960 resultados para density dependent thinning
Resumo:
P>1. There are a number of models describing population structure, many of which have the capacity to incorporate spatial habitat effects. One such model is the source-sink model, that describes a system where some habitats have a natality that is higher than mortality (source) and others have a mortality that exceeds natality (sink). A source can be maintained in the absence of migration, whereas a sink will go extinct. 2. However, the interaction between population dynamics and habitat quality is complex, and concerns have been raised about the validity of published empirical studies addressing source-sink dynamics. In particular, some of these studies fail to provide data on survival, a significant component in disentangling a sink from a low quality source. Moreover, failing to account for a density-dependent increase in mortality, or decrease in fecundity, can result in a territory being falsely assigned as a sink, when in fact, this density-dependent suppression only decreases the population size to a lower level, hence indicating a 'pseudo-sink'. 3. In this study, we investigate a long-term data set for key components of territory-specific demography (mortality and reproduction) and their relationship to habitat characteristics in the territorial, group-living Siberian jay (Perisoreus infaustus). We also assess territory-specific population growth rates (r), to test whether spatial population dynamics are consistent with the ideas of source-sink dynamics. 4. Although average mortality did not differ between sexes, habitat-specific mortality did. Female mortality was higher in older forests, a pattern not observed in males. Male mortality only increased with an increasing amount of open areas. Moreover, reproductive success was higher further away from human settlement, indicating a strong effect of human-associated nest predators. 5. Averaged over all years, 76% of the territories were sources. These territories generally consisted of less open areas, and were located further away from human settlement. 6. The source-sink model provides a tool for modelling demography in distinct habitat patches of different quality, which can aid in identifying key habitats within the landscape, and thus, reduce the risk of implementing unsound management decisions.
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Structural remodeling of the myocardium associated with mechanical overload or cardiac infarction is accompanied by the appearance of myofibroblasts. These fibroblast-like cells express alpha-smooth muscle actin (alphaSMA) and have been shown to express connexins in tissues other than heart. The present study examined whether myofibroblasts of cardiac origin establish heterocellular gap junctional coupling with cardiomyocytes and whether ensuing electrotonic interactions affect impulse propagation. For this purpose, impulse conduction characteristics (conduction velocity [theta] and maximal upstroke velocity [dV/dtmax]) were assessed optically in cultured strands of cardiomyocytes, which were coated with fibroblasts of cardiac origin. Immunocytochemistry showed that cultured fibroblasts underwent a phenotype switch to alphaSMA-positive myofibroblasts that expressed connexin 43 and 45 both among themselves and at contact sites with cardiomyocytes. Myofibroblasts affected theta and dV/dtmax in a cell density-dependent manner; a gradual increase of myofibroblast-to-cardiomyocyte ratios up to 7:100 caused an increase of both theta and dV/dtmax, which was followed by a progressive decline at higher ratios. On full coverage of the strands with myofibroblasts (ratio >20:100), theta fell <200 mm/s. This biphasic dependence of theta and dV/dtmax on myofibroblast density is reminiscent of "supernormal conduction" and is explained by a myofibroblast density-dependent gradual depolarization of the cardiomyocyte strands from -78 mV to -50 mV as measured using microelectrode recordings. These findings suggest that myofibroblasts, apart from their role in structural remodeling, might contribute to arrhythmogenesis by direct electrotonic modulation of conduction and that prevention of their appearance might represent an antiarrhythmic therapeutic target.
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Focal ectopic activity in cardiac tissue is a key factor in the initiation and perpetuation of tachyarrhythmias. Because myofibroblasts as present in fibrotic remodeled myocardia and infarct scars depolarize cardiomyocytes by heterocellular electrotonic interactions via gap junctions in vitro, we investigated using strands of cultured ventricular cardiomyocytes coated with myofibroblasts, whether this interaction might give rise to depolarization-induced abnormal automaticity. Whereas uncoated cardiomyocyte strands were invariably quiescent, myofibroblasts induced synchronized spontaneous activity in a density dependent manner. Activations appeared at spatial myofibroblast densities >15.7% and involved more than 80% of the preparations at myofibroblast densities of 50%. Spontaneous activity was based on depolarization-induced automaticity as evidenced by: (1) suppression of activity by the sarcolemmal K(ATP) channel opener P-1075; (2) induction of activity in current-clamped single cardiomyocytes undergoing depolarization to potentials similar to those induced by myofibroblasts in cardiomyocyte strands; and (3) induction of spontaneous activity in cardiomyocyte strands coated with connexin 43 transfected Hela cells but not with communication deficient HeLa wild-type cells. Apart from unveiling the mechanism underlying the hallmark of monolayer cultures of cardiomyocytes, ie, spontaneous electromechanical activity, these findings open the perspective that myofibroblasts present in structurally remodeled myocardia following pressure overload and infarction might contribute to arrhythmogenesis by induction of ectopic activity.
