A DNA test to sex most birds.

The repeatability of behaviour: a meta-analysis.

Understanding the ecological consequences of biodiversity is a fundamental challenge. Research on a key component of biodiversity, genetic diversity, has traditionally focused on its importance in evolutionary processes, but classical studies in evolutionary biology, agronomy and conservation biology indicate that genetic diversity might also have important ecological effects. Our review of the literature reveals significant effects of genetic diversity on ecological processes such as primary productivity, population recovery from disturbance, interspecific competition, community structure, and fluxes of energy and nutrients. Thus, genetic diversity can have important ecological consequences at the population, community and ecosystem levels, and in some cases the effects are comparable in magnitude to the effects of species diversity. However, it is not clear how widely these results apply in nature, as studies to date have been biased towards manipulations of plant clonal diversity, and little is known about the relative importance of genetic diversity vs. other factors that influence ecological processes of interest. Future studies should focus not only on documenting the presence of genetic diversity effects but also on identifying underlying mechanisms and predicting when such effects are likely to occur in nature.

/pdf/ecological-consequences-of-genetic-diversity-19pxvjx8hv.pdf

Ecological consequences of genetic diversity.

In this review I show that the '3/4-power scaling law' of metabolic rate is not universal, either within or among animal species. Significant variation in the scaling of metabolic rate with body mass is described mainly for animals, but also for unicells and plants. Much of this variation, which can be related to taxonomic, physiological, and/or environmental differences, is not adequately explained by existing theoretical models, which are also reviewed. As a result, synthetic explanatory schemes based on multiple boundary constraints and on the scaling of multiple energy-using processes are advocated. It is also stressed that a complete understanding of metabolic scaling will require the identification of both proximate (functional) and ultimate (evolutionary) causes. Four major types of intraspecific metabolic scaling with body mass are recognized [based on the power function R=aMb, where R is respiration (metabolic) rate, a is a constant, M is body mass, and b is the scaling exponent]: Type I: linear, negatively allometric (b 1) to one or two later phases of negative allometry (b<1). Ontogenetic changes in the metabolic intensity of four component processes (i.e. growth, reproduction, locomotion, and heat production) appear to be important in these different patterns of metabolic scaling. These changes may, in turn, be shaped by age (size)-specific patterns of mortality. In addition, major differences in interspecific metabolic scaling are described, especially with respect to mode of temperature regulation, body-size range, and activity level. A 'metabolic-level boundaries hypothesis' focusing on two major constraints (surface-area limits on resource/waste exchange processes and mass/volume limits on power production) can explain much, but not all of this variation. My analysis indicates that further empirical and theoretical work is needed to understand fully the physiological and ecological bases for the considerable variation in metabolic scaling that is observed both within and among species. Recommended approaches for doing this are discussed. I conclude that the scaling of metabolism is not the simple result of a physical law, but rather appears to be the more complex result of diverse adaptations evolved in the context of both physico-chemical and ecological constraints.

Beyond the '3/4-power law': variation in the intra- and interspecific scaling of metabolic rate in animals.

A plethora of epigenetic modifications have been described in the human genome and shown to play diverse roles in gene regulation, cellular differentiation and the onset of disease. Although individual modifications have been linked to the activity levels of various genetic functional elements, their combinatorial patterns are still unresolved and their potential for systematic de novo genome annotation remains untapped. Here, we use a multivariate Hidden Markov Model to reveal chromatin states in human T cells, based on recurrent and spatially coherent combinations of chromatin marks.We define 51 distinct chromatin states, including promoter-associated, transcription-associated, active intergenic, largescale repressed and repeat-associated states. Each chromatin state shows specific enrichments in functional annotations, sequence motifs and specific experimentally observed characteristics, suggesting distinct biological roles. This approach provides a complementary functional annotation of the human genome that reveals the genome-wide locations of diverse classes of epigenetic function.

Discovery and characterization of chromatin states for systematic annotation of the human genome

Many of the most dangerous human diseases are transmitted by insect vectors. After decades of repeated insecticide use, all of these vector species have demonstrated the capacity to evolve resistance to insecticides. Insecticide resistance is generally considered to undermine control of vector-transmitted diseases because it increases the number of vectors that survive the insecticide treatment. Disease control failure, however, need not follow from vector control failure. Here, we review evidence that insecticide resistance may have an impact on the quality of vectors and, specifically, on three key determinants of parasite transmission: vector longevity, competence, and behaviour. We argue that, in some instances, insecticide resistance is likely to result in a decrease in vector longevity, a decrease in infectiousness, or in a change in behaviour, all of which will reduce the vectorial capacity of the insect. If this effect is sufficiently large, the impact of insecticide resistance on disease management may not be as detrimental as previously thought. In other instances, however, insecticide resistance may have the opposite effect, increasing the insect's vectorial capacity, which may lead to a dramatic increase in the transmission of the disease and even to a higher prevalence than in the absence of insecticides. Either way-and there may be no simple generality-the consequence of the evolution of insecticide resistance for disease ecology deserves additional attention.

