139 research outputs found
Extraordinary Sex Ratios: Cultural Effects on Ecological Consequences
We model sex-structured population dynamics to analyze pairwise competition
between groups differing both genetically and culturally. A sex-ratio allele is
expressed in the heterogametic sex only, so that assumptions of Fisher's
analysis do not apply. Sex-ratio evolution drives cultural evolution of a
group-associated trait governing mortality in the homogametic sex. The two-sex
dynamics under resource limitation induces a strong Allee effect that depends
on both sex ratio and cultural trait values. We describe the resulting
threshold, separating extinction from positive growth, as a function of female
and male densities. When initial conditions avoid extinction due to the Allee
effect, different sex ratios cannot coexist; in our model, greater female
allocation always invades and excludes a lesser allocation. But the culturally
transmitted trait interacts with the sex ratio to determine the ecological
consequences of successful invasion. The invading female allocation may permit
population persistence at self-regulated equilibrium. For this case, the
resident culture may be excluded, or may coexist with the invader culture. That
is, a single sex-ratio allele in females and a cultural dimorphism in male
mortality can persist; a low-mortality resident trait is maintained by
father-to-son cultural transmission. Otherwise, the successfully invading
female allocation excludes the resident allele and culture, and then drives the
population to extinction via a shortage of males. Finally, we show that the
results obtained under homogeneous mixing hold, with caveats, in a spatially
explicit model with local mating and diffusive dispersal in both sexes.Comment: final version, reflecting changes in response to referees' comment
Spatial Competition: Roughening of an Experimental Interface
Limited dispersal distance generates spatial aggregation. Intraspecific interactions are then concentrated within clusters, and between-species interactions occur near cluster boundaries. Spread of a locally dispersing invader can become motion of an interface between the invading and resident species, and spatial competition will produce variation in the extent of invasive advance along the interface. Kinetic roughening theory offers a framework for quantifying the development of these fluctuations, which may structure the interface as a self-affine fractal, and so induce a series of temporal and spatial scaling relationships. For most clonal plants, advance should become spatially correlated along the interface, and width of the interface (where invader and resident compete directly) should increase as a power function of time. Once roughening equilibrates, interface width and the relative location of the most advanced invader should each scale with interface length. We tested these predictions by letting white clover (Trifolium repens) invade ryegrass (Lolium perenne). The spatial correlation of clover growth developed as anticipated by kinetic roughening theory, and both interface width and the most advanced invaderβs lead scaled with front length. However, the scaling exponents differed from those predicted by recent simulation studies, likely due to cloverβs growth morphology.
In many plant communities, limited dispersal aggregates conspecific individuals1. In particular, most invasive plants are clonal and propagate vegetatively2, so that invaders initially cluster among residents3. Aggregation of conspecifics has consequences for population interactions. Individual plants usually compete at the nearest-neighbor scale4,5. When different species each aggregate spatially and interact locally, intraspecific competition will predominate within clusters, while interspecific competition will localize at the interface between clusters6,7,8. This interaction geometry implies that the advance versus extinction of an invasive species may depend on development and subsequent movement of a between-species interface9,10.
An invading speciesβ local density declines from positive equilibrium to rarity across the width of an ecological interface11. As a competitively superior invader excludes the resident species within the interface width, the front is pushed forward. Dispersal limitation promotes spatially correlated invasive advance along the interface. These correlations, generated through lateral growth, invite application of the theory of kinetic roughening, a framework for identifying quantitative characteristics shared by different interface-growth processes12. Previous applications of the theory span materials science13, temporal pattern in parallel-computing14,15, and ecological invasion11,16.
Kinetic roughening theory predicts power-law scaling relationships governing both the development and the equilibrium statistical structure of an invader-resident interface. Our analyses emphasize scaling of both the interface width and the relative position of the βfront-runner,β the most advanced invader, a metric used at both local and regional scales17,18,19. Interestingly, the exponents of scaling relationships predicted by kinetic roughening sometimes identify an interface as a member of a particular universality class. That is, quite distinct local processes may exhibit the same dependence of interface roughening on time, and the equilibrium width may exhibit the same dependence on interface length; universality implies powerful generality13. Previously, we modeled the front produced when a dispersal limited, but competitively superior, invader advances across a habitat occupied by a resident species11,20. That modelβs kinetic roughening belongs to the KPZ universality class, for Kardar-Parisi-Zhang12.
