Soil organic carbon is not just for soil scientists: measurement recommendations for diverse practitioners.

Soil organic carbon (SOC) regulates terrestrial ecosystem functioning, provides diverse energy sources for soil microorganisms, governs soil structure, and regulates the availability of organically bound nutrients. Investigators in increasingly diverse disciplines recognize how quantifying SOC attributes can provide insight about ecological states and processes. Today, multiple research networks collect and provide SOC data, and robust, new technologies are available for managing, sharing, and analyzing large data sets. We advocate that the scientific community capitalize on these developments to augment SOC data sets via standardized protocols. We describe why such efforts are important and the breadth of disciplines for which it will be helpful, and outline a tiered approach for standardized sampling of SOC and ancillary variables that ranges from simple to more complex. We target scientists ranging from those with little to no background in soil science to those with more soil-related expertise, and offer examples of the ways in which the resulting data can be organized, shared, and discoverable.

Sensitivity of global soil carbon stocks to combined nutrient enrichment.

Soil stores approximately twice as much carbon as the atmosphere and fluctuations in the size of the soil carbon pool directly influence climate conditions. We used the Nutrient Network global change experiment to examine how anthropogenic nutrient enrichment might influence grassland soil carbon storage at a global scale. In isolation, enrichment of nitrogen and phosphorous had minimal impacts on soil carbon storage. However, when these nutrients were added in combination with potassium and micronutrients, soil carbon stocks changed considerably, with an average increase of 0.04 KgCm-2  year-1 (standard deviation 0.18 KgCm-2  year-1 ). These effects did not correlate with changes in primary productivity, suggesting that soil carbon decomposition may have been restricted. Although nutrient enrichment caused soil carbon gains most dry, sandy regions, considerable absolute losses of soil carbon may occur in high-latitude regions that store the majority of the world's soil carbon. These mechanistic insights into the sensitivity of grassland carbon stocks to nutrient enrichment can facilitate biochemical modelling efforts to project carbon cycling under future climate scenarios.

Plant nitrogen concentration and isotopic composition in residential lawns across seven US cities.

Human drivers are often proposed to be stronger than biophysical drivers in influencing ecosystem structure and function in highly urbanized areas. In residential land cover, private yards are influenced by individual homeowner preferences and actions while also experiencing large-scale human and biophysical drivers. We studied plant nitrogen (%N) and N stable isotopic composition (δ(15)N) in residential yards and paired native ecosystems in seven cities across the US that span major ecological biomes and climatic regions: Baltimore, Boston, Los Angeles, Miami, Minneapolis-St. Paul, Phoenix, and Salt Lake City. We found that residential lawns in three cities had enriched plant δ(15)N (P < 0.03) and in six cities higher plant N (%) relative to the associated native ecosystems (P < 0.05). Plant δ(15)N was progressively depleted across a gradient of urban density classes in Baltimore and Boston (P < 0.05). Lawn fertilization was associated with depleted plant δ(15)N in Boston and Los Angeles (P < 0.05), and organic fertilizer additions were associated with enriched plant δ(15)N in Los Angeles and Salt Lake City (P < 0.04). Plant δ(15)N was significantly enriched as a function of housing age in Baltimore (r (2) = 0.27, P < 0.02), Boston (r (2) = 0.27, P < 0.01), and Los Angeles (r (2) = 0.34, P < 0.01). These patterns in plant δ(15)N and plant N (%) across these cities suggests that N sources to lawns, as well as greater rates of N cycling combined with subsequent N losses, may be important drivers of plant N dynamics in lawn ecosystems at the national scale.

Sinks for nitrogen inputs in terrestrial ecosystems: a meta-analysis of 15N tracer field studies.

