I have tried to grow a tropical plant like Tamarind and mango in various parts of Texas where ever I was working. unless you keep them inside the house during the winter and protect them from freezing all of them will die if they are left out in the open during the winter. but curiously a number of other plants which are native to this region somehow miraculously survive after shedding their leaves during autumn and surviving through the bitter winter totally leafless almost looking like they are dead. and once spring arrives there is a burst of buds, fruits and leaves.
So what is special about Apple and Peach trees when compared to mangoes and Tamarind?
“plant detects the change in temperature, rather than the absolute temperature”
I always wondered what kind of time sensor temperature sensor these plants possess?
today, while I was reading about a parasite trichinella, spiralis
the author wrote “ Larvae can survive for up to a month in a dead animal at low temperatures. Animals that hibernate have a natural antifreeze molecule to help them survive the cold winters, “
So let us look at two wonderful things which I did not know about till now.
winter hardening and antifreeze proteins
Plants in temperate and polar regions adapt to winter and sub zero temperatures by relocating nutrients from leaves and shoots to storage organs Freezing temperatures induce dehydrative stress on plants, as water absorption in the root and water transport in the plant decreases Water in and between cells in the plant freezes and expands, causing tissue damage. Cold hardening is a process in which a plant undergoes physiological changes to avoid or mitigate cellular injuries caused by sub-zero temperatures. Non-acclimatized individuals can survive −5 °C, while an acclimatized individual in the same species can survive −30°. Plants that originated in the tropics, like tomato or maize, don't go through cold hardening and are unable to survive freezing temperatures.The plant starts the adaptation by exposure to cold yet still not freezing temperatures. The process can be divided into three steps. First the plant perceives low temperature, then converts the signal to activate or repress expression of appropriate genes. Finally, it uses these genes to combat the stress, caused by sub-zero temperatures, affecting its living cells. Many of the genes and responses to low-temperature stress are shared with other abiotic stresses, like drought or salinity.
When temperature drops, the membrane fluidity, RNA and DNA stability, and enzyme activity change. These, in turn, affect transcription, translation, intermediate metabolism, and photosynthesis, leading to an energy imbalance. This energy imbalance is thought to be one of the ways the plant detects low temperature. Experiments on Arabidopsis show that the plant detects the change in temperature, rather than the absolute temperature. The rate of temperature drop is directly connected to the magnitude of calcium influx, from the space between cells, into the cell. Calcium channels in the cell membrane detect the temperature drop and promotes expression of low-temperature responsible genes in alfalfa and arabidopsis. The response to the change in calcium elevation depends on the cell type and stress history. Shoot tissue will respond more than root cells, and a cell that already is adapted to cold stress will respond more than one that has not been through cold hardening before. Light doesn't control the onset of cold hardening directly, but the shortening of daylight is associated with fall and starts production of reactive oxygen species and excitation of photosystem 2, which influences low-temp signal transduction mechanisms. Plants with a compromised perception of day length have compromised cold acclimation.
Cold increases cell membrane permeability and makes the cell shrink, as water is drawn out when ice is formed in the extracellular matrix between cells.] To retain the surface area of the cell membrane so it will be able to regain its former volume when temperature rises again, the plant forms more and stronger Hechtian strands. These are tubelike structures that connect the protoplast with the cell wall. When the intracellular water freezes, the cell will expand, and without cold hardening the cell would rupture. To protect the cell membrane from expansion induced damage, the plant cell changes the proportions of almost all lipids in the cell membrane, and increases the amount of total soluble protein and other cryoprotecting molecules, like sugar and proline.
Chilling injury occurs at 0–10 degrees Celsius, as a result of membrane damage, metabolic changes, and toxic buildup. Symptoms include wilting, water soaking, necrosis, chlorosis, ion leakage, and decreased growth. Freezing injury may occur at temperatures below 0 degrees Celsius. Symptoms of extracellular freezing include structural damage, dehydration, and necrosis. If intracellular freezing occurs, it will lead to death. Freezing injury is a result of lost permeability, plasmolysis, and post-thaw cell bursting.
When spring comes, or during a mild spell in winter, plants de-harden, and if the temperature is warm for long enough – their growth resumes.
When temperature drops, the membrane fluidity, RNA and DNA stability, and enzyme activity change. These, in turn, affect transcription, translation, intermediate metabolism, and photosynthesis, leading to an energy imbalance. This energy imbalance is thought to be one of the ways the plant detects low temperature. Experiments on Arabidopsis show that the plant detects the change in temperature, rather than the absolute temperature. The rate of temperature drop is directly connected to the magnitude of calcium influx, from the space between cells, into the cell. Calcium channels in the cell membrane detect the temperature drop and promotes expression of low-temperature responsible genes in alfalfa and arabidopsis. The response to the change in calcium elevation depends on the cell type and stress history. Shoot tissue will respond more than root cells, and a cell that already is adapted to cold stress will respond more than one that has not been through cold hardening before. Light doesn't control the onset of cold hardening directly, but the shortening of daylight is associated with fall and starts production of reactive oxygen species and excitation of photosystem 2, which influences low-temp signal transduction mechanisms. Plants with a compromised perception of day length have compromised cold acclimation.
