Plants have evolved through several mechanisms by which they protect themselves from the damaging effects of UV-B radiation (Table 14.3).
Table 14.3 Protective mechanisms against damage by UV-B radiation in plants. Adapted with permission from Prasad et al. (2003b)
• DNA repair: photo-reactivation enzymes (photolyase); excision repair by removing damaged part of DNA; bypass damaged DNA and fill gaps later from sister duplex.
• Increase reflectance to avoid entry of UV-B radiation through cuticle wax, leaf hairs, and trichomes.
• Increase absorption of UV-B radiation at epidermal cells by production of pigments, such as flavonoids, carotenoid, and anthocyanins.
• Production of antioxidant enzymes (e.g., superoxide dismutase, ascorbate peroxidase, glutathione reductase) and compounds (ascorbates, alpha-tocopherol, and polyamines) that protect against oxidative stress caused by UV-B exposure.
Plants have constantly been exposed to sunlight, including UV radiation before formation of the ozone layer. In the process of evolution, certain plants developed a tolerance to solar UV-B radiation that limits the amount of DNA damage they suffer. All cellular life-forms possess DNA repair enzymes that recognize chemically modified bases, including those formed because of UV radiation. Furthermore, cells have evolved through a variety of biochemical mechanisms to restore the integrity of the genetic material after DNA damage and thus retain its stability. These processes, called "DNA repair mechanisms," include photo-reactivation, excision repair (nucleotide and base excision repair), and post-replication repair. Photoreactivation mainly involves photolyase, an enzyme responsible for the direct splitting of cyclobutane pyrimidine dimers. Excision repair is done by nicking the damaged part of DNA, removing the bases in the damaged strand, and synthesis of the gap. In post-replication repair, DNA damage is bypassed during DNA replication and the resulting gaps are filled in later using the information from the sister duplex. Such DNA repair mechanisms are observed in both nuclear and chloroplast DNA. However, different plant species and varieties within a species vary in their ability to repair the damage caused by UV-B.
Plants are exposed to UV-B radiation as it passes through the epidermal layers to reach the sensitive sites. Therefore, the surface structure, physiology, and composition of the epidermal layer play an important role in protecting (shielding) cells from UV-B radiation. The important surface characteristics of the epidermal layer, which reduces penetration of UV-B radiation, include protective structures, such as trichomes and wax coating. These structures have the capacity to attenuate, absorb, and reflect UV-B radiation because of their optimal structure and presence of chemical compounds.
Studies have also shown that UV-B radiation leads to oxidative stress in plant systems as observed in many other abiotic (temperature and light) and biotic (insects and diseases) stress conditions. Therefore, as a result of UV-B exposure, plants increase production of flavonoids and antioxidant enzymes (e.g., superoxide dismutase, ascorbate peroxidase, and glutathione reductase) that provide defense against UV-B radiation. Other chemicals, such as alpha tocopherol (vitamin E), peroxidases, ascorbates, beta carotene, and polyamines, provide protective functions against UV-B damage.
Flavonoids are produced and mainly deposited in epidermal and mesophyll layers and leaf hairs. The presence and distribution of flavonoids at different locations can provide an efficient screen to UV-B radiation. Flavonoids are very effective in screening (absorbing) UV-B radiation and reducing damage to sensitive cell organs (i.e., DNA, chloroplasts, and mitochondria). In addition, anthocyanins and carotenoids could potentially screen UV radiation, particularly in flowers, and provide protection to pollen grains. These compounds attenuate the damaging solar UV-B radiation, but they transmit photosynthetically active radiation through the epidermis. Thus, these compounds do not directly influence photosynthesis and other physiological processes.
UV-B-mediated alterations in plant growth and yield are dependent upon species sensitivity and combined responses to other abiotic and biotic stresses (Teramura and Sullivan, 1994). The inconsistencies may be explained by either genotypic differences in UV-B sensitivity, different environmental conditions under which plants were grown, and/or the intensity of UV-B (Musil et al., 2002; Kakani et al., 2003 a). A bulk of these studies conducted in growth chambers, greenhouses, or the field use different types of exposure systems that may be responsible for interpreting the results as intraspecific differential sensitivity of crop species (Runeckles and Krupa, 1994).
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