Resumo:
Although accumulating evidence indicates that local intraspecific density-dependent effects are not as rare in species-rich communities as previously suspected, there are still very few detailed and systematic neighborhood analyses of species-rich communities. Here, we provide such an analysis with the overall goal of quantifying the relative importance of inter- and intraspecific interaction strength in a primary, lowland dipterocarp forest located at Danum, Sabah, Malaysia. Using data on 10 abundant overstory dipterocarp species from two 4-ha permanent plots, we evaluated the effects of neighbors on the absolute growth rate of focal trees (from 1986 to 1996) over increasing neighborhood radii (from 1 to 20 m) with multiple regressions. Only trees 10 cm to < 100 cm girth at breast height in 1986 were considered as focal trees. Among neighborhood models with one neighbor term, models including only conspecific larger trees performed best in five out of 10 species. Negative effects of conspecific larger neighbors were most apparent in large overstory species such as those of the genus Shorea. However, neighborhood models with separate terms and radii for heterospecific and conspecific neighbors accounted for more variability in absolute growth rates than did neighborhood models with one neighbor term. The conspecific term was significant for nine out of 10 species. Moreover, in five out of 10 species, trees without conspecific neighbors had significantly higher absolute growth rates than trees with conspecific neighbors. Averaged over the 10 species, trees without conspecific neighbors grew 32.4 cm(2) in basal area from 1986 to 1996, whereas trees with conspecific neighbors only grew 14.7 cm(2) in basal area, although there was no difference in initial basal area between trees in the two groups. Averaged across the six species of the genus Shorea, negative effects of conspecific larger trees were significantly stronger than for heterospecific larger neighbors. Thus, high local densities within neighborhoods of 20 m may lead to strong intraspecific negative and, hence, density-dependent, effects even in species rich communities with low overall densities at larger spatial scales. We conjecture that the strength of conspecific effects may be correlated with the degree of host specificity of ectomycorrhizae.
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Studies of food webs suggest that limited nonrandom dispersal can play an important role in structuring food webs. It is not clear, however, whether density-dependent dispersal fits empirical patterns of food webs better than density-independent dispersal. Here, we study a spatially distributed food web, using a series of population-dispersal models that contrast density-independent and density-dependent dispersal in landscapes where sampled sites are either homogeneously or heterogeneously distributed. These models are fitted to empirical data, allowing us to infer mechanisms that are consistent with the data. Our results show that models with density-dependent dispersal fit the α, β, and γ tritrophic richness observed in empirical data best. Our results also show that density-dependent dispersal leads to a critical distance threshold beyond which site similarity (i.e., β tritrophic richness) starts to decrease much faster. Such a threshold can also be detected in the empirical data. In contrast, models with density-independent dispersal do not predict such a threshold. Moreover, preferential dispersal from more centrally located sites to peripheral sites does not provide a better fit to empirical data when compared with symmetric dispersal between sites. Our results suggest that nonrandom dispersal in heterogeneous landscapes is an important driver that shapes local and regional richness (i.e., α and γ tritrophic richness, respectively) as well as the distance-decay relationship (i.e., β tritrophic richness) in food webs.
Resumo:
1 We used simulated and experimental plant populations to analyse mortality-driven pattern formation under size-dependent competition. Larger plants had an advantage under size-asymmetric but not under symmetric competition. Initial patterns were random or clumped. 2 The simulations were individual-based and spatially explicit. Size-dependent competition was modelled with different rules to partition overlapping zones of influence. 3 The experiment used genotypes of Arabidopsis thaliana with different morphological plasticity and hence size-dependent competition. Compared with wild types, transgenic individuals over-expressed phytochrome A and had decreased plasticity because of disabled phytochrome-mediated shade avoidance. Therefore, competition among transgenics was more asymmetric compared with wild-types. 4 Density-dependent mortality under symmetric competition did not substantially change the initial spatial pattern. Conversely, simulations under asymmetric competition and experimental patterns of transgenic over-expressors showed patterns of survivors that deviated substantially from random mortality independent of initial patterns. 5 Small-scale initial patterns of wild types were regular rather than random or clumped. We hypothesize that this small-scale regularity may be explained by early shade avoidance of seedlings in their cotyledon stage. 6 Our experimental results support predictions from an individual-based simulation model and support the conclusion that regular spatial patterns of surviving individuals should be interpreted as evidence for strong, asymmetric competitive interactions and subsequent density-dependent mortality.