Effects of anthropogenic nitrogen (N) deposition and the ability of terrestrial ecosystems to store carbon (C) depend in part on the amount of N retained in the system and its partitioning among plant and soil pools. We conducted a meta-analysis of studies at 48 sites across four continents that used enriched 15N isotope tracers in order to synthesize information about total ecosystem N retention (i.e., total ecosystem 15N recovery in plant and soil pools) across natural systems and N partitioning among ecosystem pools. The greatest recoveries of ecosystem 15N tracer occurred in shrublands (mean, 89.5%) and wetlands (84.8%) followed by forests (74.9%) and grasslands (51.8%). In the short term (< 1 week after 15N tracer application), total ecosystem 15N recovery was negatively correlated with fine-root and soil 15N natural abundance, and organic soil C and N concentration but was positively correlated with mean annual temperature and mineral soil C:N. In the longer term (3-18 months after 15N tracer application), total ecosystem 15N retention was negatively correlated with foliar natural-abundance 15N but was positively correlated with mineral soil C and N concentration and C:N, showing that plant and soil natural-abundance 15N and soil C:N are good indicators of total ecosystem N retention. Foliar N concentration was not significantly related to ecosystem 15N tracer recovery, suggesting that plant N status is not a good predictor of total ecosystem N retention. Because the largest ecosystem sinks for 15N tracer were below ground in forests, shrublands, and grasslands, we conclude that growth enhancement and potential for increased C storage in aboveground biomass from atmospheric N deposition is likely to be modest in these ecosystems. Total ecosystem 15N recovery decreased with N fertilization, with an apparent threshold fertilization rate of 46 kg N x ha(-1) x yr(-1) above which most ecosystems showed net losses of applied 15N tracer in response to N fertilizer addition.

Carbon, nitrogen, and phosphorus fluxes in household ecosystems in the Minneapolis-Saint Paul, Minnesota, urban region.

Rapid worldwide urbanization calls for a better understanding of the biogeochemical cycling of those macroelements that have large environmental impacts in cities. This study, part of the Twin Cities Household Ecosystem Project, quantified fluxes of carbon (C), nitrogen (N), and phosphorus (P) at the scale of individual households in the Minneapolis-Saint Paul metropolitan area in Minnesota, USA. We estimated input and output fluxes associated with several components of household activities including air and motor vehicle travel, food consumption, home energy use, landscape, pets, and paper and plastic use for 360 owner-occupied, stand-alone households. A few component fluxes dominated total input fluxes of elements. For instance, air and motor vehicle transportation, together with home energy use, accounted for 85% of total C consumption and emissions. All total and component fluxes were skewed to varying degrees, suggesting that policies targeting disproportionately high fluxes could be an effective and efficient way to reduce pollution. For example, 20% of households contributed 75% of air travel emissions and 40% of motor vehicle emissions. Home energy use was more nearly normally distributed. Nitrogen fluxes were dominated by human diet and lawn fertilizer applications, which together accounted for 65% of total household N inputs. The majority of P inputs were associated with human diet, use of detergents, and pet food. A large portion of the variation among household fluxes of C, N, and P was related to a few biophysical variables. A better understanding of the biophysical, demographic, and behavioral drivers of household activities that contribute to C, N, and P fluxes is pivotal for developing accurate urban biogeochemical models and for informing policies aimed at reducing sources of pollution in urban ecosystems.

A genetic model to investigate drug-target interactions at the ribosomal decoding site.

Recent advances in X-ray crystallography have greatly contributed to the understanding of the structural interactions between aminoglycosides and the ribosomal decoding site. Efforts to genetically probe the functional relevance of proposed drug-nucleotide contacts have in part been hampered by the presence of multiple rRNA operons in most bacteria. A derivative of the Gram-positive Mycobacterium smegmatis was rendered single rRNA operon allelic by means of gene inactivation techniques. In this system, genetic manipulation of the single chromosomal rRNA operon results in cells carrying homogeneous populations of mutant ribosomes. An exhaustive mutagenesis study of the ribosomal A site has been performed to define the importance of individual drug-nucleotide contacts. Mutational alterations in the M. smegmatis decoding site are discussed here, comparing the results with those obtained in other organisms. Implications for the selectivity of antimicrobial agents and for the fitness cost of resistance mutations are addressed.

Mutagenesis of 16S rRNA C1409-G1491 base-pair differentiates between 6'OH and 6'NH3+ aminoglycosides.

Using a single rRNA allelic Gram-positive model system, we systematically mutagenized 16S rRNA positions 1409 and 1491 to probe the functional relevance of structural interactions between aminoglycoside antibiotics and the A-site rRNA that were suggested by X-ray crystallography. At the structural level, the interaction of the 2-deoxystreptamine aminoglycosides with the rRNA base-pair C1409-G1491 has been suggested to involve the following features: (i) ring I of the disubstituted 2-deoxystreptamines stacks upon G1491 and H-bonds to the Watson-Crick edge of A1408; (ii) ring III of the 4,5-disubstituted aminoglycosides shows hydrogen bonding to G1491. However, we found that mutants with altered 16S rRNA bases 1409 and 1491 discriminated poorly between 4,5-disubstituted and 4,6-disubstituted 2-deoxystreptamines, but differentially affected aminoglycosides with a hydroxyl group versus an ammonium group at position 6' of ring I, e.g. G1491U conferred high-level drug resistance to paromomycin and geneticin, but not to neomycin, tobramycin or gentamicin.

