A commonly held view in evolutionary biology is that new species form in response to environmental factors, such as habitat differences or barriers to individual movements that sever a population. We have developed a computer model, called EvoSpace, that illustrates how new species can emerge when a species range becomes very large compared with the dispersal distances of its individuals. This situation has been called isolation-by-distance because remote parts of the range can take different evolutionary paths even though there is no particular place where we would expect different populations to separate. When the extent of genetic difference between individuals is coupled with decreasing offspring viability (e.g., resulting from developmental problems), EvoSpace predicts that sharp spatial boundaries can emerge in arbitrary locations, separating subpopulations that occasionally persist long enough to become reproductively incompatible species. The model shows an inherent tendency toward spatial self-organization, in contrast with the traditional view of environmentally forced origins of new species. We think that isolation-by-distance is a common aspect of the evolutionary process and that spatial self-organization of gene pools may often facilitate the evolution of new species.
In amoebiasis, a human disease that is a serious health problem in many developing countries, efforts have been made to identify responsible factors for the tissue damage inflicted by the parasite Entamoeba histolytica. This amoeba lives in the lumen of the colon without causing damage to the intestinal mucosa, but under unknown circumstances becomes invasive, destroying the intestinal tissue. Bacteria in the intestinal flora have been proposed as inducers of higher amoebic virulence, but the causes or mechanisms responsible for the induction are still undetermined. Mixed intestinal infections with Entamoeba histolytica and enteropathogenic bacteria, showing exacerbated manifestations of disease, are common in endemic countries. We implemented an experimental system to study amoebic virulence in the presence of pathogenic bacteria and its consequences on epithelial cells. Results showed that amoebae that ingested enteropathogenic bacteria became more virulent, causing more damage to epithelial cells. Bacteria induced release of inflammatory proteins by the epithelial cells that attracted amoebae, facilitating amoebic contact to the epithelial cells and higher damage. Our results, although a first approach to this complex problem, provide insights into amoebic infections, as interplay with other pathogens apparently influences the intestinal environment, the behavior of cells involved and the manifestations of the disease.