Co-evolution of male and female reproductive traits across the Bruchidae (Coleoptera)

1. Despite the obvious importance of spermatozoa to individual reproductive success a general explanation of variation in spermatozoan form and function is still lacking. In species with internal fertilization, sperm not only have to interact with the physical and biochemical environment of the female reproductive tract, but frequently face competition from the sperm of rival males. Both sperm competition theory and adaptation to the selective environment of the female reproductive tract have been implicated in the evolution of spermatozoan morphological diversity. 2. Using the comparative method, we examine variation in sperm length in relation to (i) sperm competition intensity (as measured by relative testis size) and (ii) female reproductive characters, across 15 species of beetle belonging to the family Bruchidae. 3. Stepwise multiple regression within a phylogenetic framework revealed sperm length to be positively correlated with female spermathecal duct length and negatively related to spermathecal volume, but not testes size, indicating that the female reproductive environment rather than sperm competition per se exerts selection on sperm length in this taxonomic group. 4. A positive association between testes volume and the volume of the female spermatheca was also evident suggesting correlated evolution of these traits. 5. A number of models of sexual selection could lead to the correlated evolution of male and female reproductive characters, although the underlying mechanisms of cause and effect remain elusive. Divergence between species (and populations) in primary reproductive traits is likely to present a significant barrier to hetero-specific fertilization, and thus contribute to reproductive isolation

Region-specific and activity-dependent regulation of SVZ neurogenesis and recovery after stroke.

Stroke is the leading cause of adult disability. Neurogenesis after stroke is associated with repair; however, the mechanisms regulating poststroke neurogenesis and its functional effect remain unclear. Here, we investigate multiple mechanistic routes of induced neurogenesis in the poststroke brain, using both a forelimb overuse manipulation that models a clinical neurorehabilitation paradigm, as well as local manipulation of cellular activity in the peri-infarct cortex. Increased activity in the forelimb peri-infarct cortex via either modulation drives increased subventricular zone (SVZ) progenitor proliferation, migration, and neuronal maturation in peri-infarct cortex. This effect is sensitive to competition from neighboring brain regions. By using orthogonal tract tracing and rabies virus approaches in transgenic SVZ-lineage-tracing mice, SVZ-derived neurons synaptically integrate into the peri-infarct cortex; these effects are enhanced with forelimb overuse. Synaptic transmission from these newborn SVZ-derived neurons is critical for spontaneous recovery after stroke, as tetanus neurotoxin silencing specifically of the SVZ-derived neurons disrupts the formation of these synaptic connections and hinders functional recovery after stroke. SVZ-derived neurogenesis after stroke is activity-dependent, region-specific, and sensitive to modulation, and the synaptic connections formed by these newborn cells are functionally critical for poststroke recovery

A theoretical investigation of the effect of proliferation and\ud adhesion on monoclonal conversion in the colonic crypt

Colorectal cancers are initiated by the accumulation of mutations in the colonic epithelium. Using a spatially structured cell-based model of a colonic crypt, we investigate the likelihood that the progeny of a mutated cell will dominate, or be sloughed out of, a crypt. Our approach is to perform multiple simulations, varying the spatial location of the initial mutation, and its proliferative and adhesive properties, to obtain statistical distributions for the probability of domination. Our simulations lead us to make a number of predictions. The process of monoclonal conversion always occurs, and does not require that the cell which initially gave rise to the population remains in the crypt. Mutations occurring more than one to two cells from the base of the crypt are unlikely to become the dominant clone. The probability of a mutant clone persisting in the crypt is sensitive to dysregulation of adhesion, and comparison with a one-dimensional model suggests that this is caused by competition directly at the base of the crypt.\ud We also predict that increases in the extent of the spatial domain in which the mutant cells proliferate cause counter-intuitive non-linear changes to the probability of its fixation, due to effects that cannot be captured in simpler models

On the mutual exclusivity of competing hypotheses

Many philosophical accounts of scientific theory comparison take as a starting point competition between mutually exclusive alternative hypotheses. However, in scientific inquiry, it often appears that hypotheses which are in competition with one another are not mutually exclusive. For example, a hypothesis which postulates one cause of a particular event may compete with a hypothesis which postulates a strictly stronger conjunction of causes. It appears that the conjunctive hypothesis does not exclude the single-cause hypothesis, but rather entails it, since the single-cause hypothesis may be seen as a special case of the conjunctive hypothesis. The apparent existence of logical relations between competing hypotheses then presents a problem for models of scientific inference which assume that competing theories are mutually exclusive. The problem has been raised in slightly different guises for both for Inference to the Best Explanation and Bayesianism. This chapter shows how taking a hierarchical view of theory comparison allows us to resolve this problem. Scientific theory evaluation takes place at multiple levels, with more general theories competing against each other at higher levels and more specific hypotheses competing at lower levels. Higher-level theories can be seen as mutually exclusive alternatives, even while logical relations are respected at lower levels

Competition, predation, and density-dependent mortality in demersal marine fishes

