Abstract
Plants, growing naturally in the open field, despite their stationary habit that exposes them to uninterrupted atmospheric UV radiation with potential for causing extensive damage to life-forms, seldom exhibit UV-induced deleterious effect on growth and development. This apparent anomaly is explained by the fact that while UV at high intensity directly inflicts damaging effect on macromolecules, UV radiation at intermittently fluencing low dose (resulting from passage through oscillatory fluctuations in weather-related variation in aerosol/cloud cover), via photoreceptor-mediated signal transduction, epigenetically induces UV acclimation strategies in plants. Such mechanism constitutes prophylactic protection from UV radiation, providing the first line of defense. Such protective mechanism constitutes UV avoidance through UV-related upregulation in induction of internal UV screening compounds, viz., phenolics, particularly flavonoids. This is enabled by the unique plant-based feature of cellular plasticity, allowing molecular rearrangements that affect a trade-off between primary metabolism (for growth and development) and secondary metabolism for synthesis of flavonoids. Being deposited in epidermal cells, these compounds serve to restrain UV penetration into inner tissue. Due to structural specialization, flavonoids, in addition to providing internal UV screen, also provide antioxidative protection to (UV-induced or otherwise) ROS-mediated oxidative damage in cells. UV, at low dose, also upregulates antioxidative enzymes. Under cellular conditions that preclude enzymatic activity, nonenzymatic antioxidants, viz., flavonoids, may take charge: flavonoids, specifically synthesized in plants, may provide antioxidative protection in animal through dietary route. Plants avoid stress symptoms by taking to trait variation associated with UV acclimation. This is commonly evident as photomorphogenic effect such as inhibition of hypocotyl/stem extension. Such traits ensure protection of dividing cells of the emerging embryonic axis by avoiding UV exposure until cells of the embryonic axis may synthesize UV-protective compounds, viz., flavonoids, and also upregulation of CPD photolyase for repair of UV-induced DNA damage. While repair of DNA damage allows recovery, antioxidative protection allows retaliatory measures for countering UV damaging effect – both constituting part of UV acclimation strategy. Repair of DNA is also reported to occur under high-dose UV radiation; the induced damage is reinstated by homologous recombination. Species-based studies on UV acclimation mechanisms in plants elucidate an important role of the genetic complement in plants toward developing UV acclimation strategies.
Exemplary studies showcasing UV-induced damage and stimulated protection in two plant systems, (i) mature (dehydrated) rice seed during postharvest aging, collected from different locations, and (ii) young (new flush) tea leaf at different altitudes (within the same latitude), i.e., sites under different UV fluence, have also been included in this chapter.
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Sen Mandi, S. (2016). UV Acclimation Strategy in Plants. In: Natural UV Radiation in Enhancing Survival Value and Quality of Plants. Springer, New Delhi. https://doi.org/10.1007/978-81-322-2767-0_4
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