http://precedings.nature.com/users/e86d2a15d1cd8f038546fbd046ac25b2/ Documents posted by Mario Pineda-Krch Nature Publishing Group en Nature Precedings http://precedings.nature.com/images/header_logo.gif http://precedings.nature.com http://dx.doi.org/10.1038/npre.2009.3672.1 Theoretical and empirical studies are showing evidence in support of evolutionary branching and sympatric speciation due to frequency‐dependent competition. However, phenotypic diversification due to underlying genetic diversification is only one possible evolutionary response to disruptive selection. Another potentially general response is phenotypic diversification in the form of phenotypic plasticity. It has been suggested that genetic variation is favored in stable environments, whereas phenotypic plasticity is favored in unstable and fluctuating environments. We investigate the “competition” between the processes of evolutionary branching and the evolution of phenotypic plasticity in a predator‐prey model that allows both processes to occur. In this model, environmental fluctuations can be caused by complicated population dynamics. We found that the evolution of phenotypic plasticity was generally more likely than evolutionary branching when the ecological dynamics exhibited pronounced predator‐prey cycles, whereas the opposite was true when the ecological dynamics was more stable. At intermediate levels of density cycling, trimorphisms with two specialist branches and a phenotypically plastic generalist branch sometimes occurred. Our theoretical results suggest that ecological dynamics and evolutionary dynamics can often be tightly linked and that an explicit consideration of population dynamics may be essential to explain the evolutionary dynamics of diversification in natural populations. http://dx.doi.org/10.1038/npre.2009.3672.1 Mon, 24 Aug 2009 09:34:31 UTC Ecological dynamics and the basis of sympatric phenotypic diversification doi:10.1038/npre.2009.3672.1 2009-08-24 Mario Pineda-Krch Nature Precedings 2009-08-24T09:34:31Z Presentation Ecology Evolutionary Biology http://creativecommons.org/licenses/by/3.0/ http://dx.doi.org/10.1038/npre.2009.3673.1 GillespieSSA is a package for the statistical computing and graphics language and environment R. GillespieSSA provides a simple to use and extensible interface to several stochastic simulation algorithms for generating simulated trajectories of finite population continuous-time model. Currently it implements Gillespie’s exact stochastic simulation algorithm (Direct method) and several approximate methods (Explicit tau-leap, Binomial tau-leap, and Optimized tau-leap). The package also contains a library of template models that can be run as demo models and can easily be customized and extended. Currently the following models are included, decaying-dimerization reaction set, linear chain system, logistic growth model, Lotka predator-prey model, Rosenzweig-MacArthur predator-prey model, Kermack-McKendrick SIR model, and a metapopulation SIRS model. http://dx.doi.org/10.1038/npre.2009.3673.1 Mon, 24 Aug 2009 09:31:16 UTC GillespieSSA: A user-friendly stochastic simulation package for R doi:10.1038/npre.2009.3673.1 2009-08-24 Mario Pineda-Krch Nature Precedings 2009-08-24T09:31:16Z Poster Ecology http://creativecommons.org/licenses/by/3.0/ http://dx.doi.org/10.1038/npre.2009.3636.1 The contradiction between the long-term persistence of the chromosomal hotspots that initiate meiotic recombination and the self-destructive mechanism by which they act strongly suggests that our understanding of recombination is incomplete. To investigate the requirements for hotspot persistence, Rosemary Redfield and I developed a computer simulation model, hotspot, of their activity and its evolutionary consequences. http://dx.doi.org/10.1038/npre.2009.3636.1 Fri, 21 Aug 2009 20:17:03 UTC The joys and perils of recombination – The hotspot conversion paradox and the evolution of recombination doi:10.1038/npre.2009.3636.1 2009-08-21 Mario Pineda-Krch Nature Precedings 2009-08-21T20:17:03Z Presentation Genetics & Genomics Evolutionary Biology http://creativecommons.org/licenses/by/3.0/ http://dx.doi.org/10.1038/npre.2009.3637.1 The contradiction between the long-term persistence of the chromosomal hotspots that initiate meiotic recombination and the self-destructive mechanism by which they act strongly suggests that our understanding of recombination is incomplete. This “hotspot paradox” has been reinforced by the finding that biased gene conversion also removes active hotspots from human sperm. To investigate the requirements for hotspot persistence, we developed a detailed computer simulation model of their activity and its evolutionary consequences. With this model, unopposed hotspot activity could drive strong hotspots from 50% representation to extinction within 70 generations. Although the crossing over that hotspots cause can increase population fitness, this benefit was always too small to slow the loss of hotspots. Hotspots