erase the tell-tale signatures of the break-up.So it might be possible to determine whetherthe family members are intact fragments orgravitational re-accumulations of smallerpieces. This new cluster will no doubt be thefocus of attention for the asteroid communityfor some time. Meanwhile, the search for everyounger families will continue, in the hope oftaking us closer to understanding the originsof our Solar System. ■

Derek C. Richardson is in the Department ofAstronomy, University of Maryland at College Park,College Park, Maryland 20742, USA.e-mail: dcr@astro.umd.edu

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stronger in the tropics than in temperateareas. The rationale for this is that much seedand seedling destruction stems from attackby insects and fungi, which reach higherdensities in tropical regions because thetropics do not experience seasonal varia-tions and tend to remain hot and humid4,5.

Hille Ris Lambers et al.6, however, showthat density-dependent mortality acts intemperate as well as in tropical forests. Theirresults come from a forest in North Carolina,where they found that six out of seven treespecies experience density-dependent mor-tality at one or more transitions in their earlystages: from seed to seedbank; from seed orseedbank to seedling; and in seedling survival(the seedbank phase is a latent period inwhich seeds lie dormant in the soil beforegermination). The results clearly show notjust the effect of general density-dependentmortality, but also species-specific, density-dependent mortality. This suggests thatrather than the driving factors being resourcecompetition for light or nutrients alone,predators or pathogens are responsible. HilleRis Lambers et al. also compared previousstudies carried out in temperate and tropicalareas, in which several species were tested fordensity-dependent mortality, and concludethat the proportion of species affected is notgreater in the tropics.

All in all, this study6 adds support to those who claim that general ecologicalmechanisms, such as the creation of gaps invegetation that allow colonization by seed-lings, and density-dependent regulation,operate similarly in the tropics and temperatezones. So theories invoking these processesfail 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, manydifferent protocols have been used in this kind of research, producing varying andsometimes confusing results. By re-analysingtheir own data with the approaches used inother studies, the authors show that theseapproaches have invariably underestimatedthe effects of density dependence. They propose a framework for simultaneouslyassessing the impact of seedling and adultdensity on seed and seedling fate. This frame-work should now be applied in future work at various latitudes.

The authors’ main message, then, is thatthe proportion of species subject to density-dependent regulation is not lower in temperate areas than in the tropics. But theecologically more significant question may beto what extent species are actually regulatedby the process. Are the effects strong or weak?And is there a latitudinal component?Addressing these questions will require iden-tifying and quantifying latitudinal trends inthe relevant factors. Earlier work demonstrat-ed that density-dependent patterns of seedloss tend to be associated with predation by

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698 NATURE | VOL 417 | 13 JUNE 2002 | www.nature.com/nature

The latitudinal gradient in species diver-sity is arguably the most universal pat-tern in global biodiversity: the lower the

latitude, the higher the number of species ina given area. This pattern, with biodiversitypeaking in the tropics (Fig. 1), is found inmost taxonomic groups and may be as oldas life itself 1–3. For plants, one explanationcentres on a phenomenon called ‘density-dependent mortality’, in which the survivalrates of species decrease as they becomemore common, leaving space for rarerspecies. It has been suggested4,5 that density-dependent mortality is more intense at lowerlatitudes, so, at least in part, accounting forthe gradient in diversity. As they describe onpage 732 of this issue, however, Hille RisLambers and colleagues6 have tested thishypothesis and found it wanting.

It is not surprising that many researchers

have sought to find an explanation for the lati-tudinal pattern in species diversity. Biologistsstudy diversity at different scales and it isbecoming clear that scale is an importantbridging element between the various theo-ries that have been developed for regional andlocal levels. As far as trees are concerned, localprocesses such as the rate and extent at whichgaps for seedling colonization occur, as well asdensity-dependent mortality, may limit theextent to which one species excludes another,and thus promote local diversity. Density-dependent mortality, however, will maintainhigh diversity only if it is species specific —that is, if it decreases the density of a species asa function of the density of that species alone,rather than of the density of all species.

If species-specific, density-dependentmortality contributes to the latitudinal gra-dient in species diversity, the effect should be

Ecology

Density and diversity Hans ter Steege and Roderick Zagt

One explanation for the especially rich diversity of trees in the tropics isthat a process called ‘density-dependent mortality’ operates there. It turnsout, however, that this process occurs in temperate forests too.

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

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insects rather than by vertebrates, and that ifspatial and temporal availability of seeds ispredictable it can have an effect on seed loss7.So which predators determined the outcomesof the studies by Hille Ris Lambers et al.? And is there a latitudinal difference in the relative prevalence of insect and vertebratepredation, and of fungal attack? There is likely to be a difference in the fruiting time of particular plant communities, and in theoccurrence of irregular heavy fruiting thatswamps consumers and means a higher proportion of seeds escapes predation.

