Low apoplastic water potentials can affect trees by decreasing the hydraulic conductivity of xylem due to embolism and by causing dehydration stress in living cells. Low apoplastic water potentials regularly occur in trees during summer and winter. These can either be caused by loss of water due to transpiration or by freezing due to the chemical properties of ice.
In this thesis the effects of low apoplastic water potential on trees were studied by causing low water potentials with three different methods: desiccation, freezing and by adjusting the osmotic concentration of xylem sap. Tree responses in this thesis were measured with stem diameter changes, leaf gas exchange, tree temperature and xylem water potential.
Living parenchyma cells are thought to have negligible effect on xylem diameter changes but this thesis shows that the role of parenchyma can, in fact, be much more significant. Evidence for the major role of parenchyma cells in the diameter changes of frozen xylem also supported the theory of extracellular freezing. Furthermore, mesophyll cells were shown to react to freezing with a rapid depression of photosynthesis.
It was also studied how a pressure increase in the xylem conduits, resulting from low water potentials, affects tree water relations during embolism formation and ice propagation. A gas burst was detected emerging from the tree stem during freezing. A decrease in the amount of gases in the xylem conduit can benefit trees in avoiding winter embolism. It was also experimentally confirmed that the formation of embolism in trees can temporarily even help relieve water stress due to the so called ´capacitive effect´. Low apoplastic water potential affects both the xylem and living cells in trees, and the interconnectedness of these responses are also shown in this thesis.