Ectotherm body size is positively correlated with latitude, giving rise to body size clines, found in different continents. Ectotherm body size also shows a developmental response to temperature, increasing at lower developmental temperatures. To investigate the effects of temperature in the evolution and plasticity of body size dines, I used two species of the genus Drosophila as model organisms. To investigate the cellular mechanism underlying the evolution of wing size clines the two newly established D. subobscura wing size clines in the Americas were compared with the ancestral European dine. Clinal differences in Europe and South America were due to changes in cell number, whereas clinal differences in North America are due to changes in cell area. These results suggest that the cellular mechanism underlying the establishment of wing size clines is contingent and not predictable. The genetic control of body size in the D. melanogaster South American body size cline was investigated by means of QTL mapping. The results found in South America were consistent with those previously found in Australia, and in both continents the inversion In(3R)P was associated QTL controlling wing area. Genes of the insulin signalling pathway, known to affect size, were characterized in their effects under different temperature and larval crowding regimes. The evolution of plasticity of body size traits was analysed using different thermal selection regimes. The phenotypic plasticity of wing size and its cellular components was examined by rearing flies, selected under fixed or variable thermal environments, at two different experimental temperatures. Plasticity of wing size did not vary among the different selection lines, however, plasticity of both cellular components of body size did. Costs and benefits of adaptation to cyclical thermal environments were assessed with larval competition assays and by assessing size when all lines were reared under cyclic thermal conditions.

Following Drosophila embryogenesis, the morphology of the central nervous system (CNS) becomes dramatically remodelled to reflect the different locomotive and sensory requirements of the adult relative to the larva. The late embryonic onset of segment-to-segment differences in the number and mitotic capacity of neural stem cell-like precursors (termed neuroblasts: NBs) is critical to this resculpting process. My studies address the roles of homeodomain and other transcription factors in regulating thoracic and abdominal-specific patterns of neurogenesis, focusing on one embryonic and one larval example. In the embryo, dividing NBs sequentially express a temporal series of transcription factors required to link birth-order to neuronal identity. The study of a group of neurons expressing the early NB-sublineage determinant Hunchback in a thorax-specific pattern (termed the THBs) was initiated. I developed a lineage- labelling method to show that the THB-producing NBs appear to undergo a delay in their sub-lineage transition from Hunchback-positive to negative status, relative to most other NBs. Importantly, gene skipping in the canonical transcription factor series is also observed. Genetic analysis reveals that this thorax-specific pattern of neurogenesis requires homothorax but surprisingly not the thoracic Hox genes. However, in the abdomen, the Hox genes Ultrabithorax and abdominalA are required to suppress the THB phenotype. In the larva, clonal analysis and CNS-specific mutants were used to test several candidate factors potentially regulating NB divisions. This approach identified critical roles for Polycomb group genes and the transcription factor Grainyhead (Grh). I find that Grh, previously implicated as the ultimate NB-sublineage determinant in the embryo, has a differential effect on larval neurogenesis in the thorax versus the abdomen. Individual grh NB lineages in the thorax are smaller than wild type and stop dividing prematurely whereas those in the abdomen are larger and divide for an abnormally long period. Underlying the latter effect is an inability to respond to the normal NB-apoptosis inducing burst of the Hox protein AbdominalA. Thus, these studies identify Grh as a context-factor for Hox function in the larval NBs, linking late but not early AbdominalA expression with NB-apoptosis.

Asymmetric localisation of mRNA transcripts to specific sites within the cytoplasm is a widely employed mechanism for targeting of proteins and generating cell polarity. The mechanism and function of mRNA localisation has been extensively studied in Drosophila melanogaster, where, for example, the Egalitarian/Bicaudal- D/dynein complex mediates transport of mRNA transcripts, towards microtubule minus-ends, during oogenesis and in syncytial blastoderm embryos. However, it is not known whether the Egalitarian/Bicaudal-D/dynein mRNA transport machinery is required to localise mRNAs in somatic cell types in the Drosophila embryo. In this thesis, I show that the Egalitarian/Bicaudal-D/dynein complex is active in embryonic epithelial cells and neuroblasts and mediates asymmetric localisation of inscuteable, wingless and crumbs, but not miranda, mRNA transcripts, indicating that this is a general mechanism for mRNA localisation in Drosophila. I provide preliminary evidence that y-Tubulin mediates asymmetric miranda localisation. I have also explored the role of mRNA localisation in protein targeting in epithelial cells and neuroblasts, and find that asymmetric localisation of inscuteable and wingless, but not crumbs, mRNA transcripts is required to enhance the targeting of their protein products. I find that asymmetric localisation of wingless mRNA and protein is not required to support Wingless function in the embryo, although, Inscuteable activity is significantly reduced when inscuteable mRNA localisation is disrupted, and neuroblasts display defects in apico-basal polarity and metaphase spindle length. In conclusion, mRNA localisation acts to enhance protein targeting and activity in somatic cell types in the Drosophila embryo.

D. melanogaster has Afrotropical origins, colonising Europe around 10-15 thousand years ago, where they faced the challenges of a variable, seasonal environment. Individuals able to predict oncoming unfavourable winter conditions were at a selective advantage. This may have led to the evolution of seasonal diapause, a physiological response allowing flies to overwinter. In this work I studied the adaptation of the D. melanogaster overwintering strategy to different environmental conditions. Several genes have been found to modulate diapause, and some of these are characterised by two (or more) alleles whose frequencies are distributed as latitudinal clines in North America and Australia. We have studied the geographical distribution of the allele frequencies of three genes (timeless, tim; couch potato, cpo and Insulin-like-Receptor, InR) in European natural populations of D. melanogaster. Overall, our results highlight a peculiar and complex situation in Europe, as compared to North America or Australia where significant and robust clines were found for cpo and InR. Interestingly, such geographical differences correlate with the phenotype: clines in diapause are robust in North America but extremely weak in Europe, perhaps reflecting different selective pressures and colonisation dynamics in the Old World.

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