| Popis: |
Dietary restriction (DR), the limitation of calories or a particular nutrient intake without malnutrition, extends lifespan and delays ageing across a range of taxa. To understand this response better and therefore its importance in the ageing process, it is important to understand the evolutionary basis of this response and its generality across environments. Several evolutionary hypotheses about why DR increases lifespan have been proposed, and one in particular suggests DR individuals are frailer and only live longer than non-DR individuals under benign laboratory conditions. Dietary macronutrients have been found to alter infection outcomes, potentially due to altered immune responses and changes in the rate of clearing of pathogen (resistance), or other effects of diet on host-parasite interactions including the ability to withstand a given pathogen load (disease tolerance). Individuals in other host-pathogen systems have been found to alter their diet choice as a result of infection. Adult DR responses and response to infection may also be altered by juvenile environmental conditions, as juvenile diets have been shown to have important effects for multiple adult life-history traits. To understand the interactions between DR, injury and infection stress, and juvenile and adult environments, here I ask the following questions using the Drosophila melanogaster - Pseudomonas entomophila host-pathogen system, and diets differing in the ratio of macronutrients (protein to carbohydrate ratios, P:C): (i) Do additional stresses of injury and infection remove the lifespan benefit of DR, and are some diets better for D. melanogaster survival post-infection with Pseudomonas entomophila? (ii) Does larval dietary macronutrient manipulation affect adult life-history traits and survival post-infection? (iii) Do infected D. melanogaster individuals have altered diet preference post-infection with P. entomophila? and (iv) Does diet affect host resistance or disease tolerance with P. entomophila infection? By addressing these questions, I hope to improve our understanding of the evolutionary basis of the DR response and its generality across environments. In chapter 2, I show that the benefits of DR response remain even with injury and infection stress, where with decreasing P:C, survival increases and the rate of ageing decreases, as does reproduction. Low P:C diets are particularly bad for survival post-infection with P. entomophila, and injury stress has no additional effect on survival in comparison to the control group. In chapter 3, I show that intermediate to high larval P:C increases measures of larval development and increases adult reproduction, however larval P:C does not alter adult lifespan or infection outcomes. In chapter 4, I show that short-term diet preference does not change with injury or P. entomophila infection. In chapter 5, I show that although higher P:C increases post-infection survival with P. entomophila, this may not due to increased resistance, as bacterial loads and a measure of the immune response to P. entomophila, AMP gene expression, are similar across two P:C diets. These data suggest a potential role of increased disease tolerance on the higher P:C diet with P. entomophila, requiring further study. Taken together, these data suggest that the response to DR, achieved through lowering P:C ratio, is relatively unaffected by the additional stresses of infection and injury; that adult, not juvenile, dietary macronutrient manipulation alters infection outcomes; and that this may be independent of changes in bacterial clearance. This suggests that the most likely evolutionary explanation for the DR response is that it is an adaptive shift in relative investment in life-history traits that is consistent across environments, particularly exposure to infection and injury. Furthermore, these results provide further evidence of differential effects of P:C depending on the host-pathogen pair, requiring further study to understand these complex interactions across systems. |