We begin by analyzing spatial competition as a problem for kinetic roughening theory, and then report a field experiment testing the predictions. We let Dutch white clover (Trifolium repens) advance into plots of perennial ryegrass (Lolium perenne). We monitored the development of spatial correlations along the fronts, and estimated a series of power-law scaling relationships from roughened fronts of different lengths. The exponents implied by the observed scaling allowed us, in addition, to ask if the experimental interface belonged to the KPZ universality class12,13
Spatial Dynamics of Invasion: The Geometry of Introduced Species
Many exotic species combine low probability of establishment at each
introduction with rapid population growth once introduction does succeed. To
analyze this phenomenon, we note that invaders often cluster spatially when
rare, and consequently an introduced exotic's population dynamics should depend
on locally structured interactions. Ecological theory for spatially structured
invasion relies on deterministic approximations, and determinism does not
address the observed uncertainty of the exotic-introduction process. We take a
new approach to the population dynamics of invasion and, by extension, to the
general question of invasibility in any spatial ecology. We apply the physical
theory for nucleation of spatial systems to a lattice-based model of
competition between plant species, a resident and an invader, and the analysis
reaches conclusions that differ qualitatively from the standard ecological
theories. Nucleation theory distinguishes between dynamics of single-cluster
and multi-cluster invasion. Low introduction rates and small system size
produce single-cluster dynamics, where success or failure of introduction is
inherently stochastic. Single-cluster invasion occurs only if the cluster
reaches a critical size, typically preceded by a number of failed attempts. For
this case, we identify the functional form of the probability distribution of
time elapsing until invasion succeeds. Although multi-cluster invasion for
sufficiently large systems exhibits spatial averaging and almost-deterministic
dynamics of the global densities, an analytical approximation from nucleation
theory, known as Avrami's law, describes our simulation results far better than
standard ecological approximations.Comment: 25 pages (pdf
Interference competition and invasion: spatial structure, novel weapons and resistance zones
Certain invasive plants may rely on interference mechanisms (allelopathy,
e.g.) to gain competitive superiority over native species. But expending
resources on interference presumably exacts a cost in another life-history
trait, so that the significance of interference competition for invasion
ecology remains uncertain. We model ecological invasion when combined effects
of preemptive and interference competition govern interactions at the
neighborhood scale. We consider three cases. Under "novel weapons," only the
initially rare invader exercises interference. For "resistance zones" only the
resident species interferes, and finally we take both species as interference
competitors. Interference increases the other species' mortality, opening space
for colonization. However, a species exercising greater interference has
reduced propagation, which can hinder its colonization of open sites.
Interference never enhances a rare invader's growth in the homogeneously mixing
approximation to our model. But interference can significantly increase an
invader's competitiveness, and its growth when rare, if interactions are
structured spatially. That is, interference can increase an invader's success
when colonization of open sites depends on local, rather than global, species
densities. In contrast, interference enhances the common, resident species'
resistance to invasion independently of spatial structure, unless the
propagation-cost is too great. Increases in background mortality (i.e.,
mortality not due to interference) always reduce the effectiveness of
interference competition
Ecological Invasion, Roughened Fronts, and a Competitor's Extreme Advance: Integrating Stochastic Spatial-Growth Models
Both community ecology and conservation biology seek further understanding of
factors governing the advance of an invasive species. We model biological
invasion as an individual-based, stochastic process on a two-dimensional
landscape. An ecologically superior invader and a resident species compete for
space preemptively. Our general model includes the basic contact process and a
variant of the Eden model as special cases. We employ the concept of a
"roughened" front to quantify effects of discreteness and stochasticity on
invasion; we emphasize the probability distribution of the front-runner's
relative position. That is, we analyze the location of the most advanced
invader as the extreme deviation about the front's mean position. We find that
a class of models with different assumptions about neighborhood interactions
exhibit universal characteristics. That is, key features of the invasion
dynamics span a class of models, independently of locally detailed demographic
rules. Our results integrate theories of invasive spatial growth and generate
novel hypotheses linking habitat or landscape size (length of the invading
front) to invasion velocity, and to the relative position of the most advanced
invader.Comment: The original publication is available at
www.springerlink.com/content/8528v8563r7u2742
Current evidence for a modulation of low back pain by human genetic variants
The manifestation of chronic back pain depends on structural, psychosocial, occupational and genetic influences. Heritability estimates for back pain range from 30% to 45%. Genetic influences are caused by genes affecting intervertebral disc degeneration or the immune response and genes involved in pain perception, signalling and psychological processing. This inter-individual variability which is partly due to genetic differences would require an individualized pain management to prevent the transition from acute to chronic back pain or improve the outcome. The genetic profile may help to define patients at high risk for chronic pain. We summarize genetic factors that (i) impact on intervertebral disc stability, namely Collagen IX, COL9A3, COL11A1, COL11A2, COL1A1, aggrecan (AGAN), cartilage intermediate layer protein, vitamin D receptor, metalloproteinsase-3 (MMP3), MMP9, and thrombospondin-2, (ii) modify inflammation, namely interleukin-1 (IL-1) locus genes and IL-6 and (iii) and pain signalling namely guanine triphosphate (GTP) cyclohydrolase 1, catechol-O-methyltransferase, ΞΌ opioid receptor (OPMR1), melanocortin 1 receptor (MC1R), transient receptor potential channel A1 and fatty acid amide hydrolase and analgesic drug metabolism (cytochrome P450 [CYP]2D6, CYP2C9)
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