Aggressiveness and size: a model and two tests

Individual variation in aggressive behavior in animals might be caused by adaptive covariation with body size. We developed a model that predicts the benefits of aggressiveness as a function of body size. The model indicated that individuals of intermediate sizes would derive the greatest benefits from being aggressive. If we assume that the cost of aggression is approximately uniform with respect to body size, selection should favor higher aggression in intermediate-sized individuals than in large or small individuals. This prediction was tested by stimulating male Madagascar hissing cockroaches, Gromphadorhina portentosa, with disembodied antennae and recording the males' aggressive responses. Antennae from larger males evoked weaker responses in subjects, suggesting that males obtained information about their opponents' size from the opponents' antennae alone. After accounting for this effect, we found support for the key prediction of our model: aggressiveness peaked at intermediate sizes. Data from actual male-male interactions validated that the antenna assay accurately measured aggressiveness. Analysis of an independent data set generated by staging male-male interactions also supported the prediction that intermediate-sized males were most aggressive. We conclude that adaptive covariation between body size and aggressiveness explains some interindividual variation in aggressiveness.     

Stress and muscular dystrophy: a genetic screen for dystroglycan and dystrophin interactors in Drosophila identifies cellular stress response components

In Drosophila, like in humans, Dystrophin Glycoprotein Complex (DGC) deficiencies cause a life span shortening disease, associated with muscle dysfunction. We performed the first in vivo genetic interaction screen in ageing dystrophic muscles and identified genes that have not been shown before to have a role in the development of muscular dystrophy and interact with dystrophin and/or dystroglycan. Mutations in many of the found interacting genes cause age-dependent morphological and heat-induced physiological defects in muscles, suggesting their importance in the tissue. Majority of them is phylogenetically conserved and implicated in human disorders, mainly tumors and myopathies. Functionally they can be divided into three main categories: proteins involved in communication between muscle and neuron, and interestingly, in mechanical and cellular stress response pathways. Our data show that stress induces muscle degeneration and accelerates age-dependent muscular dystrophy. Dystrophic muscles are already compromised; and as a consequence they are less adaptive and more sensitive to energetic stress and to changes in the ambient temperature. However, only dystroglycan, but not dystrophin deficiency causes extreme myodegeneration induced by energetic stress suggesting that dystroglycan might be a component of the low-energy pathway and act as a transducer of energetic stress in normal and dystrophic muscles.     

The cost of sex: quantifying energetic investment in gamete production by males and females

The relative energetic investment in reproduction between the sexes forms the basis of sexual selection and life history theories in evolutionary biology. It is often assumed that males invest considerably less in gametes than females, but quantifying the energetic cost of gamete production in both sexes has remained a difficult challenge. For a broad diversity of species (invertebrates, reptiles, amphibians, fishes, birds, and mammals), we compared the cost of gamete production between the sexes in terms of the investment in gonad tissue and the rate of gamete biomass production. Investment in gonad biomass was nearly proportional to body mass in both sexes, but gamete biomass production rate was approximately two to four orders of magnitude higher in females. In both males and females, gamete biomass production rate increased with organism mass as a power law, much like individual metabolic rate. This suggests that whole-organism energetics may act as a primary constraint on gamete production among species. Residual variation in sperm production rate was positively correlated with relative testes size. Together, these results suggest that understanding the heterogeneity in rates of gamete production among species requires joint consideration of the effects of gonad mass and metabolism.     

Ovulatory shifts in human female ornamentation: near ovulation, women dress to impress

Humans differ from many other primates in the apparent absence of obvious advertisements of fertility within the ovulatory cycle. However, recent studies demonstrate increases in women's sexual motivation near ovulation, raising the question of whether human ovulation could be marked by observable changes in overt behavior. Using a sample of 30 partnered women photographed at high and low fertility cycle phases, we show that readily-observable behaviors - self-grooming and ornamentation through attractive choice of dress - increase during the fertile phase of the ovulatory cycle. At above-chance levels, 42 judges selected photographs of women in their fertile (59.5%) rather than luteal phase (40.5%) as "trying to look more attractive." Moreover, the closer women were to ovulation when photographed in the fertile window, the more frequently their fertile photograph was chosen. Although an emerging literature indicates a variety of changes in women across the cycle, the ornamentation effect is striking in both its magnitude and its status as an overt behavioral difference that can be easily observed by others. It may help explain the previously documented finding that men's mate retention efforts increase as their partners approach ovulation.     

Weather, not climate, defines distributions of vagile bird species

Background

Accurate predictions of species distributions are essential for climate change impact assessments. However the standard practice of using long-term climate averages to train species distribution models might mute important temporal patterns of species distribution. The benefit of using temporally explicit weather and distribution data has not been assessed. We hypothesized that short-term weather associated with the time a species was recorded should be superior to long-term climate measures for predicting distributions of mobile species.

Methodology

We tested our hypothesis by generating distribution models for 157 bird species found in Australian tropical savannas (ATS) using modelling algorithm Maxent. The variable weather of the ATS supports a bird assemblage with variable movement patterns and a high incidence of nomadism. We developed “weather” models by relating climatic variables (mean temperature, rainfall, rainfall seasonality and temperature seasonality) from the three month, six month and one year period preceding each bird record over a 58 year period (1950–2008). These weather models were compared against models built using long-term (30 year) averages of the same climatic variables.

Conclusions

Weather models consistently achieved higher model scores than climate models, particularly for wide-ranging, nomadic and desert species. Climate models predicted larger range areas for species, whereas weather models quantified fluctuations in habitat suitability across months, seasons and years. Models based on long-term climate averages over-estimate availability of suitable habitat and species'' climatic tolerances, masking species potential vulnerability to climate change. Our results demonstrate that dynamic approaches to distribution modelling, such as incorporating organism-appropriate temporal scales, improves understanding of species distributions.     

Osteoactivin promotes breast cancer metastasis to bone

The skeleton is a preferred site of metastasis in patients with disseminated breast cancer. We have used 4T1 mouse mammary carcinoma cells, which metastasize to bone from the mammary fat pads of immunocompetent mice, to identify novel genes involved in this process. In vivo selection of parental cells resulted in the isolation of independent, aggressively bone metastatic breast cancer populations with reduced metastasis to the lung. Gene expression profiling identified osteoactivin as a candidate that is highly and selectively expressed in aggressively bone metastatic breast cancer cells. These cells displayed enhanced migratory and invasive characteristics in vitro, the latter requiring sustained osteoactivin expression. Osteoactivin depletion in these cells, by small interfering RNA, also lead to a loss of matrix metalloproteinase-3 expression, whereas forced osteoactivin expression in parental 4T1 cells was sufficient to elevate matrix metalloproteinase-3 levels, suggesting that this matrix metalloproteinase may be an important mediator of osteoactivin function. Overexpression of osteoactivin in an independent, weakly bone metastatic breast cancer cell model significantly enhanced the formation of osteolytic bone metastases in vivo. Finally, high levels of osteoactivin expression in primary human breast cancers correlate with estrogen receptor-negative status and increasing tumor grade. Thus, we have identified osteoactivin as a protein that is expressed in aggressive human breast cancers and is capable of promoting breast cancer metastasis to bone.