Density-dependent Way Research Articles

Density-dependent private benefit leads to bacterial mutualism.

Microorganisms produce and secrete materials that are beneficial for themselves and their neighbors. We modeled the situation when cells can produce different costly secretions which increase the carrying capacity of the population. Strains that lose the function of producing one or more secretions avoid the cost of production and can exhaust the producers. However, secreting substances provides a private benefit for the producers in a density-dependent way. We developed a model to examine the outcome of the selection among different types of producer strains from the nonproducer strain to the partial producers, to the full producer strain. We were interested in circumstances under which selection maintains partners that produce complementary secreted materials thus forming an interdependent mutualistic interaction. We show that interdependent mutualism is selected under a broad range of conditions if private benefit decreases with density. Selection frequently causes the coexistence of more and less generalist cooperative strains, thus cooperation and exploitation co-occur. Interdependent mutualism is evolved under more specific circumstances if private benefit increases with density and these general observations are valid in a well-mixed and a structured deme model. We show that the applied population structure allows the invasion of rare cooperators and supports cooperation ingeneral.

Cell density-dependent regulation of microcystin synthetase genes (mcy) expression and microcystin-LR production in Microcystis aeruginosa that mimics quorum sensing

As the secondary metabolites of cyanobacterial harmful algal blooms (Cyano-HABs), microcystins (MCs) were generated under various environmental and cellular conditions. The understanding of the causes of MCs generation is of great interest in the field of water treatment and environmental science. In this work, we studied how Microcystis aeruginosa (FACHB-905) cell densities affect the MCs synthetase genes (mcy) expression, microcystin-LR (MC-LR) and quorum sensing molecules (Acyl-homoserine lactones (AHLs)) production. An electrochemical sensor was developed here for sensitive and quantitative detection of MC-LR that cultured at different cell densities. The results showed that mcy expression and MC-LR concentration started to increase when the cell density reached ca. 22 × 106 cells/mL, and was significantly increased with increasing cell densities. Moreover, the up-regulation of AHLs with increasing cell densities revealed that MC-LR is quorum sensing-mediated. Our results undoubtedly confirmed that MC-LR was produced in a cell density-dependent way that mimics quorum sensing, and the minimum cell density (ca. 22 × 106 cells/mL) that was required to produce MC-LR was provided and offered a reference standard for the prevention and control of MCs pollution in the actual water environment.

The dual impact of Ostreopsis cf. ovata on Mytilus galloprovincialis and Paracentrotus lividus: Toxin accumulation and pathological aspects

Blooms of the toxic dinoflagellates Ostreopsis have become common along rocky shores of the Mediterranean Sea. In addition to health problems for beach-goers, Ostreopsis toxins may accumulate in benthic marine animals used for human consumption, which however at times have shown signals of stress and even mortality. In order to elucidate the actual relationships between Ostreopsis and benthic invertebrates, we exposed mussels Mytilus galloprovincialis and sea urchins Paracentrotus lividus from the Gulf of Naples to cultures and natural material of O. cf. ovata and assessed feeding and adverse effects on the animals, along with their acquired toxicity. Mussels exposed to O. cf. ovata for 24 hours filtered the microalgae at different rates, depending on both mussel size and microalgal density, and became weakly toxic in some cases. Under longer exposure most animals died and all survivors were toxic. Detoxification of a naturally toxic mussel populations from an area affected by O. cf. ovata blooms took more than two weeks. Sea urchins fed with the red alga Asparagopsis taxiformis epiphytised by O. cf. ovata did not show damages and became mildly toxic in some cases. However, the direct exposure of sea urchins to O. cf. ovata cultures caused the partial or total loss of the spines in a density-dependent way, with the death of the animals at the highest microalgal concentrations. Milder effects were registered with sonicated cultures or toxin extracts. Our results indicate that the balance between toxicity and animal health in these invertebrates depends on the mode and intensity of exposure to the toxic microalga, while the response varies between the two species but also within the same species. This scenario matches the variety of responses of benthic populations recorded in the natural environment in areas affected by O. cf. ovata blooms.

