The following article will guide you about how plants cope with high temperature. The four ways are: 1. Acclimation to High Temperature 2. Membrane Composition 3. Morphological Adaptations and 4. Heat-Shock Proteins.
Way # 1. Acclimation to High Temperature:
Brief exposure of plants to sub-lethal temperatures may increase their thermo-.tolerance. Light and other factors may cause an increase in tolerance to heat, but plant’s acclimation to higher temperatures is minimal (a few degrees only) as compared to other stresses such as freezing and drought. For example, soybean seedlings exposed to 2 hours at 40°C can subsequently survive an otherwise lethal 2 hours exposure at 45°C. Although, some changes occurring during acclimation to heat stress are reversible, but if the stress is too severe, irreversible changes may occur which may prove to be lethal.
Way # 2. Membrane Composition:
In high-temperature tolerant species such as agave and cacti, there is greater proportion of saturated fatty acids (with higher melting points) in their membrane lipids. This enables such plants to maintain fluidity and stability of their membranes at higher temperatures.
Way # 3. Morphological Adaptations:
Plants avoid intense solar radiations and overheating in the same way as in drought resistance by developing morphological adaptations that include:
(i) More vertical orientation of leaves,
(ii) Rolling their leaves along the axis (as in grasses),
(iii) Reflective leaf hairs,
(iv) Waxy leaf surfaces and
(v) Smaller deeply dissected leaves to minimise the boundary layer thickness and thus maximise heat loss by convection and conduction.
Way # 4. Heat-Shock Proteins (HSPs):
Although, in response to heart-shock stress or heat stress, synthesis of most of the normal proteins is suppressed, but the plants produce a unique set of low molecular mass proteins which are known as heat-shock proteins (HSPs). Most of the HSPs function to help cells endure heat stress by acting as molecular chaperones protecting essential enzymes and nucleic acids from heat denaturation and mis-folding. They also prevent dis-assembly of multimeric aggregates during heat stress.
Heat-shock proteins were originally discovered in fruit fly (Drosophila melanogaster), but they have since been discovered in variety of animals including man, plants, fungi and micro-organisms. HSPs are synthesized in cells very rapidly in response to heat-shock. For example, when soybean seedlings are suddenly exposed from 25°C to 40°C (i.e., just below the lethal temperature), new m-RNA transcripts can be detected within 3-5 minutes and bulk of newly synthesized HSPs within 30 minutes. With the return of normal temperature, HSPs are no longer produced and the pattern of protein synthesis also returns to normal. (Transcription of HSPs m-RNAs is believed to be mediated by a specific heat shock factors or HSF).
The molecular mass of HSPs ranges from 15-114 kDa. Based on their size, five major classes of HSPs are found in plants. Different HSPs are localized in cell in cytosol, ER, mitochondria, chloroplasts and nucleus. Ubiquitin, an 8 kDa protein found in all eukaryotes is also a HSP that is involved in targeting other proteins for prototeolytic degradation. Major classes of HSPs in plants, their probable function and localization in cell are given in table 23.1.
Although HSPs in plants were first observed in response to heat shock treatment that hardly occurs in nature, HSPs are also produced in response to gradual rise in higher temperature in paints under field conditions. HSPs have also been observed in normal unstressed cells, but their concentrations do not increase in response to heat stress.
(The induction of HSPs is not limited to heat stress alone. Other stresses such as ABA treatment, water deficit, wounding, low temperature and salinity also result in new set of proteins called stress proteins. Although some stress proteins may be similar to HSPs and may gain cross protection against another stress, but there is no universal set of stress proteins).