SYMP 21-4 - Killing in the name of science: Changes in tree physiology during induced lethal drought and carbon starvation

Thursday, August 9, 2012: 2:35 PM
Portland Blrm 253, Oregon Convention Center
Henrik Hartmann1, S. E. Trumbore2 and Waldemar Ziegler2, (1)Biological Processes, Max Planck Institute for Biogeochemistry, Jena, QC, Germany, (2)Biogeochemical Processes, Max Planck Institute for Biogeochemistry, Jena, Germany
Background/Question/Methods

Global occurrences of forest dieback have been linked to drought and heat and this phenomenon is expected to increase with anticipated climatic change. However, there is no thorough understanding of drought-induced mortality mechanisms. Recent theoretical advances suggest interactive effects of hydraulic failure, carbon limitation and carbon translocation as causes of drought-induced tree mortality but there is still an imminent need for more data assimilation especially from studies that kill trees. In a series of combined field- and greenhouse experiments, we are currently investigating responses in tree physiology with respect to water transport, carbon assimilation and allocation, carbon metabolism and storage use, and whole-tree carbon balance under induced lethal drought and carbon starvation. Both treatments provoke a negative net carbon balance but the latter allows maintaining plant water potentials at adequate levels for carbon translocation. This approach thus facilitates the partitioning of drought effects on carbon metabolism and carbon transport. Treatments were carried out until tree death occurred and provide data for broadening our understanding of tree physiology under lethal drought.

Results/Conclusions

Experimental drought killed trees (young Norway spruce) within 3 months and caused a rapid decline in carbon assimilation. Although droughted trees maintained photosynthesis early in the morning and during mild cloudy days even during advanced drought, the sustained respirational demand soon forced trees into a negative carbon balance. Available carbon was deviated from growth to maintenance. Drought did not cause irreversible xylem cavitation but phloem functioning seemed impeded as 13Cδ signals in root NSC were uncoupled from needles/branches. The 13Cδ signature of root-respired CO2 indicated the use of stored carbon early during drought and root tissue NSC concentrations were very low at the end of the experiment. However, NSC concentrations in needles and branches increased in trees exposed to drying-rewetting cycles. This increase may be interpreted as a change in carbon allocation to promote osmoregulation. Taken together, our results indicate that drought-induced changes in carbon pools and allocation are not defined at the organism level but rather within functional units. Additional data from the greenhouse experiment will hopefully show whether maintenance of carbon pools in above-ground tissues was a purposed promotion of drought tolerance (osmoregulation) or resulted from reduced carbon translocation.