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1 Light availability may be crucial for understanding dynamics of plant–herbivore interactions in temperate and tropical forest communities. This is because local light availability can influence both tree seedling tolerance and susceptibility to herbivory – yet how they mediate levels of insect herbivory that vary with the density of host population is virtually unknown. Here we tested predictions of three key, non-mutually exclusive hypotheses of plant–herbivore interactions: the Limiting Resource Model (LRM), the Plant Vigour Hypothesis (PVH), and the Janzen-Connell Mechanism (JCM). 2 In an Amazonian forest, we planted Swietenia macrophylla seedlings (c. 5 months old) into natural canopy gaps and the shaded understorey and simulated the damage patterns of the specialist herbivore moth, Steniscadia poliophaea, by clipping seedling leaves. Over the next 8 months, we monitored seedling performance in terms of growth and survivorship and also quantified herbivory to new young leaves on a seasonal basis. 3 In support of the LRM, severe leaf damage (≥ 50%) was lethal for Swietenia macrophylla seedlings in the understorey, but in gaps only reduced seedling growth. In support of the PVH, gap seedlings suffered greater post-simulated herbivory (up to 100% defoliation) by S. poliophaea caterpillars than their understorey counterparts. 4 Adding a novel dimension to the Janzen–Connell hypothesis, we found that early wet season herbivory of seedlings in gaps increased with conspecific adult density within a 125-m radius; whereas in the understorey only those seedlings within 50 m of a Swietenia tree were attacked by caterpillars. 5 Synthesis. These results suggest lepidopterans that need young leaves for food may forage more widely in forests to find seedlings in light-rich canopy gaps. Moths may achieve this successfully by being first attracted to gaps, and then searching within them for suitable hosts. A conceptual model, integrating conspecific adult tree density with light-driven changes in seedling tolerance/vigour and their susceptibility to herbivory and mortality, is presented. Spatial variation in the light available to tree seedlings often affects their tolerance and vigour, which may have important consequences for leaf-chewing insects and the scale of density-dependent herbivory in forests.
Resumo:
Conspecific effects of neighbours on small-tree survival may have a role in tree population dynamics and community composition of tropical forests. This notion was tested with data from two 4-ha plots in lowland forest at Danum, Sabah (Borneo), for a 21-year interval (censuses at 1986, 1996, 2001, 2007). Species with ≥45 focal trees 10 to <100 cm stem girth per plot in 1986 were selected. Logistic regressions fitted mean focal tree size and mean inverse-distance-weighted basal area abundance of neighbours (within 20 m), for the periods over which each focus tree was alive. Coefficients of variation of neighbourhood basal area abundance, both spatially and temporally, quantified the changing environment of each focus tree. Fits were critically and individually evaluated, with corrections for spatial autocorrelation. Conspecific effects at Danum was generally very weak or non-existent: species’ mortality rates varied also across plots. The main reasons appear to be that (1) species were not dense enough to interact despite frequent although weak spatial aggregation, and their neighbourhoods were highly differing in species composition; and (2) these neighbourhoods were highly variable temporally, meaning that focus trees experienced stochastically fluctuating neighbourhood environments. Only one species, Dimorphocalyx muricatus, showed strong conspecific effects (varying between plots) which can be explained by its distinct ecology. This understorey species is highly aggregated on ridges and is drought-tolerant. That this functionally and habitat-specialized species, has implied intraspecific density-dependent feedback in its dynamics is a remarkable indication of the overall processes maintaining stability of the Danum forest.
