WHY DOES DROUGHT KILL TREES? INTERACTIONS BETWEEN WATER, CARBON, AND FUNGAL SYMBIONTS

One of the global causes of forest die-off is climate-change induced drought. Drought kills trees by reducing water supply and non-structural carbohydrate (NSC) availability and by increasing susceptibility to negative biotic interactions. However, we lack an understanding of how water, NSC, and biotic agents interact. As a result, we still cannot accurately predict drought-induced mortality. The overarching goal of my dissertation is to increase our understanding of the interacting mechanisms leading to drought-induced mortality (DIM) and to identify physiological variables that accurately predict risk of DIM. Via greenhouse experiments with Pinus ponderosa (ponderosa pine) seedlings, I addressed three overarching research questions: (1) which physiological variables are good predictors of DIM?, (2) What is the role of NSC on plant water relations and DIM?, and (3) Do fungal symbionts affect plant water relations by altering host NSC during periods of carbon deficit? I first show that plant water content integrates the negative effects of reduced water supply and NSC availability under drought and it accurately predicts DIM risk. Further, plant water content shows a threshold at which DIM risk increases. I also provide evidence that plants use NSC to retain water in living tissues and maintain plant water content above critical mortality thresholds. Next, I show that plant water content is a good predictor of DIM risk across populations of ponderosa pine despite differences in morphology, physiology, and drought strategies. The integrative nature of plant water content is relevant because it can be detected remotely, which may allow large-scale assessments of mortality risk. Lastly, I show that fungal symbionts connecting multiple plant hosts can become parasitic and deplete NSC in some hosts. Such a depletion impairs plant water relations, which could increase host vulnerability to drought. My dissertation provides insight on physiological mechanisms leading to DIM and identifies simple physiological variables useful for monitoring DIM risk