Insufficient Astrocyte-Derived Brain-Derived Neurotrophic Factor Contributes to Propofol-Induced Neuron Death Through Akt/Glycogen Synthase Kinase 3β/Mitochondrial Fission Pathway.

Growing animal evidence demonstrates that prolonged exposure to propofol during brain development induces widespread neuronal cell death, but there is little information on the role of astrocytes. Astrocytes can release neurotrophic growth factors such as brain-derived neurotrophic factor (BDNF), which can exert the protective effect on neurons in paracrine fashion. We hypothesize that during propofol anesthesia, BDNF released from developing astrocytes may not be sufficient to prevent propofol-induced neurotoxicity. Hippocampal astrocytes and neurons isolated from neonatal Sprague Dawley rats were exposed to propofol at a clinically relevant dose of 30 μM or dimethyl sulfoxide as control for 6 hours. Propofol-induced cell death was determined by propidium iodide (PI) staining in astrocyte-alone cultures, neuron-alone cultures, or cocultures containing either low or high density of astrocytes (1:9 or 1:1 ratio of astrocytes to neurons ratio [ANR], respectively). The astrocyte-conditioned medium was collected 12 hours after propofol exposure and measured by protein array assay. BDNF concentration in astrocyte-conditioned medium was quantified using enzyme-linked immunosorbent assay. Neuron-alone cultures were treated with BDNF, tyrosine receptor kinase B inhibitor cyclotraxin-B, glycogen synthase kinase 3β (GSK3β) inhibitor CHIR99021, or mitochondrial fission inhibitor Mdivi-1 before propofol exposure. Western blot was performed for quantification of the level of protein kinase B and GSK3β. Mitochondrial shape was visualized through translocase of the outer membrane 20 staining. Propofol increased cell death in neurons by 1.8-fold (% of PI-positive cells [PI%] = 18.6; 95% confidence interval [CI], 15.2-21.9, P < .05) but did not influence astrocyte viability. The neuronal death was attenuated by a high ANR (1:1 cocultures; fold change [FC] = 1.17, 95% CI, 0.96-1.38, P < .05), but not with a low ANR [1:9 cocultures; FC = 1.87, 95% CI, 1.48-2.26, P > .05]). Astrocytes secreted BDNF in a cell density-dependent way and propofol decreased BDNF secretion from astrocytes. Administration of BDNF, CHIR99021, or Mdivi-1 significantly attenuated the propofol-induced neuronal death and aberrant mitochondria in neuron-alone cultures (FC = 0.8, 95% CI, 0.62-0.98; FC = 1.22, 95% CI, 1.11-1.32; FC = 1.35, 95% CI, 1.16-1.54, respectively, P < .05) and the cocultures with a low ANR (1:9; FC = 0.85, 95% CI, 0.74-0.97; FC = 1.08, 95% CI, 0.84-1.32; FC = 1.25, 95% CI, 1.1-1.39, respectively, P < .05). Blocking BDNF receptor or protein kinase B activity abolished astrocyte-induced neuroprotection in the cocultures with a high ANR (1:1). Astrocytes attenuate propofol-induced neurotoxicity through BDNF-mediated cell survival pathway suggesting multiple neuroprotective strategies such as administration of BDNF, astrocyte-conditioned medium, decreasing mitochondrial fission, or inhibition of GSK3β.

Properties of strongly magnetized ultradense matter and its effects on magnetar pulsations

We investigate the effect of strong magnetic fields on the adiabatic radial oscillations of hadronic stars. We describe magnetized hadronic matter within the framework of the relativistic nonlinear Walecka model and integrate the equations of relativistic radial oscillations to determine the fundamental pulsation mode. We consider that the magnetic field increases, in a density dependent way, from the surface, where it has a typical magnetar value of ${10}^{15}\phantom{\rule{4pt}{0ex}}\mathrm{G}$, to the interior of the star, where it can be as large as $3\ifmmode\times\else\texttimes\fi{}{10}^{18}\phantom{\rule{4pt}{0ex}}\mathrm{G}$. We show that magnetic fields of the order of ${10}^{18}\phantom{\rule{4pt}{0ex}}\mathrm{G}$ at the stellar core produce a significant change in the frequency of neutron star pulsations with respect to unmagnetized objects. If radial pulsations are excited in magnetar flares, they can leave an imprint in the flare lightcurves and open a new window for the study of highly magnetized ultradense matter.