Phosphorylation-dependent proline isomerization catalyzed by Pin1 is essential for tumor cell survival and entry into mitosis.

Pin1, a member of the parvulin family of peptidyl-prolyl cis-trans isomerases (PPIases) has been implicated in the G2-M transition of the mammalian cell cycle. Pin1 interacts with a series of mitotic phosphoproteins, including Polo-like kinase-1, Cdc25C, and Cdc27, and is thought to act as a phosphorylation-dependent PPIase for these target molecules. Pin1 recognizes phosphorylated serine-proline or threonine-proline peptide-bonds in test substrates up to 1300-fold better than in the respective unphosphorylated peptides. To test directly whether Pin1 regulates the G2-M transition and/or progression through mitosis by catalyzing phosphorylation-dependent prolyl isomerization of essential mitotic targets, we examined the consequences of Pin1 depletion, achieved by (a) overexpression of Pin1 antisense RNA, (b) overexpression of dominant-negative Pin1, and (c) by a known small-molecule Pin1-PPIase inhibitor, juglone. The results of all of the three lines of investigation show that the catalytic activity of Pin1 is essential for tumor cell survival and entry into mitosis.

Consequences of changing biodiversity.

Human alteration of the global environment has triggered the sixth major extinction event in the history of life and caused widespread changes in the global distribution of organisms. These changes in biodiversity alter ecosystem processes and change the resilience of ecosystems to environmental change. This has profound consequences for services that humans derive from ecosystems. The large ecological and societal consequences of changing biodiversity should be minimized to preserve options for future solutions to global environmental problems.

Arctic and boreal ecosystems of western North America as components of the climate system.

Synthesis of results from several Arctic and boreal research programmes provides evidence for the strong role of high-latitude ecosystems in the climate system. Average surface air temperature has increased 0.3 °C per decade during the twentieth century in the western North American Arctic and boreal forest zones. Precipitation has also increased, but changes in soil moisture are uncertain. Disturbance rates have increased in the boreal forest; for example, there has been a doubling of the area burned in North America in the past 20 years. The disturbance regime in tundra may not have changed. Tundra has a 3-6-fold higher winter albedo than boreal forest, but summer albedo and energy partitioning differ more strongly among ecosystems within either tundra or boreal forest than between these two biomes. This indicates a need to improve our understanding of vegetation dynamics within, as well as between, biomes. If regional surface warming were to continue, changes in albedo and energy absorption would likely act as a positive feedback to regional warming due to earlier melting of snow and, over the long term, the northward movement of treeline. Surface drying and a change in dominance from mosses to vascular plants would also enhance sensible heat flux and regional warming in tundra. In the boreal forest of western North America, deciduous forests have twice the albedo of conifer forests in both winter and summer, 50-80% higher evapotranspiration, and therefore only 30-50% of the sensible heat flux of conifers in summer. Therefore, a warming-induced increase in fire frequency that increased the proportion of deciduous forests in the landscape, would act as a negative feedback to regional warming. Changes in thermokarst and the aerial extent of wetlands, lakes, and ponds would alter high-latitude methane flux. There is currently a wide discrepancy among estimates of the size and direction of CO2 flux between high-latitude ecosystems and the atmosphere. These discrepancies relate more strongly to the approach and assumptions for extrapolation than to inconsistencies in the underlying data. Inverse modelling from atmospheric CO2 concentrations suggests that high latitudes are neutral or net sinks for atmospheric CO2 , whereas field measurements suggest that high latitudes are neutral or a net CO2 source. Both approaches rely on assumptions that are difficult to verify. The most parsimonious explanation of the available data is that drying in tundra and disturbance in boreal forest enhance CO2 efflux. Nevertheless, many areas of both tundra and boreal forests remain net sinks due to regional variation in climate and local variation in topographically determined soil moisture. Improved understanding of the role of high-latitude ecosystems in the climate system requires a concerted research effort that focuses on geographical variation in the processes controlling land-atmosphere exchange, species composition, and ecosystem structure. Future studies must be conducted over a long enough time-period to detect and quantify ecosystem feedbacks.

