Potential effects of gas hydrate on human welfare

For almost 30 years. serious interest has been directed toward natural gas hydrate, a crystalline solid composed of water and methane, as a potential (i) energy resource, (ii) factor in global climate change, and (iii) submarine geohazard. Although each of these issues can affect human welfare, only (iii) is considered to be of immediate importance. Assessments of gas hydrate as an energy resource have often been overly optimistic, based in part on its very high methane content and on its worldwide occurrence in continental margins. Although these attributes are attractive, geologic settings, reservoir properties, and phase-equilibria considerations diminish the energy resource potential of natural gas hydrate. The possible role of gas hydrate in global climate change has been often overstated. Although methane is a “greenhouse” gas in the atmosphere, much methane from dissociated gas hydrate may never reach the atmosphere, but rather may be converted to carbon dioxide and sequestered by the hydrosphere/biosphere before reaching the atmosphere. Thus, methane from gas hydrate may have little opportunity to affect global climate change. However, submarine geohazards (such as sediment instabilities and slope failures on local and regional scales, leading to debris flows, slumps, slides, and possible tsunamis) caused by gas-hydrate dissociation are of immediate and increasing importance as humankind moves to exploit seabed resources in ever-deepening waters of coastal oceans. The vulnerability of gas hydrate to temperature and sea level changes enhances the instability of deep-water oceanic sediments, and thus human activities and installations in this setting can be affected.

Reorganization of an arid ecosystem in response to recent climate change

Natural ecosystems contain many individuals and species interacting with each other and with their abiotic environment. Such systems can be expected to exhibit complex dynamics in which small perturbations can be amplified to cause large changes. Here, we document the reorganization of an arid ecosystem that has occurred since the late 1970s. The density of woody shrubs increased 3-fold. Several previously common animal species went locally extinct, while other previously rare species increased. While these changes are symptomatic of desertification, they were not caused by livestock grazing or drought, the principal causes of historical desertification. The changes apparently were caused by a shift in regional climate: since 1977 winter precipitation throughout the region was substantially higher than average for this century. These changes illustrate the kinds of large, unexpected responses of complex natural ecosystems that can occur in response to both natural perturbations and human activities.

Late Quaternary extinction of a tree species in eastern North America

Widespread species- and genus-level extinctions of mammals in North America and Europe occurred during the last deglaciation [16,000–9,000 yr B.P. (by 14C)], a period of rapid and often abrupt climatic and vegetational change. These extinctions are variously ascribed to environmental change and overkill by human hunters. By contrast, plant extinctions since the Middle Pleistocene are undocumented, suggesting that plant species have been able to respond to environmental changes of the past several glacial/interglacial cycles by migration. We provide evidence from morphological studies of fossil cones and anatomical studies of fossil needles that a now-extinct species of spruce (Picea critchfieldii sp. nov.) was widespread in eastern North America during the Last Glacial Maximum. P. critchfieldii was dominant in vegetation of the Lower Mississippi Valley, and extended at least as far east as western Georgia. P. critchfieldii disappeared during the last deglaciation, and its extinction is not directly attributable to human activities. Similarly widespread plant species may be at risk of extinction in the face of future climate change.

Rhizobium gone native: Unexpected plasmid stability of indigenous Rhizobium leguminosarum

Lateral transfer of bacterial plasmids is thought to play an important role in microbial evolution and population dynamics. However, this assumption is based primarily on investigations of medically or agriculturally important bacterial species. To explore the role of lateral transfer in the evolution of bacterial systems not under intensive, human-mediated selection, we examined the association of genotypes at plasmid-encoded and chromosomal loci of native Rhizobium, the nitrogen-fixing symbiont of legumes. To this end, Rhizobium leguminosarum strains nodulating sympatric species of native Trifolium were characterized genetically at plasmid-encoded symbiotic (sym) regions (nodulation AB and nodulation CIJT loci) and a repeated chromosomal locus not involved in the symbiosis with legumes. Restriction fragment length polymorphism analysis was used to distinguish genetic groups at plasmid and chromosomal loci. The correlation between major sym and chromosomal genotypes and the distribution of genotypes across host plant species and sampling location were determined using χ2 analysis. In contrast to findings of previous studies, a strict association existed between major sym plasmid and chromosomal genetic groups, suggesting a lack of successful sym plasmid transfer between major Rhizobium chromosomal types. These data indicate that previous observations of sym plasmid transfer in agricultural settings may seriously overestimate the rates of successful conjugation in systems not impacted by human activities. In addition, a nonrandom distribution of Rhizobium genotypes across host plant species and sampling site demonstrates the importance of both factors in shaping Rhizobium population dynamics.

