The Butterflies of Serengeti Nkwabi, Ally K; Metzger, Kristine L; Sinclair, Anthony R. E
Serengeti IV,
04/2015
Book Chapter
In savanna habitats the abundances of butterflies change with season, related to their food supply which is determined by rainfall. Consequently interannual abundances change markedly depending on ...wet or dry years. These data reflect general insect abundance for which data are much more difficult to obtain. In general we find that environmental variability has marked influences on the biodiversity of butterflies in the Serengeti ecosystem. Temporal fluctuations, both seasonally and interannually affect their abundance. Habitat heterogeneity enhances species richness considerably, but disturbances both natural and human-induced reduce this richness; grazing by wildebeest, burning, and agriculture all reduce richness. In particular, habitat modification through agriculture results in the loss of most of the restricted range species. Conservation, therefore, should be aware that the diversity of Serengeti is determined by the many different habitats that occur within it, and that too much disturbance could reduce such diversity.
Plant diversity within the Serengeti ecosystem is often overlooked. A logical focus is on broad factors such as climate, topographic heterogeneity and fire frequency. Subsequently, the issue of ...compositional stability through time and space and what factors may influence the turnover of species through time. The chapter concludes by comparing plant diversity in the savanna/grassland habitats of Serengeti to other, similar grassland and savanna systems around the world.
Cellular proliferation depends on refilling the tricarboxylic acid (TCA) cycle to support biomass production (anaplerosis). The two major anaplerotic pathways in cells are pyruvate conversion to ...oxaloacetate via pyruvate carboxylase (PC) and glutamine conversion to a-ketoglutarate. Cancers often show an organ-specific reliance on either pathway. However, it remains unknown whether they adapt their mode of anaplerosis when metastasizing to a distant organ. We measured PC-dependent anaplerosis in breast-cancer-derived lung metastases compared to their primary cancers using in vivo C-13 tracer analysis. We discovered that lung metastases have higher PC-dependent anaplerosis compared to primary breast cancers. Based on in vitro analysis and a mathematical model for the determination of compartment-specific metabolite concentrations, we found that mitochondrial pyruvate concentrations can promote PC-dependent anaplerosis via enzyme kinetics. In conclusion, we show that breast cancer cells proliferating as lung metastases activate PC-dependent anaplerosis in response to the lung microenvironment.
PDF