Cold increases cell membrane permeability and makes the cell shrink, as water is drawn out when ice is formed in the extracellular matrix between cells.] To retain the surface area of the cell membrane so it will be able to regain its former volume when temperature rises again, the plant forms more and stronger Hechtian strands. These are tubelike structures that connect the protoplast with the cell wall. When the intracellular water freezes, the cell will expand, and without cold hardening the cell would rupture. To protect the cell membrane from expansion induced damage, the plant cell changes the proportions of almost all lipids in the cell membrane, and increases the amount of total soluble protein and other cryoprotecting molecules, like sugar and proline.
Chilling injury occurs at 0–10 degrees Celsius, as a result of membrane damage, metabolic changes, and toxic buildup. Symptoms include wilting, water soaking, necrosis, chlorosis, ion leakage, and decreased growth. Freezing injury may occur at temperatures below 0 degrees Celsius. Symptoms of extracellular freezing include structural damage, dehydration, and necrosis. If intracellular freezing occurs, it will lead to death. Freezing injury is a result of lost permeability, plasmolysis, and post-thaw cell bursting.
When spring comes, or during a mild spell in winter, plants de-harden, and if the temperature is warm for long enough – their growth resumes.
Molecule of the Month
Antifreeze Proteins
Small antifreeze proteins protect cells from damage by ice
Antifreeze protein from the cold-water ocean pout, with the ice-binding portion in lighter blue.
Download high quality TIFF image
Ice is a big problem for organisms that live in cold climates. Once the temperature dips below freezing, ice crystals steadily grow and burst cells. This danger, however, has not limited the spread of life on Earth to temperate regions. Organisms of all types--plants, animals, fungi and bacteria--have developed ways to combat the deadly growth of ice crystals. In some cases, they pack their cells with small antifreeze compounds like sugars or glycerol. But in cases where extra help is needed, cells make specialized antifreeze proteins to protect themselves as the temperature drops.
Nice Ice
Antifreeze proteins don't stop the growth of ice crystals, but they limit the growth to manageable sizes. For this reason, they are also known as ice-restructuring proteins. This is necessary because of an unusual property of ice called recrystallization. When water begins to freeze, many small crystals form, but then a few small crystals dominate and grow larger and larger, stealing water molecules from the surrounding small crystals. Antifreeze proteins counteract this recrystallization effect. They bind to the surface of the small ice crystals and slow or prevent the growth into larger dangerous crystals.
Supercooling
Antifreeze proteins lower the freezing point of water by a few degrees, but surprisingly, they don't change the melting point. This process of depressing the freezing point while not effecting the melting point is termed thermal hysteresis. The most effective antifreeze proteins are made by insects, which lower the freezing point by about 6 degrees. However, antifreeze proteins, even the ones from plants and bacteria that have smaller effects on freezing point, are useful in another way. They are placed outside cells where they control the size of ice crystals and prevent catastrophic ice crystal formation when the temperature drops below the (lowered) freezing point.
Icy Ice Cream
Antifreeze proteins have been useful in industry. For instance, natural antifreeze proteins purified from cold-water ocean pout (shown here from PDB entry 1kdf ) have been used as a preservative in ice cream. They coat the fine ice crystals that give ice cream its smooth texture, and prevent it from recrystallizing during storage and delivery into chunky, icy ice cream. Researchers are also experimenting with antifreeze proteins as a way to preserve tissues and organs that are stored at low temperatures, reducing the possible damage from ice crystals.
Several different antifreeze proteins, with the ice-binding portions in lighter blue.
Download high quality TIFF image
Many Solutions to the Same Problem
Antifreeze proteins are a perfect example of convergent evolution. Looking at the proteins used by different organisms, we see that many different proteins have been selected to serve this same function. Several examples are included here. All of these are small proteins with a flat surface that is rich in threonine (colored lighter blue here), which binds to the surface of ice crystals. These include two proteins from fish, the ocean pout (1kdf ) and the winter flounder (1wfb ), and three very active proteins from insects, the yellow mealworm beetle (1ezg ), the spruce budworm moth (1eww ), and the
Antifreeze proteins are examples of convergent evolution. Can you find other examples in the PDB where two entirely different proteins perform the same function?
The insect antifreeze proteins are examples of solenoidal folds, where the protein chain loops around like a spring. Compare the way the chain is folded in the beetle and moth proteins with the entirely different type of looping fold in the snow flea protein. Can you find other examples of solenoidal folds in the PDB
References
S. Venkatesh and C. Dayananda (2008) Properties, potentials, and prospects of antifreeze proteins. Critical Reviews in Biotechnology 28, 57-82.
A. Regand and H. D. Goff (2006) Ice recrystallization inhibition in ice cream as affected by ice restructuring proteins from winter wheat grass. Journal of Dairy Science 89, 49-57.
Z. Jia and P. L. Davies (2002) Antifreeze proteins: an unusual receptor-ligand interaction. Trends in Biochemical Sciences 27, 101-106.
Some Beautiful photographs of Trichinella spiralis
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