Loss of speciation rate will impoverish future diversity

Human activities have greatly reduced the amount of the earth's area available to wild species. As the area they have left declines, so will their rates of speciation. This loss of speciation will occur for two reasons: species with larger geographical ranges speciate faster; and loss of area drives up extinction rates, thus reducing the number of species available for speciation. Theory predicts steady states in species diversity, and fossils suggest that these have typified life for most of the past 500 million years. Modern and fossil evidence indicates that, at the scale of the whole earth and its major biogeographical provinces, those steady states respond linearly, or nearly so, to available area. Hence, a loss of x% of area will produce a loss of about x% of species. Local samples of habitats merely echo the diversity available in the whole province of which they are a part. So, conservation tactics that rely on remnant patches to preserve diversity cannot succeed for long. Instead, diversity will decay to a depauperate steady state in two phases. The first will involve deterministic extinctions, reflecting the loss of all areas in which a species can ordinarily sustain its demographics. The second will be stochastic, reflecting accidents brought on by global warming, new diseases, and commingling the species of the separate bio-provinces. A new kind of conservation effort, reconciliation ecology, can avoid this decay. Reconciliation ecology discovers how to modify and diversify anthropogenic habitats so that they harbor a wide variety of species. It develops management techniques that allow humans to share their geographical range with wild species.

Disrupting evolutionary processes: The effect of habitat fragmentation on collared lizards in the Missouri Ozarks

Humans affect biodiversity at the genetic, species, community, and ecosystem levels. This impact on genetic diversity is critical, because genetic diversity is the raw material of evolutionary change, including adaptation and speciation. Two forces affecting genetic variation are genetic drift (which decreases genetic variation within but increases genetic differentiation among local populations) and gene flow (which increases variation within but decreases differentiation among local populations). Humans activities often augment drift and diminish gene flow for many species, which reduces genetic variation in local populations and prevents the spread of adaptive complexes outside their population of origin, thereby disrupting adaptive processes both locally and globally within a species. These impacts are illustrated with collared lizards (Crotaphytus collaris) in the Missouri Ozarks. Forest fire suppression has reduced habitat and disrupted gene flow in this lizard, thereby altering the balance toward drift and away from gene flow. This balance can be restored by managed landscape burns. Some have argued that, although human-induced fragmentation disrupts adaptation, it will also ultimately produce new species through founder effects. However, population genetic theory and experiments predict that most fragmentation events caused by human activities will facilitate not speciation, but local extinction. Founder events have played an important role in the macroevolution of certain groups, but only when ecological opportunities are expanding rather than contracting. The general impact of human activities on genetic diversity disrupts or diminishes the capacity for adaptation, speciation, and macroevolutionary change. This impact will ultimately diminish biodiversity at all levels.