If indeed the small-scale processesobserved 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 specifictemporal scales (Fig. 2). At the large spatialscale at which the gradient is evident, theanswer must, at least partly, lie in the balancebetween speciation and extinction. A furtherquestion then centres on the relative impor-tance of local processes in this balance. It is obvious that there are several mechanismsthat can contribute to the latitudinal

gradient1–4,8. There is unlikely to be a simpleanswer, and any explanation probably con-sists of a mix of local, regional, global andhistorical factors. ■

Hans ter Steege is at the International Institute forGeoinformation Science and Earth Observation(ITC), PO Box 6, NL-7500 AA Enschede, The Netherlands.e-mail: tersteege@itc.nlRoderick Zagt is at the National Herbarium of theNetherlands, Utrecht University Branch, W. C. vanUnnik Building, Heidelberglaan 2, 3584 CSUtrecht, The Netherlands.e-mail: lipaugus@luna.nl1. 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).

which leads to the formation of the charac-teristic ‘fatty streaks’. Inflammatory whiteblood cells congregate at these damagedareas through their interaction with adhe-sion molecules expressed by cells in theendothelial layer, which lines the inside ofblood vessels. This can then set off a cascadeof inflammatory processes and further lipiddeposition, leading eventually to full-blownatherosclerosis with plaque formation in theartery wall. Atherosclerosis is thus viewed asa chronic inflammatory disease of the blood-vessel wall2,3. An early event — the develop-ment of arterial damage and fatty deposits —is the capture, by cells called macrophages, oflipoproteins retained in the arterial wall,resulting in the formation of lipid-laden‘foam cells’. Although it has not been shownexperimentally, the ‘response-to-retention’hypothesis proposes that the retention andmodification of these lipoproteins in thearterial lining is one of the initiating eventsthat triggers the inflammatory response4.

Among the many risk factors for cardio-vascular disease are raised concentrations of blood cholesterol, especially cholesteroltransported by low-density lipoproteins(LDLs) containing the protein apoB100 (anapolipoprotein). Results from clinical trialsin which concentrations of cholesterol in the blood stream were pharmacologicallylowered established LDL cholesterolunequivocally as a culprit in atherosclerosis.But what triggers the accumulation of cholesterol-containing lipoproteins in thesub-endothelial space of the arterial wall? Aslong ago as 1949, Mogen Faber5 suggestedthat proteoglycans are involved — these arecomponents of the extracellular matrix thatare produced, for instance, by smooth-muscle cells that have migrated into theplaque. But because of a lack of suitable animal models, the effects of an interactionbetween proteoglycans and lipoproteins onatherogenesis have not been amenable toexperimental testing in vivo — until now.

Skålén et al.1 have analysed the suscepti-bility to atherosclerosis of transgenic micecarrying human apoB100 genes with a range of mutations that yield proteins withreduced affinity for proteoglycans6. Theyshow that, when fed a diet that promotesatherogenesis, these mice develop plaquesmore slowly than control mice expressingthe normal human apoB100 protein. TheLDL particles from transgenic mice carryingnormal and mutated human apoB100 weretransported similarly across the endotheliallining of the wall and showed the same susceptibility to oxidation, inflammatoryproperties and capture by macrophages. SoSkålén et al. conclude that the retention of apoB100 lipoproteins by proteoglycansimmediately beneath the endothelial layer isa central event in early atherogenesis.

The strengths, as well as the limitations,of this study lie in the fact that Skålén and

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NATURE | VOL 417 | 13 JUNE 2002 | www.nature.com/nature 699

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 andextinction and, to a certain extent, by immigration. These processes determine the number ofregional 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 interspeciescompetition, 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.

Speciation

Immigration

Extinction

Environmental filtersRegionaldiversity Dispersal limitation

Localdiversity

Predation

Random extinction

Interspeciescompetition

Atherosclerosis is a disease of the arterialwall that is characterized by chol-esterol accumulation and culminates

in potentially life-threatening conditionssuch as heart attack, stroke and angina. Howthe process starts is poorly understood. Intheir paper on page 750 of this issue, how-ever, Skålén and colleagues1 show that at least

part of the explanation lies in a highly specificinteraction between proteoglycans, whichare components of the artery wall, and a constituent of lipoproteins called apoB.

The atherogenic process starts at an earlyage with the deposition in blood-vessel wallsof lipids such as cholesterol, derived fromlipoproteins circulating in the bloodstream,

Cardiovascular biology

A cholesterol tetherBart Staels

The build-up of cholesterol in the walls of arteries is a hallmark ofatherosclerosis. Work with transgenic mice has revealed a specificinteraction through which cholesterol deposition is initiated.

© 2002 Nature Publishing Group