Functional Responses of Three Neotropical Mirid Predators to Eggs of Tuta absoluta on Tomato.

Tuta absoluta (Meyrick) has quickly developed into a significant tomato pest worldwide. While the recently found mirid predators Macrolophus basicornis (Stal), Engytatus varians (Distant) and Campyloneuropsis infumatus (Carvalho) of this pest are able to establish and reproduce on tomato, biological knowledge of these mirids is still limited. Here we describe the functional response of the three mirid predators of the tomato pest T. absoluta when offered a range of prey densities (four, eight, 16, 32, 64, 128 and 256 eggs) during a 24 h period inside cylindrical plastic cages in the laboratory. Engytatus varians and M. basicornis showed a type III functional response, whereas C. infumatus showed a type II functional response. At the highest prey densities, C. infumatus consumed an average of 51.0 eggs, E. varians 91.1 eggs, and M. basicornis 100.8 eggs. Taking all information into account that we have collected of these three Neotropical mirid species, we predict that M. basicornis might be the best candidate for control of the tomato borer in Brazil: it has the highest fecundity, the largest maximum predation capacity, and it reacts in a density-dependent way to the widest prey range.

Integration of Metabolic and Quorum Sensing Signals Governing the Decision to Cooperate in a Bacterial Social Trait.

Many unicellular organisms live in multicellular communities that rely on cooperation between cells. However, cooperative traits are vulnerable to exploitation by non-cooperators (cheaters). We expand our understanding of the molecular mechanisms that allow multicellular systems to remain robust in the face of cheating by dissecting the dynamic regulation of cooperative rhamnolipids required for swarming in Pseudomonas aeruginosa. We combine mathematical modeling and experiments to quantitatively characterize the integration of metabolic and population density signals (quorum sensing) governing expression of the rhamnolipid synthesis operon rhlAB. The combined computational/experimental analysis reveals that when nutrients are abundant, rhlAB promoter activity increases gradually in a density dependent way. When growth slows down due to nutrient limitation, rhlAB promoter activity can stop abruptly, decrease gradually or even increase depending on whether the growth-limiting nutrient is the carbon source, nitrogen source or iron. Starvation by specific nutrients drives growth on intracellular nutrient pools as well as the qualitative rhlAB promoter response, which itself is modulated by quorum sensing. Our quantitative analysis suggests a supply-driven activation that integrates metabolic prudence with quorum sensing in a non-digital manner and allows P. aeruginosa cells to invest in cooperation only when the population size is large enough (quorum sensing) and individual cells have enough metabolic resources to do so (metabolic prudence). Thus, the quantitative description of rhlAB regulatory dynamics brings a greater understating to the regulation required to make swarming cooperation stable.

AI-2 quorum-sensing inhibitors affect the starvation response and reduce virulence in several Vibrio species, most likely by interfering with LuxPQ

The increase of disease outbreaks caused by Vibrio species in aquatic organisms as well as in humans, together with the emergence of antibiotic resistance in Vibrio species, has led to a growing interest in alternative disease control measures. Quorum sensing (QS) is a mechanism for regulating microbial gene expression in a cell density-dependent way. While there is good evidence for the involvement of auto-inducer 2 (AI-2)-based interspecies QS in the control of virulence in multiple Vibrio species, only few inhibitors of this system are known. From the screening of a small panel of nucleoside analogues for their ability to disturb AI-2-based QS, an adenosine derivative with a p-methoxyphenylpropionamide moiety at C-3' emerged as a promising hit. Its mechanism of inhibition was elucidated by measuring the effect on bioluminescence in a series of Vibrio harveyi AI-2 QS mutants. Our results indicate that this compound, as well as a truncated analogue lacking the adenine base, block AI-2-based QS without interfering with bacterial growth. The active compounds affected neither the bioluminescence system as such nor the production of AI-2, but most likely interfered with the signal transduction pathway at the level of LuxPQ in V. harveyi. The most active nucleoside analogue (designated LMC-21) was found to reduce the Vibrio species starvation response, to affect biofilm formation in Vibrio anguillarum, Vibrio vulnificus and Vibrio cholerae, to reduce pigment and protease production in V. anguillarum, and to protect gnotobiotic Artemia from V. harveyi-induced mortality.