could not be maintained by plausible rates of de novo mutation, nor by crossover interference, which alters the frequency and/or spacing of crossovers. Competition among hotspots for activity-limiting factors also did not prevent their extinction, although the rate of hotspot loss was slowed. Key factors were the probability that the initiating hotspot allele is destroyed and the nonmeiotic contributions hotspots make to fitness. Experimental investigation of these deserves high priority, because until the paradox is resolved all components of the mechanism are open to doubt. http://dx.doi.org/10.1038/npre.2009.3637.1 Tue, 18 Aug 2009 20:29:58 UTC The hotspot conversion paradox doi:10.1038/npre.2009.3637.1 2009-08-18 Mario Pineda-Krch Nature Precedings 2009-08-18T20:29:58Z Presentation Genetics & Genomics Evolutionary Biology http://creativecommons.org/licenses/by/3.0/ http://dx.doi.org/10.1038/npre.2009.3638.1 Overview of the Special Interdisciplinary Minisymposium at the 2009 meeting of the Society for Mathematical Biology on modeling of forest insect population dynamics. http://dx.doi.org/10.1038/npre.2009.3638.1 Tue, 18 Aug 2009 08:07:59 UTC Modeling forest insect population dynamics doi:10.1038/npre.2009.3638.1 2009-08-18 Mario Pineda-Krch Nature Precedings 2009-08-18T08:07:59Z Presentation Ecology http://creativecommons.org/licenses/by/3.0/ http://dx.doi.org/10.1038/npre.2007.57.1 Traits determining ecological interactions and dynamics are generally subject to natural selection. That genetically based individual variation in ecological traits can influence population dynamics has interested population biologist from various perspectives. Population ecologists recognized the need to incorporate individual variation in models of population regulation, while evolutionary biologists wish to understand genetic and evolutionary dynamics, e.g. of life history traits, in density-regulated populations. But how does adaptation in ecological traits affect population dynamics? In this project we investigated how ecological dynamics changes as a consequence of adaptive evolution in ecological traits using an individual-based predator-prey model. http://dx.doi.org/10.1038/npre.2007.57.1 Mon, 18 Jun 2007 03:57:37 UTC Adaptive evolution and then what? doi:10.1038/npre.2007.57.1 2009-03-04 Mario Pineda-Krch Nature Precedings 2007-06-18T03:57:37Z Poster Ecology Evolutionary Biology http://creativecommons.org/licenses/by/2.5/ http://dx.doi.org/10.1038/npre.2007.56.1 An increasing number of studies are showing evidence in support of sympatric speciation. One basic question remains, however. When a population has undergone a branching in its phenotype, is this due to an evolutionary branching in the underlying genotype or due to phenotypic plasticity modifying a single genotype? Thus, phenotypic plasticity has come to be viewed as a trait subject to selection, just like any other phenotypic character1,2. Here we present a model addressing the conditions under which a predator phenotype experiencing selection for two alternative optimal phenotypes gives rise to genetically based phenotypic branching or to phenotypic plasticity, allowing the corresponding genotype to give rise to two alternative, well-adapted phenotypes. http://dx.doi.org/10.1038/npre.2007.56.1 Sat, 16 Jun 2007 10:03:20 UTC Fluctuating population dynamics promotes the evolution of phenotypic plasticity doi:10.1038/npre.2007.56.1 2007-06-16 Mario Pineda-Krch Nature Precedings 2007-06-16T10:03:20Z Poster Ecology http://creativecommons.org/licenses/by/2.5/ http://dx.doi.org/10.1038/npre.2007.48.1 Periodic predator-prey dynamics in constant environments are usually taken as indicative of deterministic limit cycles. It is known, however, that demographic stochasticity in finite populations can also give rise to regular population cycles, even when the corresponding deterministic models predict a stable equilibrium. The existence of quasi-cycles substantially expands the scope for natural patterns of periodic population oscillations caused by ecological interactions, thereby complicating the conclusive interpretation of such patterns. It is, however, feasible and straightforward to accurately distinguish between the two types of cycle through the combined analysis of autocorrelations and marginal distributions of population sizes. By confronting these results with real ecological time series even short and imperfect time series allow quasi-cycles and limit cycles to be distinguished reliably.This work has been published in:Pineda-Krch M, Blok HJ, Dieckmann U, Doebeli M. 2007. A tale of two cycles – Distinguishing between true limit cycles and quasi-cycles in finite predator-prey populations. Oikos 116: 53-64. http://dx.doi.org/10.1038/npre.2007.48.1 Thu, 14 Jun 2007 05:22:34 UTC Noise, cycles, and noisy cycles in finite populations doi:10.1038/npre.2007.48.1 2007-06-14 Mario Pineda-Krch Nature Precedings 2007-06-14T05:22:34Z Presentation Ecology http://creativecommons.org/licenses/by/2.5/