Abstract
Plants that remain active during winter are subject to freezing of living and nonliving tissues, including the vascular system. In living tissues, freezing can cause intracellular ice formation, which can kill the cells, or extracellular ice formation, which may protect the cells from damage. If extracellular freezing occurs, cellular dehydration becomes the main problem, although mechanical damage to cell membranes may also occur. Within the nonliving conduits of the xylem, freezing temperatures are likely to cause cavitation resulting in losses of xylem function, depending on the size of the conduits as well as the freezing temperature and tension in the xylem. Phloem transport is also limited by cold temperatures as sap becomes more viscous and as sink strength and rates of phloem unloading decline, slowing the bulk flow of phloem sap. To remain active in winter, therefore, plants must prevent intracellular freezing in their living tissues, including in the phloem system, and maintain some xylem function, even if the soil is frozen. Woody plants that become dormant during winter discard their most vulnerable living tissues, but still need to prevent intracellular freezing in stems and roots, and must be able to recover xylem and phloem function in the spring. The potentially lethal stresses caused by freezing and low temperatures and the strategies woody plants use to survive these stresses are the subject of this chapter. The chapter discusses the primary mechanisms plants use to control freezing dynamics and reduce freezing injury in living tissues, as well as the physiological transformations that take place during cold acclimation. It also focuses on the limitations to long distance transport in the xylem and phloem and how the vascular systems of woody plants have adapted.
Original language | English (US) |
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Title of host publication | Vascular Transport in Plants |
Publisher | Elsevier |
Pages | 401-424 |
Number of pages | 24 |
ISBN (Electronic) | 9780120884575 |
DOIs | |
State | Published - Jan 1 2005 |
Bibliographical note
Publisher Copyright:© 2005 Elsevier Inc. All rights reserved.