Resumo:
Classical quorum-sensing (autoinduction) regulation, as exemplified by the lux system of Vibrio fischeri, requires N-acyl homoserine lactone (AHL) signals to stimulate cognate transcriptional activators for the cell density-dependent expression of specific target gene systems. For Pantoea stewartii subsp. stewartii, a bacterial pathogen of sweet corn and maize, the extracellular polysaccharide (EPS) stewartan is a major virulence factor, and its production is controlled by quorum sensing in a population density-dependent manner. Two genes, esaI and esaR, encode essential regulatory proteins for quorum sensing. EsaI is the AHL signal synthase, and EsaR is the cognate gene regulator. esaI, DeltaesaR, and DeltaesaI-esaR mutations were constructed to establish the regulatory role of EsaR. We report here that strains containing an esaR mutation produce high levels of EPS independently of cell density and in the absence of the AHL signal. Our data indicate that quorum-sensing regulation in P. s. subsp. stewartii, in contrast to most other described systems, uses EsaR to repress EPS synthesis at low cell density, and that derepression requires micromolar amounts of AHL. In addition, derepressed esaR strains, which synthesize EPS constitutively at low cell densities, were significantly less virulent than the wild-type parent. This finding suggests that quorum sensing in P. s. subsp. stewartii may be a mechanism to delay the expression of EPS during the early stages of infection so that it does not interfere with other mechanisms of pathogenesis.
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Snow cover has dramatic effects on the structure and functioning of Arctic ecosystems in winter. In the tundra, the subnivean space is the primary habitat of wintering small mammals and may be critical for their survival and reproduction. We have investigated the effects of snow cover and habitat features on the distributions of collared lemming (Dicrostonyx groenlandicus) and brown lemming (Lemmus trimucronatus) winter nests, as well as on their probabilities of reproduction and predation by stoats (Mustela erminea) and arctic foxes (Vulpes lagopus). We sampled 193 lemming winter nests and measured habitat features at all of these nests and at random sites at two spatial scales. We also monitored overwinter ground temperature at a subsample of nest and random sites. Our results demonstrate that nests were primarily located in areas with high micro-topography heterogeneity, steep slopes, deep snow cover providing thermal protection (reduced daily temperature fluctuations) and a high abundance of mosses. The probability of reproduction increased in collared lemming nests at low elevation and in brown lemming nests with high availability of some graminoid species. The probability of predation by stoats was density dependent and was higher in nests used by collared lemmings. Snow cover did not affect the probability of predation of lemming nests by stoats, but deep snow cover limited predation attempts by arctic foxes. We conclude that snow cover plays a key role in the spatial structure of wintering lemming populations and potentially in their population dynamics in the Arctic.
Resumo:
Classical quorum-sensing (autoinduction) regulation, as exemplified by the lux system of Vibrio fischeri, requires N-acyl homoserine lactone (AHL) signals to stimulate cognate transcriptional activators for the cell density-dependent expression of specific target gene systems. For Pantoea stewartii subsp. stewartii, a bacterial pathogen of sweet corn and maize, the extracellular polysaccharide (EPS) stewartan is a major virulence factor, and its production is controlled by quorum sensing in a population density-dependent manner. Two genes, esaI and esaR, encode essential regulatory proteins for quorum sensing. EsaI is the AHL signal synthase, and EsaR is the cognate gene regulator. esaI, ΔesaR, and ΔesaI-esaR mutations were constructed to establish the regulatory role of EsaR. We report here that strains containing an esaR mutation produce high levels of EPS independently of cell density and in the absence of the AHL signal. Our data indicate that quorum-sensing regulation in P. s. subsp. stewartii, in contrast to most other described systems, uses EsaR to repress EPS synthesis at low cell density, and that derepression requires micromolar amounts of AHL. In addition, derepressed esaR strains, which synthesize EPS constitutively at low cell densities, were significantly less virulent than the wild-type parent. This finding suggests that quorum sensing in P. s. subsp. stewartii may be a mechanism to delay the expression of EPS during the early stages of infection so that it does not interfere with other mechanisms of pathogenesis.
Resumo:
Bacteria communicate with each other to coordinate expression of specific genes in a cell density-dependent fashion, a phenomenon called quorum sensing and response. Although we know that quorum sensing via acyl-homoserine lactone (HSL) signals controls expression of several virulence genes in the human pathogen Pseudomonas aeruginosa, the number and types of genes controlled by quorum sensing have not been studied systematically. We have constructed a library of random insertions in the chromosome of a P. aeruginosa acyl-HSL synthesis mutant by using a transposon containing a promoterless lacZ. This library was screened for acyl-HSL induction of lacZ. Thirty-nine quorum sensing-regulated genes were identified. The genes were organized into classes depending on the pattern of regulation. About half of the genes appear to be in seven operons, some seem organized in large patches on the genome. Many of the quorum sensing-regulated genes code for putative virulence factors or production of secondary metabolites. Many of the genes identified showed a high level of induction by acyl-HSL signaling.