The haemolysin-secreting ShlB protein of the outer membrane of Serratia marcescens: determination of surface-exposed residues and formation of ion-permeable pores by ShlB mutants in artificial lipid bilayer membranes.

The ShlB protein in the outer membrane of Serratia marcescens is the only protein known to be involved in secretion of the ShlA protein across the outer membrane. At the same time, ShlB converts ShlA into a haemolytic and a cytolytic toxin. Surface-exposed residues of ShlB were determined by reaction of an M2 monoclonal antibody with the M2 epitope DYKDDDDK inserted at 25 sites along the entire ShlB polypeptide. The antibody bound to the M2 epitope at 17 sites in intact cells, which indicated surface exposure of the epitope, and to 23 sites in isolated outer membranes. Two insertion mutants contained no ShlB(M2) protein in the outer membrane. The ShlB derivatives activated and/or secreted ShlA. To gain insights into the secretion mechanism, we studied whether highly purified ShlB and ShlB deletion derivatives formed pores in artificial lipid bilayer membranes. Wild-type ShlB formed channels with very low single channel conductance that rarely assumed an open channel configuration. In contrast, open channels with a considerably higher single channel conductance were observed with the deletion mutants ShlB(Delta65-186), ShlB(Delta87-153), and ShlB(Delta126-200). ShlB(Delta126-200) frequently formed permanently open channels, whereas the conductance caused by ShlB(Delta65-186) and ShlB(Delta87-153) did not assume a stationary value, but fluctuated rapidly between open and closed configurations. The results demonstrate the orientation of large portions of ShlB in the outer membrane and suggest that ShlB may function as a specialized pore through which ShlA is secreted.

YopJ of Yersinia pseudotuberculosis is required for the inhibition of macrophage TNF-alpha production and downregulation of the MAP kinases p38 and JNK.

Exposure of macrophages to lipopolysaccharide (LPS) leads to production of the pro-inflammatory cytokine, tumour necrosis factor alpha (TNF-alpha). Previous studies have suggested that pathogenic Yersinia spp. inhibit LPS-mediated production of TNF-alpha in macrophages, and that one of the Yop proteins secreted by the plasmid-encoded type III pathway is required for this activity. We found that TNF-alpha production was inhibited when J774A.1 murine macrophages were infected with wild-type Y. pseudotuberculosis but not with an isogenic ysc mutant defective for Yop secretion. We inactivated multiple yop genes to identify which of these factors are required for the inhibition of TNF-alpha production. A mutant unable to express yopJ was defective for the inhibition of TNF-alpha production. Production of TNF-alpha is regulated at the transcriptional and translational levels by several mitogen-activated protein (MAP) kinases. The MAP kinases p38 and JNK underwent sustained activation in macrophages infected with the yopJ mutant. Conversely, p38 and JNK were downregulated in macrophages infected with the wild-type strain. The ability of the yopJ mutant to downregulate p38 and JNK and to inhibit production of TNF-alpha was restored by the expression of yopJ+ in trans. Therefore, YopJ is required for Y. pseudotuberculosis to downregulate MAP kinases and inhibit the production of TNF-alpha in macrophages.

Specific phosphatidylethanolamine dependence of Serratia marcescens cytotoxin activity.