The relative roles of competition and predation in demographic density dependence are poorly known. A tractable experimental design to determine such effects and their interactions for demersal (seafloor oriented) fishes and similar sedentary species is cross-factoring multiple densities of new recruits with the presence and absence of predators. This design allows one to distinguish between density-dependent mortality due to competition alone, predation alone, or an interaction between the two, especially when supplemental field observations are available. To date, 14 species of marine fish have been examined with some variant of this design, and for 12 species predation was demonstrated to be the sole or major cause of density dependence. However, as competition may be slow acting relative to predation, the importance of competition can be underestimated in short-term experiments. On the Great Barrier Reef, we conducted a long-term field experiment in which multiple densities of new recruits of a planktivorous damselfish were cross-factored with the presence or absence of resident piscivorous fish on patch reefs. During the first 10 months, no density-dependent mortality was detected, regardless of whether resident predators were present or absent. By the end of the experiment at 17 months, per capita mortality was strongly density dependent and highly compensatory in both predator treatments; all reefs ultimately supported nearly the same adult density regardless of experimental treatment. Examination of treatment effect sizes suggested that competition was the main source of density-dependent mortality, with predation being merely a proximate agent of death. We hypothesize that predators were ineffective in this system compared with similar studies elsewhere because prey density was low relative to ample prey refuges provided by highly complex corals. Combined with previous studies, these findings indicate that density-dependent mortality in demersal marine fishes is often caused by interplay of predation and competition, whose roles may be altered by variation in habitat complexity and larval supply. These conclusions are relevant to marine fisheries models, which typically assume that density dependence is due solely to intraspecific competition

Evolution of female multiple mating : A quantitative model of the “sexually selected sperm” hypothesis

This article is protected by copyright. All rights reserved. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.Peer reviewedPublisher PD

The economic implications of a multiple species approach to bioeconomic modelling : a thesis presented in partial fulfilment of the requirements for the degree of Master of Applied Economics at Massey University, Palmerston North, New Zealand

Human activity frequently leads to the endangerment or extinction of other species. While ecologists study the biological facets of species loss, economics, as the science of understanding people's behaviour, has been charged with investigating the incentives underlying the actions people take that lead to this loss. One approach economists have taken to gain this understanding is to develop models of endangered species that include both economic and biological components, known as bioeconomic models. While ecologists frequently note the importance of modelling entire ecosystems rather than single species, most bioeconomic models in the current literature focus only on a single species. This thesis addresses the economic significance of this assumption through the development of a series of multiple species models and demonstrates, using African Wildlife as an example, the importance of interrelationships and economic values to the survival of endangered species. From these models one can infer the conditions under which a single species model may be appropriate, at least in general terms. If species are independent, and either the opportunity cost of capital or the value of habitat is very low relative to the value of the species in question, then a single species model may yield results similar to that of a multiple species model. In contrast, if species are independent and these additional conditions are not met, a single species model may significantly underestimate both optimal stock levels and land allocation. However, species do not live independently; they interact with species with which they share habitat and, when species interact, the potential for misapplication of the single species framework is even greater. When species compete, the single species framework consistently produces higher stock levels than the multiple species framework, the greater the level of competition the greater the difference. In a predator-prey relationship, the relative values of predator and prey are critical to determining the outcome of the multiple species model. It is demonstrated that the inclusion of at least all economically valuable species in an ecosystem is important when constructing bioeconomic models. Using single species models where multiple species are economically significant could lead to misleading results and ultimately to incorrect policy decisions

Pre-integration lateral inhibition enhances unsupervised learning

A large and influential class of neural network architectures use post-integration lateral inhibition as a mechanism for competition. We argue that these algorithms are computationally deficient in that they fail to generate, or learn, appropriate perceptual representations under certain circumstances. An alternative neural network architecture is presented in which nodes compete for the right to receive inputs rather than for the right to generate outputs. This form of competition, implemented through pre-integration lateral inhibition, does provide appropriate coding properties and can be used to efficiently learn such representations. Furthermore, this architecture is consistent with both neuro-anatomical and neuro-physiological data. We thus argue that pre-integration lateral inhibition has computational advantages over conventional neural network architectures while remaining equally biologically plausible

Immune-mediated competition in rodent malaria is most likely caused by induced changes in innate immune clearance of merozoites

Malarial infections are often genetically diverse, leading to competitive interactions between parasites. A quantitative understanding of the competition between strains is essential to understand a wide range of issues, including the evolution of virulence and drug resistance. In this study, we use dynamical-model based Bayesian inference to investigate the cause of competitive suppression of an avirulent clone of Plasmodium chabaudi (AS) by a virulent clone (AJ) in immuno-deficient and competent mice. We test whether competitive suppression is caused by clone-specific differences in one or more of the following processes: adaptive immune clearance of merozoites and parasitised red blood cells (RBCs), background loss of merozoites and parasitised RBCs, RBC age preference, RBC infection rate, burst size, and within-RBC interference. These processes were parameterised in dynamical mathematical models and fitted to experimental data. We found that just one parameter μ, the ratio of background loss rate of merozoites to invasion rate of mature RBCs, needed to be clone-specific to predict the data. Interestingly, μ was found to be the same for both clones in single-clone infections, but different between the clones in mixed infections. The size of this difference was largest in immuno-competent mice and smallest in immuno-deficient mice. This explains why competitive suppression was alleviated in immuno-deficient mice. We found that competitive suppression acts early in infection, even before the day of peak parasitaemia. These results lead us to argue that the innate immune response clearing merozoites is the most likely, but not necessarily the only, mediator of competitive interactions between virulent and avirulent clones. Moreover, in mixed infections we predict there to be an interaction between the clones and the innate immune response which induces changes in the strength of its clearance of merozoites. What this interaction is unknown, but future refinement of the model, challenged with other datasets, may lead to its discovery