Freeze Injury: How it Occurs and What to do about It.
With the first Arctic blast hitting the eastern part of the United States this weekend, I thought it might be a good time to look at freeze injury (a component of winter injury) is some detail. Freeze tolerance of plants is not constitutive, but induced in response to low, nonfreezing temperatures (< 50 F) during the fall or early winter. This process is known as cold acclimation. It explains why a plant species growing at a warm temperature that is exposed to freezing is killed, while that same plant exposed to a cold acclimation prior to sub zero temperatures survives.
Fall management practices influence the cold acclimation process. For example, if you are trying to promote turf growth through the fall by covering greens, it might be advisable during late fall to expose these greens to cool temperatures below 50° F but above 32° F. This will allow your turf to cold acclimate, or sometimes referred to as hardening off.
Freeze injury is a potential problem on warm season turfgrasses like bermudagrass and seashore paspalum and cool season turfgrasses primarily annual bluegrass and ryegrass - along their northern range of adaptation. Freeze tolerance or conversely injury is due in large part to how the turfgrass plant reacts to cell dehydration. Once temperatures fall before freezing water begins to freeze intercellularly causing a decrease in water potential outside the cell. Unfrozen water within the cell moves down this gradient out of the cell toward the ice crystals in the intercellular spaces. Literally dehydration is occurring to the cell. The colder the temperatures the more water travels down the gradient toward the frozen water. At 14° F, 90% of the osmotically active water will move out of the cell into intercellular spaces (Thomashow, 1998).
The freezing point is believed to be higher intercellularly than intracellulary, which is a good thing because intracellularly freezing is fatal. As water leaves the cell, the plasma membrane (syn. plasmalemma) contract and pull away from the cell wall. With the arrival of warm temperatures the ice present intercellularly melts and the water flows back into the cell where hydration takes place. If no damage has occurred to the plasma membrane (punctured, ruptured) then the cell is alive and well. However, if the cell rehydrates and damage has occurred to the plasma membrane cell death is eminent.
The most prevalent type of freeze injury that occurs on golf courses in the United States occurs at relatively high freezing temperatures 25° to 28° F during late winter/early spring. This type of freeze injury is sometimes described as “expansion-induced lysis” because it occurs during freeze/thaw cycles. The expansion/contraction of the plasma membrane in plants that have broken cold acclimation can lead to death. Ice rapidly forming or rapid collapse of the plasma membrane can result in ruptures in the membrane. Excessive water around the crown of the plant during these freeze/thaw cycles in late winter increases the severity of the damage.
A second type of freeze injury that occurs at lower temperatures involves changes in the plasma membrane. Where expansion-induced lysis is a result of mechanical damage, at temperatures below 25° F and more likely around 14° F loss of cell responsiveness occurs because of membrane changes. The plasma membrane becomes more rigid, and loses its ability to be pliable through structural or phase changes (Gordon-Kamm and Steponkus, 1984). Technically, the plasma membrane undergoes a phase transition from lamellar-to- hexagonalII. Actually it is this work (Gordon-Kamm and Steponkus, 1984) that demonstrated that freeze-induced phase transitions are a consequence of dehydration rather than subzero temperatures per se. The severity of dehydration increases however with decreasing temperature.
Freeze resistance is comprised of two components – freeze tolerance and freeze avoidance. Freeze tolerance is the plant’s response to the freeze temperature. Without a doubt the singular most important tolerance mechanism of plants is plasma membrane stabilization through cold acclimation. Where plasma membranes from nonacclimated plants suffer expansion-induced lysis and phase transition, membranes from cold acclimated plants do not (Thomashow, 1998).
Turfgrass investigations that looked at plasma mebrane bilayer constituents found that cold tolerance of cultivars of both bermudagrass and seashore paspalum involved fatty acids. The presence of unsaturated fatty acids like linolenic acid tend to be associated with lower freeze tolerance than those cultivars with proportionally higher saturated fatty acids (Cyril et al., 2002).
Freeze avoidance is where the plant is present, but not exposed to the freeze. For example, if the air temperature is sub zero but the turf is covered with snow, the plants crown or stems are not “feeling” the sub zero temperatures. The temperature under the snow cover is considerably warmer.
Turf managers have some control of increasing the likelihood of winter survival by:
* Raising the mowing height on warm season turfgrasses during the fall. This will provide more some protection to the growing point during freezing temperatures.
* Provide drainage for removal of water from excessively wet areas. During freeze/thaw cycles the presence of excessive moisture can enhance freeze injury.
* Reduce thatch. A significant thatch layer results in the plant’s growing point to lose contact with the soil as it “rises” into the thatch layer. This will expose the plant more readily to freezing temperatures.
* Potassium fertilization. On warm season turfgrasses potassium is often applied for increasing the chances of winter survival. Potassium is an ion that helps lower the osmotic potential of the cell decreasing water the potential for water flow from the cell.
* Reduce the likelihood of excessive growth going into the winter. Overstimulation of growth promotes succulent high water content cells that are more likely to encounter freeze injury.
* Minimize shading. Although not fully researched, a degree of correlation has occurred with freeze injury and degree of shading. Shading may contribute to increased freeze injury due to plant cells tend to be 1) more succulent in shade and have larger intercellular spaces, 2) lower carbohydrate levels, which may influence water potential, as well as the energy requirements of the turf and 4) shaded areas tend to be wetter, which may contribute to the severity of freeze/thaw cycles in late winter.
Cyril, J., G.L. Powell, R.R. Duncan, and W.V. Baird. 2002. Changes in membrane polar lipid fatty acids of seashore paspalum in response to low temperature exposure. Crop Science 42:2031-2037.
Gordon-Kamm, W.J. and P.L. Steponkus. 1984. Lamellar-to hexagonalII phase transitions in the plasma membrane of isolated protoplasts after freeze-induced dehydration. Proceeding of the National Academy of Science 81:6373-6377.
Thomashow, M.F. 1998. Role of cold-responsive genes in plant freezing tolerance. Plant Physiology 118:1-8.
About the author
Dr. Karl Danneberger is a professor of Turfgrass Science at The Ohio State University. Dr. Danneberger's contact information can be found here. You may also follow Dr. Danneberger on Twitter: