,3,8, all operating at specific temporal scales (Fig. 2). At the large spatial scale at which the gradient is evident, the answer must, at least partly, lie in the balance between speciation and extinction. A further question then centres on the relative importance of local processes in this balance. It is obvious that there are several mechanisms that can contribute to the latitudinal

gradient1–4,8. There is unlikely to be a simple answer, and any explanation probably consists of a mix of local, regional, global and historical factors. ■ Hans ter Steege is at the International Institute for Geoinformation Science and Earth Observation (ITC), PO Box 6, NL-7500 AA Enschede, The Netherlands. e-mail: [email protected] Roderick Zagt is at the National Herbarium of the Netherlands, Utrecht University Branch, W. C. van Unnik Building, Heidelberglaan 2, 3584 CS Utrecht, The Netherlands. e-mail: [email protected] 1. Gaston, K. J. Nature 504, 220–227 (2000). 2. Rosenzweig, M. L. Species Diversity in Space and Time (Cambridge Univ. Press, 1995). 3. Huston, M. Biological Diversity: The Coexistence of Species on Changing Landscapes (Cambridge Univ. Press, 1994). 4. Givnish, T. J. J. Ecol. 87, 193–210 (1999). 5. Harms, K. E. et al. Nature 404, 493–495 (2000). 6. Hille Ris Lambers, J., Clark, J. S. & Beckage, B. Nature 417, 732–735 (2002). 7. Hammond, D. S. & Brown, V. K. in Dynamics of Tropical Communities (eds Newbery, D. N., Prins, H. H. T. & Brown, V. K.) 51–78 (Blackwell Science, London, 1998). 8. Ricklefs, R. E. & Schluter, D. Species Diversity in Ecological Communities (Univ. Chicago Press, 1993). 9. Hubbell, S. P. The Unified Theory of Biodiversity and Biogeography (Princeton Univ. Press, 2001).

Cardiovascular biology

A cholesterol tether Bart Staels The build-up of cholesterol in the walls of arteries is a hallmark of atherosclerosis. Work with transgenic mice has revealed a specific interaction through which cholesterol deposition is initiated. therosclerosis is a disease of the arterial wall that is characterized by cholesterol accumulation and culminates in potentially life-threatening conditions such as heart attack, stroke and angina. How the process starts is poorly understood. In their paper on page 750 of this issue, however, Skålén and colleagues1 show that at least

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part of the explanation lies in a highly specific interaction between proteoglycans, which are components of the artery wall, and a constituent of lipoproteins called apoB. The atherogenic process starts at an early age with the deposition in blood-vessel walls of lipids such as cholesterol, derived from lipoproteins circulating in the bloodstream, © 2002 Nature Publishing Group

which leads to the formation of the characteristic ‘fatty streaks’. Inflammatory white blood cells congregate at these damaged areas through their interaction with adhesion molecules expressed by cells in the endothelial layer, which lines the inside of blood vessels. This can then set off a cascade of inflammatory processes and further lipid deposition, leading eventually to full-blown atherosclerosis with plaque formation in the artery wall. Atherosclerosis is thus viewed as a chronic inflammatory disease of the bloodvessel wall2,3. An early event — the development of arterial damage and fatty deposits — is the capture, by cells called macrophages, of lipoproteins retained in the arterial wall, resulting in the formation of lipid-laden ‘foam cells’. Although it has not been shown experimentally, the ‘response-to-retention’ hypothesis proposes that the retention and modification of these lipoproteins in the arterial lining is one of the initiating events that triggers the inflammatory response4. Among the many risk factors for cardiovascular disease are raised concentrations of blood cholesterol, especially cholesterol transported by low-density lipoproteins (LDLs) containing the protein apoB100 (an apolipoprotein). Results from clinical trials in which concentrations of cholesterol in the blood stream were pharmacologically lowered established LDL cholesterol unequivocally as a culprit in atherosclerosis. But what triggers the accumulation of cholesterol-containing lipoproteins in the sub-endothelial space of the arterial wall? As long ago as 1949, Mogen Faber5 suggested that proteoglycans are involved — these are components of the extracellular matrix that are produced, for instance, by smoothmuscle cells that have migrated into the plaque. But because of a lack of suitable animal models, the effects of an interaction between proteoglycans and lipoproteins on atherogenesis have not been amenable to experimental testing in vivo — until now. Skålén et al.1 have analysed the susceptibility to atherosclerosis of transgenic mice carrying human apoB100 genes with a range of mutations that yield proteins with reduced affinity for proteoglycans6. They show that, when fed a diet that promotes atherogenesis, these mice develop plaques more slowly than control mice expressing the normal human apoB100 protein. The LDL particles from transgenic mice carrying normal and mutated human apoB100 were transported similarly across the endothelial lining of the wall and showed the same susceptibility to oxidation, inflammatory properties and capture by macrophages. So Skålén et al. conclude that the retention of apoB100 lipoproteins by proteoglycans immediately beneath the endothelial layer is a central event in early atherogenesis. The strengths, as well as the limitations, of this study lie in the fact that Skålén and 699