Erratum

After the paper was published, a writing error was detected in the mathematical formula used to calculate the population increase rates. Because of this error, the statistical analyses of population increase rates were based on erroneous values. We recalculated the population increase rates using a corrected formula: where Nt is the catch index for a trapping occasion, Nt+T is the catch index for the following trapping occasion, and T is the time (in months) elapsed between the trapping occasions. To avoid division by zero, zero values were replaced with a value corresponding to a catch of 0.5 individuals in the trapping occasion. A reanalysis of the population increase rates revealed that the results published under subheading ‘Population increase rate’ (page 336 in the original article) and in Fig. 7 (page 339) were partly misleading. The main difference between the published results and the corrected results can be seen by comparing the previously published Fig. 7 with the corrected Fig. 7. In the corrected results, direct density dependence is more prevalent than in the previously published results. The difference is obvious particularly in autumn (population growth from August to October). In addition to the changes in Fig. 7, the results of regression analyses (page 336 right column) changed somewhat. In contrast to the previously published results, age structure did not explain a significant proportion of the variation in the population increase rates. The only variable that entered the stepwise regression models was productivity (the mean litter size multiplied by the proportion of females breeding), and even this variable could only explain 9% of the current population increase rate of bank voles (F1,48=5.0, P=0.03). In other species none of the variables studied entered the models. Corrected Fig. 7. Density dependence of the population increase rate. Pearson correlation coefficients for the relationship of the population increase rate with the density of the species studied (dots), pooled density of voles (circles), and regional mean density of voles (squares) with time lags from 0 to 12 months, separately for each species (field voles, sibling voles, bank voles, and common shrews) and season (spring=April to June, summer=June to August, autumn=August to October, and winter=October to April). Data from short line trappings in 1986–1992. Significant correlations are shown with an asterisk above (positive correlations) or below (negative correlations) the line. The corrected results reveal clear interspecific and seasonal differences in the relative importance of direct and delayed density dependence. In common shrews and bank voles, direct density dependence appears to prevail throughout the year (Fig. 7). The only exception is a negative relationship with previous vole densities (a time lag of 8–10 months) in bank voles in spring (population growth from April to June). In field voles, direct density dependence dominates in autumn but delayed density dependence from winter to the following summer (October to June). In sibling voles, the results resemble those of field voles with the exception that direct density dependence appears to be relatively more important in spring (Fig. 7). In contrast to the results of the original article, the corrected results suggest that the cessation of population growth at the population peak in August should be attributed to factors operating in a directly density dependent way at that part of the year. The corrected results also suggest that the delayed density dependent feedback loop necessary to generate the 3-year population cycle in Microtus voles operates during the period from late autumn to the following summer (October to June). These corrected results do not change the main conclusion of the original article: our results indicate that changes in survival rather than in reproduction drive the 3-year population cycles of voles.

Concurrent density dependence and independence in populations of arctic ground squirrels.

No population increases without limit. The processes that prevent this can operate in either a density-dependent way (acting with increasing severity to increase mortality rates or decrease reproductive rates as density increases), a density-independent way, or in both ways simultaneously. However, ecologists disagree for two main reasons about the relative roles and influences that density-dependent and density-independent processes have in determining population size. First, empirical studies showing both processes operating simultaneously are rare. Second, time-series analyses of long-term census data sometimes overestimate dependence. By using a density-perturbation experiment on arctic ground squirrels, we show concurrent density-dependent and density-independent declines in weaning rates, followed by density-dependent declines in overwinter survival during hibernation. These two processes result in strong, density-dependent convergence of experimentally increased populations to those of control populations that had been at low, stable levels.

