Intrasexual competition and eating restriction in heterosexual and homosexual individuals

Restrictive eating attitudes and behaviors have been hypothesized to be related to processes of intrasexual competition. According to this perspective, within-sex competition for status serves the adaptive purpose of attracting mates. As such, status competition salience may lead to concerns of mating desirability. For heterosexual women and gay men, such concerns revolve around appearing youthful and, thus, thinner. Following this logic, we examined how exposure to high-status and competitive (but not thin or highly attractive) same-sex individuals would influence body image and eating attitudes in heterosexual and in gay/lesbian individuals. Results indicated that for heterosexuals, intrasexual competition cues led to greater body image dissatisfaction and more restrictive eating attitudes for women, but not for men. In contrast, for homosexual individuals, intrasexual competition cues led to worse body image and eating attitudes for gay men, but not for lesbian women. These findings support the idea that the ultimate explanation for eating disorders is related to intrasexual competition.     

Shared or Unshared Parental Care in Overwintering Brent Geese (Branta bernicla hrota)

We examine brood size effects on the behaviour of wintering parent and juvenile brent geese (Branta bernicla hrota) to test predictions of shared and unshared parental care models. The behaviour of both parents and offspring appear to be influenced by declining food availability over the winter. Parental vigilance increased with brood size and may be explained by vigilance having functions in addition to antipredator behaviour where the benefits are shared among the brood. There was no increase in parental aggression with brood size and this does not fit the prediction of shared care. Nevertheless, large families are able to monopolize better feeding areas compared with smaller families and large families static feed more but walk feed less than do small families, the former apparently being the preferred mode. The presence of additional young, rather than increasing the amount of parental aggression, seems to enhance the family's competitive ability. Because parents with large broods benefit from enhanced access to resources there is likely to be no additional significant cost in the parental care of larger broods (sensu Trivers 1972 ).     

SEXUAL SIZE DIMORPHISM AND REPRODUCTIVE INVESTMENT BY FEMALE SPIDERS: A COMPARATIVE ANALYSIS

We investigate the association between female reproductive investment, absolute size, and sexual size dimorphism in spiders to test the predictions of the fecundity-advantage hypothesis. The relationships between absolute size and sexual size dimorphism and aspects of female reproductive output are examined in comparative analyses using phylogenetically independent contrasts. We provide support for the idea that allometry for sexual dimorphism is the result of variation in female size more so than male size. Regression analyses suggest selection for increased fecundity in females. We argue that fecundity selection provides the only general explanation for the evolution of sexual size dimorphism in spiders.     

Analysis of the 5q31 33 locus shows an association between single nucleotide polymorphism variants in the IL-5 gene and symptomatic infection with the human blood fluke, Schistosoma japonicum

Genetic studies of human susceptibility to Schistosoma (blood fluke) infections have previously identified a genetic locus determining infection intensity with the African species, Schistosoma mansoni, in the 5q31-33 region of the human genome that is known to contain the Th2 immune response cluster, including the genes encoding the IL-4, IL-5, and IL-13 cytokines. These cytokines are key players in inflammatory immune responses and have previously been implicated in human susceptibility to infection with the Asian species, S. japonicum. In a nested case control study, we genotyped 30 HapMap tagging single nucleotide polymorphisms (SNPs) across these three genes in 159 individuals identified as putatively susceptible to reinfection with S. japonicum and in 133 putatively resistant individuals. A third group comprising 113 individuals demonstrating symptomatic infection was also included. The results provided no significant association at a global level between reinfection predisposition and any of the individual SNPs or haplotype blocks. However, two tagging SNPs in IL-5 demonstrated globally significant association with susceptibility to symptomatic infection. They were in strong linkage disequilibrium with each other and were found to belong to the same haplotype block that also provided a significant association after permutation testing. This haplotype was located in the 3'-untranslated region of IL-5, suggesting that variants in this region of IL-5 may modulate the immune response in these individuals with symptomatic infection.     

Expression of protein phosphatase 2A mutants and silencing of the regulatory B alpha subunit induce a selective loss of acetylated and detyrosinated microtubules

Carboxymethylation and phosphorylation of protein phosphatase 2A (PP2A) catalytic C subunit are evolutionary conserved mechanisms that critically control PP2A holoenzyme assembly and substrate specificity. Down-regulation of PP2A methylation and PP2A enzymes containing the B alpha regulatory subunit occur in Alzheimer's disease. In this study, we show that expressed wild-type and methylation- (L309 Delta) and phosphorylation- (T304D, T304A, Y307F, and Y307E) site mutants of PP2A C subunit differentially bind to B, B', and B'-type regulatory subunits in NIH 3T3 fibroblasts and neuro-2a (N2a) neuroblastoma cells. They also display distinct binding affinity for microtubules (MTs). Relative to controls, expression of the wild-type, T304A and Y307F C subunits in N2a cells promotes the accumulation of acetylated and detyrosinated MTs. However, expression of the Y307E, L309 Delta, and T304D mutants, which are impaired in their ability to associate with the B alpha subunit, induces their loss. Silencing of B alpha subunit in N2a and NIH 3T3 cells is sufficient to induce a similar breakdown of acetylated and detyrosinated MTs. It also confers increased sensitivity to nocodazole-induced MT depolymerization. Our findings suggest that changes in intracellular PP2A subunit composition can modulate MT dynamics. They support the hypothesis that reduced amounts of neuronal B alpha-containing PP2A heterotrimers contribute to MT destabilization in Alzheimer's disease.     

Genome partitioning of genetic variation for height from 11,214 sibling pairs

Height has been used for more than a century as a model by which to understand quantitative genetic variation in humans. We report that the entire genome appears to contribute to its additive genetic variance. We used genotypes and phenotypes of 11,214 sibling pairs from three countries to partition additive genetic variance across the genome. Using genome scans to estimate the proportion of the genomes of each chromosome from siblings that were identical by descent, we estimated the heritability of height contributed by each of the 22 autosomes and the X chromosome. We show that additive genetic variance is spread across multiple chromosomes and that at least six chromosomes (i.e., 3, 4, 8, 15, 17, and 18) are responsible for the observed variation. Indeed, the data are not inconsistent with a uniform spread of trait loci throughout the genome. Our estimate of the variance explained by a chromosome is correlated with the number of times suggestive or significant linkage with height has been reported for that chromosome. Variance due to dominance was not significant but was difficult to assess because of the high sampling correlation between additive and dominance components. Results were consistent with the absence of any large between-chromosome epistatic effects. Notwithstanding the proposed architecture of complex traits that involves widespread gene-gene and gene-environment interactions, our results suggest that variation in height in humans can be explained by many loci distributed over all autosomes, with an additive mode of gene action.