The cytolytic and haemolytic activity of Serratia marcescens is determined by the ShlA protein, which is secreted across the outer membrane with the aid of the ShlB protein. In the absence of ShlB, inactive ShlA* remains in the periplasm of Escherichia col transformed with an shlA-encoding plasmid, which indicates that ShlB converts ShlA* to active ShlA. ShlA* in a periplasmic extract and partially purified ShlA* were activated in vitro by partially purified ShlB. When both proteins were highly purified, ShlA* was only activated by ShlB when phosphatidylethanolamine (PE) or phosphatidylserine was added to the assay, while phosphatidylglycerol contributed little to ShlA* activation. Lyso-PE, cardiolipin, phosphatidylcholine, phosphatidic acid, lipopolysaccharide and various detergents could not substitute for PE. Although radioactively labelled PE was so tightly associated with ShlA that it remained bound to ShlA after heating and SDS-PAGE, it was not covalently linked to ShlA as PE could be removed by thin-layer chromatography with organic solvents. The number of PE molecules associated per molecule of ShlA was 3.9 +/- 2.2. Active ShlA was inactivated by treatment with phospholipase A2, which indicated that PE is also required for ShlA activity. ShlA-255 (containing the 255 N-terminal amino acids of ShlA) reversibly complemented ShlA* to active ShlA and was inactivated by phospholipase A2, which demonstrated that PE binds to the N-terminal portion of ShlA; this region has previously been found to be involved in ShlA secretion and activation. Electrospray mass spectroscopy of ShlA-255 determined a molar mass that corresponded to that of unmodified ShlA-255. An E. coli mutant that synthesized only minute amounts of PE did not secrete ShlA but contained residual cell-bound haemolytic activity. Since PE binds strongly to ShlA* in the absence of ShlB without converting ShlA* to haemolytic ShlA, ShlB presumably imposes a conformation on ShlA that brings PE into a position to mediate interaction of the hydrophilic haemolysin with the lipid bilayer of the eukaryotic membrane.

Involvement of mitogen-activated protein kinase pathways in the nuclear responses and cytokine production induced by Salmonella typhimurium in cultured intestinal epithelial cells.

Central to the pathogenesis of Salmonella typhimurium is its ability to engage the host cell in a two-way biochemical interaction. As a consequence of this interaction, a dedicated protein secretion system, termed type III, is activated in these bacteria and directs the translocation of signaling proteins into the host cell. Secretion of these proteins stimulates host cell signal transduction pathways that lead to a variety of cellular responses. An important feature of S. typhimurium pathogenesis is the induction of a profound inflammatory response in the intestinal epithelium. In this report, we show that S. typhimurium induces host cell signal transduction pathways that lead to the activation of the transcription factors NF-kappaB and AP-1, resulting in the production of proinflammatory cytokines such as IL-8. We also show that S. typhimurium infection of cultured intestinal epithelial cells results in the activation of the mitogen-activated protein (MAP) kinases ERK, JNK, and p38. Induction of these signaling pathways and the synthesis of IL-8 was strictly dependent on the function of the invasion-associated type III protein secretion system encoded by S. typhimurium. Pretreatment of cells with the highly specific p38 MAP kinase inhibitor SB 203580 prevented S. typhimurium-induced IL-8 production. These results indicate that the inflammatory response induced by S. typhimurium may be due to the specific stimulation of MAP kinase signaling pathways leading to nuclear responses.

Requirement of CDC42 for Salmonella-induced cytoskeletal and nuclear responses.

The bacterial pathogen Salmonella typhimurium triggers host cell signaling pathways that lead to cytoskeletal and nuclear responses required for pathogenesis. Here, the role of the small guanosine triphosphate (GTP)-binding protein CDC42Hs in these responses was examined. Expression of a dominant interfering mutant of CDC42 (CDC42HsN17) prevented S. typhimurium-induced cytoskeletal reorganization and subsequent macropinocytosis and bacterial internalization into host cells. Cells expressing constitutively active CDC42 (CDC42HsV12) internalized an S. typhimurium mutant unable to trigger host cell responses. Furthermore, expression of CDC42HsN17 prevented S. typhimurium-induced JNK kinase activation. These results indicate that CDC42 is required for bacterial invasion and induction of nuclear responses in host cells.

Enterobacterial hemolysins: activation, secretion and pore formation.

Two types of enterobacterial hemolysins have been studied in detail: the Escherichia coli alpha-hemolysin and the Serratia marcescens hemolysin. Although they have similar properties, they differ entirely in the number and structure of the proteins that determine their hemolytic activities, in the mechanism and the subcellular location of activation and in their secretion mechanisms.

Activation and secretion of Serratia hemolysin.