Pollinator-Induced Density Dependence in Deceptive Species

Many animal-pollinated species experience low visitation rates and, in some cases, stand on the brink of extinction because they are poorly fertilized. Among these plants, some are deceptive species (flowering plants that do not offer any reward to their pollinators). A learning process that pollinators undergo determines visitation rate in those food frauds that do not mimic rewarding models. Pollinators that visit cheating species avoid them after having experienced the absence of reward a few times and then visit rewarding plants. We modeled this learning process, using classical optimal foraging and game theory tools, and applied our model to survey how visitation rate can be adjusted in deceptive species in a density-dependent way and how it can influence the population dynamics of those species. We found pollinator behavior to induce positive density dependence at low density (Allee effect) and therefore to create a threshold density under which population survival is not possible. Moreover, negative density dependence occurs at high density so that in most cases pollination limitation creates a stable demographic equilibrium. Stochastic simulations were performed to investigate the stability of populations at these equilibria and estimate their mean time to extinction. Because some parameters such as pollinator density or habitat fragmentation were explicitly taken into account, we tried to describe environmental conditions conducive to a deceptive plant's survival.

Population dynamics of the wood mouse Apodemus sylvaticus (Rodentia: Muridae) in a Sitka spruce successional mosaic

A population of wood mice, Apodemus sylvaticus (L.), was studied by capture‐mark‐recapture, in five 0.81 ha grids within a habitat mosaic produced by the felling of a plantation of mature Sitka spruce (Picea sitchensis Carriere). From May 1990 to June 1992, we estimated population sizes, survival (total and by weight classes), recruitment, and home‐range sizes, usually at monthly intervals, for the study area taken as a whole. Inter‐grid movements were frequent for both sexes, supporting the assumption that the population could be analysed in this way. Wood mice were more abundant in 1991 than in 1990, associated with increased seed supply. In both years, numbers were low in spring and increased gradually towards an autumn peak, which was of similar size in both years. Male home‐range areas varied seasonally, and were negatively correlated with population sizes, while female home ranges showed little seasonal variation. Survival and recruitment both declined sharply in late autumn, apparently in a densitydependent way. Except for this latter result, the population dynamics in a heterogeneous coniferous woodland were consistent with those described previously for this species in more homogeneous deciduous woodlands, suggesting that the same regulatory processes are operating in both habitats.

Density Dependence, Stochasticity, Compensation and Predator Regulation

This paper presents conceptual models of how density dependence and regulation operates in populations. Limitation is a process which sets the potential equilibrium level, and is caused by all forms of mortality or reproductive loss. Random variations in these mortalities will cause the population to fluctuate about the equilibrium. Regulation is the tendency of the population to return, through density dependent factors, to the equilibrium level when disturbed from it. The strength of density dependence determines whether a stable equilibrium, limit cycle or chaotic behaviour occurs. A population rarely, if ever, remains at its equilibrium because of disturbances. Because the amplitude of population fluctuations is determined by both the strength of density dependence and the size of the density independent mortalities, knowledge of both are required to understand population dynamics. Compensation is the ability of a mortality factor to counteract the effects of another one and requires a change in strength of the density dependence. Exact compensation rarely, if ever, occurs. Predators can act in a density dependent way to hold prey numbers at low levels. They can also act in an inverse density dependent (depensatory) way, which at high prey densities limits but not regulates the prey, but at low densities may cause the extinction of prey. Predation can produce special cases of multiple stable states and stable limit cycles. We discuss some of the criticisms of density dependence.

Proliferation control in cloned normal and malignant human cells

A method for cloning of a variety of normal and malignant human cells in culture is described. Palladium is precipitated on agarose through masks prefabricated by a photolithographic technique. Practically any pattern can be produced where cells exclusively settle and multiply as ‘miniclones’ on the metal ‘islands’. This communication establishes 1. 1. that ‘miniclones’ settle and multiply with the same efficiency as cells of a mass population, thus constituting an unbiased cell sample 2. 2. that certain malignant lines cannot be studied with the unmodified technique suitable for normal glia-like cells because of excessive translocation between islands 3. 3. that this can be circumvented by the interposition of a thin agar overlay between the cells and the fluid medium. Proliferation of normal glia-like cells was inhibited on palladium islands in a cell density-dependent way. On sufficiently small islands even single cells could be prevented from dividing. Circles of about 3 000 μm 2 prevented multiplication of about 50% of single cells otherwise capable of division, suggesting that cell-to-cell contacts may not be necessary for proliferation inhibition of normal cells.