An environmental model of self-compatibility transitions in the solanaceae plant family

Higher level selection processes such as species selection are not generally predicted to overpower individual selection on character traits. Goldberg et al. provide a model derived from collected life history data and argue that species selection is maintaining self-incompatibility in the Solanaceae plant family. This model applies only on the level of the species, not representing the underlying interactions between individuals and the environment. We propose a new model with environmental variation at the individual level that may explain the maintenance and frequency of loss of this character trait. We use individual based modelling techniques to explore our hypothesis, and compare it with that originally proposed. The results show alternative values required for the mutation rate to produce the species level transition frequency under the opposing models, given certain assumptions. Future work is suggested to refine the parameter relationships, test for robustness, and determine if individual models of higher complexity will exhibit similar outcomes

Mediating exposure in public interactions

Mobile computing and public interactions together open up a new range of challenges in interaction design. To date a very gregarious model of interaction has been assumed. However, the public setting will invoke feelings of shyness and a desire to control the personal exposure associated with interactions. In this paper we discuss these issues and our initial tests of a system which affords a control beyond "engage or don't engage"

The evolution of group traits: modelling natural selection on trait prevalence within and between groups

One of evolution's greatest innovations was group living; indeed, it is fundamental to our daily lives as humans. Yet despite intense theoretical and empirical work, the details of how group living arose and is maintained are poorly understood. A central question in this area concerns the strength of natural selection operating between groups of organisms (group selection) because some think this is key to the evolution of group behaviour. It is, however, challenging to measure natural selection occurring between groups and between the individuals within those groups simultaneously. Consequently, a number of contentious theoretical issues have plagued group selection research for a number of decades, and empirical work on this topic is often misinterpreted. In this thesis, I investigate three biological systems that are candidates for group selection where empirical data is readily available. Using techniques from theoretical and computational biology - simulations, game theory and population genetics - I model evolution occurring at multiple levels simultaneously (multi-level selection), shedding light on the evolution and maintenance of group traits. First, I consider the evolution of a trait - lateralization - at the population- and colony-level in eusocial organisms, which have a reproductive structure that promotes group organisation and cooperation. I provide an evolutionary explanation for the strength of lateralization in colonies of the red wood ant, Formica rufa, as a compromise between intraspecific and predatory interactions. After extending the analysis to involve predators targeting multiple colonies simultaneously, I show that populations should tend towards an equal distribution of left- and right- lateralized colonies, resulting in zero population-level lateralization. This contradicts the established view that sociality should produce strong levels of lateralization at the population level. Second, I study a sub-social spider, Anelosimus studiosus, which is a group-living species that has recently been claimed to exhibit group-level adaptation. I use evolutionary game theory to explain the evolution of colony aggression with individual costs and benefits, providing an alternative to the existing group-level interpretation. The model generates a striking fit to the data without any between-group interactions. Therefore, I conclude that more evidence is needed to infer group-level adaptation in this colonial spider. Third, I study the Solanaceae, a plant family whose breeding system is reported to have undergone species selection - group selection acting on whole species. I investigate the evolution of self-fertilization over the family's phylogenetic history. By integrating an existing phylogeny with models of breeding system evolution at the individual level, I find the average selection pressure - and attendant properties of populations - expected to have characterised the Solanaceae over ~36 million years. In conclusion, I have shown the power of modelling approaches to clarify evolutionary explanations, to question existing interpretations, and to identify experiments that can help researchers identify the true causes of trait evolution

The evolution of handedness: why are ant colonies left- and right-handed?

No description supplie

Identification of Intracellular and Plasma Membrane Calcium Channel Homologues in Pathogenic Parasites

Ca2+ channels regulate many crucial processes within cells and their abnormal activity can be damaging to cell survival, suggesting that they might represent attractive therapeutic targets in pathogenic organisms. Parasitic diseases such as malaria, leishmaniasis, trypanosomiasis and schistosomiasis are responsible for millions of deaths each year worldwide. The genomes of many pathogenic parasites have recently been sequenced, opening the way for rational design of targeted therapies. We analyzed genomes of pathogenic protozoan parasites as well as the genome of Schistosoma mansoni, and show the existence within them of genes encoding homologues of mammalian intracellular Ca2+ release channels: inositol 1,4,5-trisphosphate receptors (IP3Rs), ryanodine receptors (RyRs), two-pore Ca2+ channels (TPCs) and intracellular transient receptor potential (Trp) channels. The genomes of Trypanosoma, Leishmania and S. mansoni parasites encode IP3R/RyR and Trp channel homologues, and that of S. mansoni additionally encodes a TPC homologue. In contrast, apicomplexan parasites lack genes encoding IP3R/RyR homologues and possess only genes encoding TPC and Trp channel homologues (Toxoplasma gondii) or Trp channel homologues alone. The genomes of parasites also encode homologues of mammalian Ca2+ influx channels, including voltage-gated Ca2+ channels and plasma membrane Trp channels. The genome of S. mansoni also encodes Orai Ca2+ channel and STIM Ca2+ sensor homologues, suggesting that store-operated Ca2+ entry may occur in this parasite. Many anti-parasitic agents alter parasite Ca2+ homeostasis and some are known modulators of mammalian Ca2+ channels, suggesting that parasite Ca2+ channel homologues might be the targets of some current anti-parasitic drugs. Differences between human and parasite Ca2+ channels suggest that pathogen-specific targeting of these channels may be an attractive therapeutic prospect

Critical Role for CD38-mediated Ca2+ Signaling in Thrombin-induced Procoagulant Activity of Mouse Platelets and Hemostasis*

CD38, a multifunctional enzyme that catalyzes the synthesis of intracellular Ca2+ messengers, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP), is known to be expressed on platelets. However, the role of CD38 in platelets remains unclear. Our present results show that treatment of platelets with thrombin results in a rapid and sustained Ca2+ signal, resulting from a coordinated interplay of Ca2+-mobilizing messengers, inositol 1,4,5-trisphosphate, cADPR, and NAADP. By dissecting the signaling pathway using various agents, we delineated that cADPR and NAADP are sequentially produced through CD38 internalization by protein kinase C via myosin heavy chain IIA following phospholipase C activation in thrombin-induced platelets. An inositol 1,4,5-trisphosphate receptor antagonist blocked the thrombin-induced formation of cADPR and NAADP as well as Ca2+ signals. An indispensable response of platelets relying on cytosolic calcium is the surface exposure of phosphatidylserine (PS), which implicates platelet procoagulant activity. Scrutinizing this parameter reveals that CD38+/+ platelets fully express PS on the surface when stimulated with thrombin, whereas this response was decreased on CD38−/− platelets. Similarly, PS exposure and Ca2+ signals were attenuated when platelets were incubated with 8-bromo-cADPR, bafilomycin A1, and a PKC inhibitor. Furthermore, in vivo, CD38-deficient mice exhibited longer bleeding times and unstable formation of thrombus than wild type mice. These results demonstrate that CD38 plays an essential role in thrombin-induced procoagulant activity of platelets and hemostasis via Ca2+ signaling mediated by its products, cADPR and NAADP