The hemolysin of Serratia marcescens (ShlA) is secreted into the culture medium and forms small pores of a defined size in erythrocytes and in black lipid membranes. The protein is synthesized as an inactive precursor of 1608 residues which is translocated across the cytoplasmic membrane by the Sec-export system. In the absence of the outer membrane protein ShlB, the ShlA protein (designated ShlA*) stays in the periplasm and displays about 0.1% of the activity of the secreted form. Secretion of ShlA with the help of ShlB is accompanied by its conversion to the hemolytic form. A ShlA derivative consisting of the N-terminal 238 residues of ShlA is secreted by ShlB, showing that the secretion signal resides in the amino terminal part of ShlA. ShlA* can be activated in vitro by a cell lysate containing ShlB, the activated ShlA remains hemolytic upon removal of ShlB. The assumed covalent modification of ShlA* by ShlB occurs in the N-terminus of ShlA since an amino terminal fragment (M(r) 28,000) secreted by ShlB, and a trypsin fragment of ShlA (M(r) 15,000) are both able to convert ShlA* to a hemolytic protein. In contrast to the permanent modification of ShlA* by ShlB, ShlA activity achieved by complementation with the ShlA fragments is abolished upon removal of the fragments. Apparently, the N-terminal portion of ShlA contains the information for secretion through the outer membrane and for insertion into the erythrocyte membrane. This information is lacking in ShlA* formed in the absence of ShlB but contained in the ShlA fragments formed in the presence of ShlB. The latter bind to ShlA* and direct ShlA* into the erythrocyte membrane. The fragments themselves are too short to build pores. The HpmA hemolysin of Proteus mirabilis shows extensive homology to ShlA. In vitro activation of HpmA* by ShlB and complementation by the 28 kDa ShlA fragment indicates a common activation mechanism.

Serratia marcescens forms a new type of cytolysin.

Most Serratia marcescens strains produce a new type of cytolysin (hemolysin) which is also found in other Serratia species. The hemolytic polypeptide ShlA (M(r) 162 101) is secreted across the outer membrane through the help of the ShlB protein which also involves conversion of an inactive precursor in an hemolytically active form. Both proteins are synthesized with signal sequences which are released during export across the cytoplasmic membrane. Mutants expressing inactive ShlB derivatives are impaired in activation and secretion suggesting a tight coupling between both processes. The region of ShlA for activation and secretion is confined to the N-terminal 16% of the polypeptide which contains the sequence NPNG which is also found in the Proteus hemolysin, the Bordetella pertussis filamentous hemagglutinin and two highly expressed outer membrane proteins of Haemophilus influenzae. Substitution of the first asparagine (N) residue by isoleucine converts the Serratia hemolysin into an inactive secretion incompetent form. It is concluded that this region is recognized by ShlB for activation and secretion of ShlA. The Serratia hemolysin forms defined pores in erythrocyte membranes.

In vitro activation of the Serratia marcescens hemolysin through modification and complementation.

The hemolytic activity of Serratia marcescens is determined by two polypeptides, termed ShlA and ShlB. ShlA is synthesized as an inactive precursor (ShlA*) and secreted with the help of ShlB, which is located in the outer membrane. In this study, it is shown that a cell lysate containing ShlB as well as partially purified ShlB converted ShlA* to the active ShlA hemolysin. ShlA remained active after removal of ShlB by column chromatography. In contrast to the stable modification of ShlA* by ShlB, a reversible activation was achieved by adding to ShlA* an N-terminal fragment of ShlA (ShlA16), consisting of 269 amino acid residues of ShlA and 18 residues of the vector. The nonhemolytic ShlA16 complemented ShlA* only when it was synthesized in an ShlB-producing cell. A deletion derivative of ShlA*, lacking residues 4 to 117, was complemented by ShlA16 but not activated by ShlB. Activation of ShlA* by ShlB at 4 degrees C proceeded at a much slower rate than complementation by ShlA16. It is concluded that ShlA* is modified by ShlB. ShlA16 modified by ShlB complements the missing modification of ShlA* in trans. Modification by ShlB occurs in the N-terminal part of ShlA*, which is also the reaction in vivo which results in active ShlA hemolysin in the culture supernatant. The HpmA hemolysin of Proteus mirabilis, which is very similar to ShlA, was also activated in vitro by ShlB and complemented by ShlA16.

Effects of plant species on nutrient cycling.

Plant species create positive feedbacks to patterns of nutrient cycling in natural ecosystems. For example, in nutrient-poor ecosystems, plants grow slowly, use nutrients efficiently and produce poor-quality litter that decomposes slowly and deters herbivores. /n contrast, plant species from nutrient-rich ecosystems grow rapidly, produce readily degradable litter and sustain high rates of herbivory, further enhancing rates of nutrient cycling. Plants may also create positive feedbacks to nutrient cycling because of species' differences in carbon deposition and competition with microbes for nutrients in the rhizosphere. New research is showing that species' effects can be as or more important than abiotic factors, such as climate, in controlling ecosystem fertility.