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FLK-1/vascular endothelial growth factor receptor 2 (VEGFR-2) is one of the receptors for VEGF. In this study we examined the effect of cell density on activation of VEGFR-2. VEGF induces only very slight tyrosine phosphorylation of VEGFR-2 in confluent (95–100% confluent) pig aortic endothelial (PAE) cells. In contrast, robust VEGF-dependent tyrosine phosphorylation of VEGFR-2 was observed in cells plated in sparse culture conditions (60–65% confluent). A similar cell density-dependent phenomenon was observed in different endothelial cells but not in NIH-3T3 fibroblast cells expressing VEGFR-2. Stimulating cells with high concentrations of VEGF or replacing the extracellular domain of VEGFR-2 with that of the colony-stimulating factor 1 receptor did not alleviate the sensitivity of VEGFR-2 to cell density, indicating that the confluent cells were probably not secreting an antagonist to VEGF. Furthermore, in PAE cells, ectopically introduced platelet-derived growth factor α receptor could be activated at both high and low cell density conditions, indicating that the density effect was not universal for all receptor tyrosine kinases expressed in endothelial cells. In addition to lowering the density of cells, removing divalent cations from the medium of confluent cells potentiated VEGFR-2 phosphorylation in response to VEGF. These findings suggested that cell–cell contact may be playing a role in regulating the activation of VEGFR-2. To this end, pretreatment of confluent PAE cells with a neutralizing anti-cadherin-5 antibody potentiated the response of VEGFR-2 to VEGF. Our data demonstrate that endothelial cell density plays a critical role in regulating VEGFR-2 activity, and that the underlying mechanism appears to involve cadherin-5.
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The use of Moloney murine leukemia virus (Mo-MLV)-based vectors to deliver therapeutic genes into target cells is limited by their inability to transduce nondividing cells. To test the capacity of HIV-based vectors to deliver genes into nondividing cells, we have generated replication-defective HIV type 1 (HIV-1) reporter vectors carrying neomycin phosphotransferase or mouse heat stable antigen, replacing the HIV-1 sequences encoding gp160. These vectors also harbor inactive vpr, vpu, and nef coding regions. Pseudotyped HIV-1 particles carrying either the ecotropic or the amphotropic Mo-MLV envelope proteins or the vesicular stomatitis virus G protein were released after single or double transfections of either human 293T or monkey COS-7 cells with titers of up to 107 colony-forming units per milliliter. A simple ultrafiltration procedure resulted in an additional 10- to 20-fold concentration of the pseudotyped particles. These vectors along with Mo-MLV-based vectors were used to transduce primary human skin fibroblasts and human peripheral blood CD34+ cells. The HIV-1 vector system was significantly more efficient than its Mo-MLV-based counterpart in transducing human skin fibroblasts arrested at the G0/G1 stage of the cell cycle by density-dependent inhibition of growth. Human CD34+ cells were transduced efficiently using HIV-1 pseudotype particles without prior stimulation with cytokines.
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Directionality in populations of replicating organisms can be parametrized in terms of a statistical concept: evolutionary entropy. This parameter, a measure of the variability in the age of reproducing individuals in a population, is isometric with the macroscopic variable body size. Evolutionary trends in entropy due to mutation and natural selection fall into patterns modulated by ecological and demographic constraints, which are delineated as follows: (i) density-dependent conditions (a unidirectional increase in evolutionary entropy), and (ii) density-independent conditions, (a) slow exponential growth (an increase in entropy); (b) rapid exponential growth, low degree of iteroparity (a decrease in entropy); and (c) rapid exponential growth, high degree of iteroparity (random, nondirectional change in entropy). Directionality in aggregates of inanimate matter can be parametrized in terms of the statistical concept, thermodynamic entropy, a measure of disorder. Directional trends in entropy in aggregates of matter fall into patterns determined by the nature of the adiabatic constraints, which are characterized as follows: (i) irreversible processes (an increase in thermodynamic entropy) and (ii) reversible processes (a constant value for entropy). This article analyzes the relation between the concepts that underlie the directionality principles in evolutionary biology and physical systems. For models of cellular populations, an analytic relation is derived between generation time, the average length of the cell cycle, and temperature. This correspondence between generation time, an evolutionary parameter, and temperature, a thermodynamic variable, is exploited to show that the increase in evolutionary entropy that characterizes population processes under density-dependent conditions represents a nonequilibrium analogue of the second law of thermodynamics.