The current biodiversity extinction event: Scenarios for mitigation and recovery

The current massive degradation of habitat and extinction of species is taking place on a catastrophically short timescale, and their effects will fundamentally reset the future evolution of the planet's biota. The fossil record suggests that recovery of global ecosystems has required millions or even tens of millions of years. Thus, intervention by humans, the very agents of the current environmental crisis, is required for any possibility of short-term recovery or maintenance of the biota. Many current recovery efforts have deficiencies, including insufficient information on the diversity and distribution of species, ecological processes, and magnitude and interaction of threats to biodiversity (pollution, overharvesting, climate change, disruption of biogeochemical cycles, introduced or invasive species, habitat loss and fragmentation through land use, disruption of community structure in habitats, and others). A much greater and more urgently applied investment to address these deficiencies is obviously warranted. Conservation and restoration in human-dominated ecosystems must strengthen connections between human activities, such as agricultural or harvesting practices, and relevant research generated in the biological, earth, and atmospheric sciences. Certain threats to biodiversity require intensive international cooperation and input from the scientific community to mitigate their harmful effects, including climate change and alteration of global biogeochemical cycles. In a world already transformed by human activity, the connection between humans and the ecosystems they depend on must frame any strategy for the recovery of the biota.

Global climate change

Most of the last 100,000 years or longer has been characterized by large, abrupt, regional-to-global climate changes. Agriculture and industry have developed during anomalously stable climatic conditions. New, high-resolution analyses of sediment cores using multiproxy and physically based transfer functions allow increasingly confident interpretation of these past changes as having been caused by “band jumps” between modes of operation of the climate system. Recurrence of such band jumps is possible and might be affected by human activities.

Recombination activities of HsDmc1 protein, the meiotic human homolog of RecA protein

Meiosis-specific homologs of RecA protein have been identified in Saccharomyces cerevisiae and higher eukaryotes including mammals, but their enzymatic activities have not been described. We have purified the human protein HsDmc1 produced in Escherichia coli from a cloned copy of the cDNA. The recombinant enzyme had DNA-dependent ATPase activity with an estimated kcat of 1.5 min−1. DNase protection experiments with oligonucleotides as substrates indicated that HsDmc1 protein binds preferentially to single-stranded DNA with a stoichiometry of approximately one molecule of protein per three nucleotide residues. HsDmc1 protein catalyzed the formation of D-loops in superhelical DNA, as well as strand exchange between single-stranded and double-stranded oligonucleotides. The requirements for strand exchange catalyzed by HsDmc1 were similar to those of RecA protein, but exchange caused by HsDmc1 was not supported by ATPγS.

Novel Regulation of Type IV Collagenase (Matrix Metalloproteinase-9 and -2) Activities by Transforming Growth Factor-β1 in Human Prostate Cancer Cell Lines

The type IV collagenases/gelatinases matrix metalloproteinase-2 (MMP-2) and MMP-9 play a variety of important roles in both physiological and pathological processes and are regulated by various growth factors, including transforming growth factor-β1 (TGF-β1), in several cell types. Previous studies have suggested that cellular control of one or both collagenases can occur through direct transcriptional mechanisms and/or after secretion through proenzyme processing and interactions with metalloproteinase inhibitors. Using human prostate cancer cell lines, we have found that TGF-β1 induces the MMP-9 proenzyme; however, this induction does not result from direct effects on gene transcription but, instead, through a protein synthesis–requiring process leading to increased MMP-9 mRNA stability. In addition, we have examined levels of TGF-β1 regulation of MMP-2 in one prostate cancer cell line and found that TGF-β1 induces higher secreted levels of this collagenase through increased stability of the secreted 72-kDa proenzyme. These results identify two novel nontranscriptional pathways for the cellular regulation of MMP-9 and MMP-2 collagenase gene expression and activities.

Scanning electrochemical microscopy of living cells: Different redox activities of nonmetastatic and metastatic human breast cells

Electrochemical methods have been widely used to monitor physiologically important molecules in biological systems. This report describes the first application of the scanning electrochemical microscope (SECM) to probe the redox activity of individual living cells. The possibilities of measuring the rate and investigating the pathway of transmembrane charge transfer are demonstrated. By this approach, significant differences are detected in the redox responses given by nonmotile, nontransformed human breast epithelial cells, breast cells with a high level of motility (engendered by overexpression of protein kinase Cα), and highly metastatic breast cancer cells. SECM analysis of the three cell lines reveals reproducible differences with respect to the kinetics of charge transfer by several redox mediators.