/pdf/insecticide-control-of-vector-borne-diseases-when-is-2oh45uywye.pdf

Insecticide control of vector-borne diseases: when is insecticide resistance a problem?

A growing body of evidence points towards epigenetic mechanisms being responsible for a wide range of biological phenomena, from the plasticity of plant growth and development to the nutritional control of caste determination in honeybees and the etiology of human disease (e.g., cancer). With the (partial) elucidation of the molecular basis of epigenetic variation and the heritability of certain of these changes, the field of evolutionary epigenetics is flourishing. Despite this, the role of epigenetics in shaping host–pathogen interactions has received comparatively little attention. Yet there is plenty of evidence supporting the implication of epigenetic mechanisms in the modulation of the biological interaction between hosts and pathogens. The phenotypic plasticity of many key parasite life-history traits appears to be under epigenetic control. Moreover, pathogen-induced effects in host phenotype may have transgenerational consequences, and the bases of these changes and their heritability probably have an epigenetic component. The significance of epigenetic modifications may, however, go beyond providing a mechanistic basis for host and pathogen plasticity. Epigenetic epidemiology has recently emerged as a promising area for future research on infectious diseases. In addition, the incorporation of epigenetic inheritance and epigenetic plasticity mechanisms to evolutionary models and empirical studies of host–pathogen interactions will provide new insights into the evolution and coevolution of these associations. Here, we review the evidence available for the role epigenetics on host–pathogen interactions, and the utility and versatility of the epigenetic technologies available that can be cross-applied to host–pathogen studies. We conclude with recommendations and directions for future research on the burgeoning field of epigenetics as applied to host–pathogen interactions.

/pdf/epigenetics-of-host-pathogen-interactions-the-road-ahead-and-3m5i3edyu0.pdf

Epigenetics of host-pathogen interactions: the road ahead and the road behind.

A prerequisite for honest handicaps is that there are significant condition–dependent costs in the expression of sexual traits. In the wolf spider Hygrolycosa rubrofasciata (Ohlert), sexual signalling (drumming) is costly in terms of increased mortality. Here we investigated whether this mortality may be caused by increased energy expenditure. During sexual signalling, metabolic rate was 22 times higher than at rest and four times higher than when males were actively moving. Metabolic rate per unit mass was positively related to absolute body mass during sexual signalling but not during other activities. This positive relationship is novel to any studies of metabolic rates. Indeed, it seems that the largest males can drum only 12 times per minute before reaching the maximum sustainable metabolic rate, whereas the smallest males may drum up to 39 times per minute. However, there is no relationship between body mass and drumming rate, indicating that larger males are able to compensate for the higher cost of drumming. There was a quadratic relationship between relative abdomen mass and overall body mass, which may provide a partial explanation for the increased energy expenditure of largest males while drumming. Altogether, our results indicate that sexual signalling is highly energetically demanding, which may be the main reason for the honesty of signalling in this species. In addition, the energetic costs are surprisingly strongly size dependent, which may compensate any disadvantage of small male size.

/pdf/energetic-costs-of-size-and-sexual-signalling-in-a-wolf-2jpxquv5ky.pdf

Energetic costs of size and sexual signalling in a wolf spider

https://www.cell.com/trends/parasitology/pdf/S1471-4922(06)00058-4.pdf

Nitric oxide: an antiparasitic molecule of invertebrates

Knowledge of the relationship between body size and fitness is essential in many models of parasitoid evolutionary ecology. One clear point emerging from previous studies is that the relationship between size and fitness can depend strongly (qualitatively and quantitatively) on the environment in which it is measured. Our results show that, in the parasitoid wasp Nasonia vitripennis, the relationship between parasitoid size and fitness is strongly dependent on the nutritional status of the female; being small is more costly when food is not available. Lipid availability is the main factor mediating the relationship between size and fitness. Small females suffer disproportionately the costs of not feeding because they emerge with small lipid reserves and thus have to rely more heavily on carbohydrates for survival and reproduction. In other words, feeding is more important for small females. Our results (1) provide a physiological explanation for why laboratory estimates of the size–fitness relationship are not as steep as field estimates and (2) suggest that females are likely to show size-dependent foraging and feeding strategies.

/pdf/the-physiological-costs-of-being-small-in-a-parasitic-wasp-z9m004wpe9.pdf

Ana Rivero

Papers

Insecticide control of vector-borne diseases: when is insecticide resistance a problem?

Epigenetics of host-pathogen interactions: the road ahead and the road behind.

Energetic costs of size and sexual signalling in a wolf spider

Nitric oxide: an antiparasitic molecule of invertebrates

The physiological costs of being small in a parasitic wasp