Abstract:
The form and function of biological systems are moulded by the action of ecological and evolutionary forces at different organisational scales. This thesis uses theoretical and empirical tools to investigate these processes in organismal and sub-organismal contexts, by looking at the biology of dispersal and cancer.
In the first section, we select laboratory populations of Drosophila melanogaster for higher dispersal under poor larval nutrition. We find that the evolutionary trajectory followed by such populations is very different from populations selected under standard larval nutrition, both in terms of the dispersal kernel shape and other traits associated with higher dispersal. This points to a qualitatively different dispersal “syndrome” that can respond to the nutritional context and we discuss the eco-evolutionary implications of such lability in the context of range expansion, population stability and climate change.
In the second section, we explore ecological processes in prostate cancer, which consists of three types of cells. All three cell types compete for one resource (oxygen), while two of the three compete for a second resource (testosterone). Modelling these interactions using a Lotka-Volterra based resource consumption framework, we show that coexistence between the three cell types is a function of both resource availability and utilisation efficiency. Since one of the three cell types is also drug-resistant, we use the same mathematical framework to identify chemotherapy regimes that exploit within-tumour resource competition to improve therapeutic efficacy. This ties in with an emerging “tumour ecology” perspective that could enable the use of intra-tumour heterogeneity towards better cancer management strategies. Finally, we investigate whether having more cells automatically entails a higher cancer risk. Empirically, the answer to this question varies depending on whether one is looking at larger organs, larger conspecifics, or larger species, but it is not clear what leads to such scale specificity. Using an agent-based model of how a cell compartment arises from a single cell, we investigate the ways in which developmental constraints interact with somatic evolution among cells to determine the scaling of cancer risk with cell number. Our results identify the conditions under which cancer risk could increase with having more cells, and importantly, those under which it cannot.