Anti-HIV-1 and chemotactic activities of human stromal cell-derived factor 1α (SDF-1α) and SDF-1β are abolished by CD26/dipeptidyl peptidase IV-mediated cleavage

CD26 is a leukocyte-activation antigen that is expressed on T lymphocytes and macrophages and possesses dipeptidyl peptidase IV (DPPIV) activity, whose natural substrates have not been identified yet. CXC chemokines, stromal cell-derived factor 1α (SDF-1α) and 1β (SDF-1β), sharing the receptor CXCR-4, are highly efficacious chemoattractants for resting lymphocytes and CD34+ progenitor cells, and they efficiently block the CXCR-4-mediated entry into cells of T cell line tropic strains of HIV type 1 (HIV-1). Here we show that both the chemotactic and antiviral activities of these chemokines are abrogated by DPPIV-mediated specific removal of the N-terminal dipeptide, not only when the chemokines are produced in transformed mouse L cell line to express human CD26 but also when they were exposed to a human T cell line (H9) physiologically expressing CD26. Mutagenesis of SDF-1α confirmed the critical requirement of the N-terminal dipeptide for its chemotactic and antiviral activities. These data suggest that CD26-mediated cleavage of SDF-1α and SDF-1β likely occurs in human bodies and promotes HIV-1 replication and disease progression. They may also explain why memory function of CD4+ cells is preferentially lost in HIV-1 infection. Furthermore, CD26 would modulate various other biological processes in which SDF-1α and SDF-1β are involved.

DNA-binding and strand-annealing activities of human Mre11: implications for its roles in DNA double-strand break repair pathways

DNA double-strand breaks (DSBs) in eukaryotic cells can be repaired by non-homologous end-joining or homologous recombination. The complex containing the Mre11, Rad50 and Nbs1 proteins has been implicated in both DSB repair pathways, even though they are mechanistically different. To get a better understanding of the properties of the human Mre11 (hMre11) protein, we investigated some of its biochemical activities. We found that hMre11 binds both double- and single-stranded (ss)DNA, with a preference for ssDNA. hMre11 does not require DNA ends for efficient binding. Interestingly, hMre11 mediates the annealing of complementary ssDNA molecules. In contrast to the annealing activity of the homologous recombination protein hRad52, the activity of hMre11 is abrogated by the ssDNA binding protein hRPA. We discuss the possible implications of the results for the role(s) of hMre11 in both DSB repair pathways.

Disparate actions of hydroxyurea in potentiation of purine and pyrimidine 2',3'-dideoxynucleoside activities against replication of human immunodeficiency virus.

We and other groups have recently reported the potentiation by ribonucleotide reductase inhibitors such as hydroxyurea of the anti-human immunodeficiency virus type 1 (HIV-1) activity of purine and pyrimidine 2',3'-dideoxynucleosides in both resting and phytohemagglutinin-stimulated peripheral blood mononuclear cells. Little agreement prevails, however, as to the mechanism of the synergistic effects described. We report here that in phytohemagglutinin-stimulated peripheral blood mononuclear cells, two mechanisms exist for the potentiation of the anti-HIV-1 activity by low-dose hydroxyurea of the purine-based dideoxynucleoside 2',3'-dideoxyinosine and the pyrimidine-based dideoxynucleosides 3'-azido-3'-deoxythymidine and 2',3'-dideoxycytidine. For 2',3'-dideoxyinosine, the enhancement arises from a specific depletion of dATP by hydroxyurea, resulting in a favorable shift of the 2',3'-dideoxyadenosine 5'-triphosphate/dATP ratio. For the pyrimidine dideoxynucleosides 3'-azido-3'-deoxythymidine and 2',3'-dideoxycytidine, the more modest anti-HIV enhancement results from hydroxyurea-induced increases of pyrimidine kinase activities in the salvage pathway and, hence, increased 5'-phosphorylation of these drugs, while depletion of the corresponding deoxynucleoside 5'-triphosphates (dTTP and dCTP) plays no significant role.