Abstract

A process-based model integrating the effects of UV-B radiation through epidermis, cellular DNA, and its consequences to the leaf expansion was developed from key parameters in the published literature. Enhanced UV-B radiation-induced DNA damage significantly delayed cell division, resulting in significant reductions in leaf growth and development. Ambient UV-B radiation-induced DNA damage significantly reduced the leaf growth of species with high relative epidermal absorbance at longer wavelengths and average/low pyrimidine cyclobutane dimers (CPD) photorepair rates. Leaf expansion was highly dependent on the number of CPD present in the DNA, as a result of UV-B radiation dose, quantitative and qualitative absorptive properties of epidermal pigments, and repair mechanisms. Formation of pyrimidine-pyrimidone (6-4) photoproducts (6-4PP) has no effect on the leaf expansion. Repair mechanisms could not solely prevent the UV-B radiation interference with the cell division. Avoidance or effective shielding by increased or modified qualitative epidermal absorptance was required. Sustained increased UV-B radiation levels are more detrimental than short, high doses of UV-B radiation. The combination of low temperature and increased UV-B radiation was more significant in the level of UV-B radiation-induced damage than UV-B radiation alone. Slow-growing leaves were more affected by increased UV-B radiation than fast-growing leaves.

Highlights

  • Ultraviolet (UV) radiation has been a natural environmental stress factor for organisms since the pre-Cambrian era (Lowry et al 1980; Rettberg et al 1998; Cockell and Horneck 2001)

  • We were able to examine a variety of questions that were difficult to approach through experimental research, including the following: (1) Are long, sustained increased UV-B radiation levels more detrimental than short, high doses of UV-B radiation? (2) Are fast-growing leaves more adaptive than slow-growing leaves? (3) Are different relative absorption spectra of flavonoids and related phenolics compounds responsible for the observed physiology of the leaf? (4) How important is DNA repair in leaf development? and (5) Is there an interaction between temperature and UV-B radiation-induced effects?

  • In addition to model analysis simulations, the following scenarios were considered: increased UV-B radiation in combination with different epidermal absorption spectra and Cyclobutane pyrimidine dimer (CPD) repair rates; increased UV-B radiation dose concentrated spread over the leaf expansion period or concentrated in 1, 2, or 3 days; leaves growing in different periods of the growing season under increased UV-B radiation; leaves growing under three temperature regimes under increased UV-B radiation; and slow, medium, and fast-growing leaves under increased UV-B radiation regime

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Summary

Introduction

Ultraviolet (UV) radiation has been a natural environmental stress factor for organisms since the pre-Cambrian era (Lowry et al 1980; Rettberg et al 1998; Cockell and Horneck 2001). While the connection between UV-B radiation, induction of DNA damage, and cell cycle arrest or apoptosis seems clear (Britt 1996; Lo et al 2005; Weber 2005; De Lima-Bessa et al 2008), the mechanisms of UV-B radiation-induced reduced cell expansion rates are less understood (Hectors et al 2010). Our model simulated the leaf optical properties (reflectance, absorptance, and transmittance) under various levels of UV-B irradiation, the absorptance of epidermal secondary metabolites, the UV-B radiation targeting of signaling proteins and their photomorphogenic effects on cell expansion, the UV-B radiation induction of DNA injuries, their repair through UVA/PAR or ATP-catalyzed repair mechanisms, their consequences on leaf cell cycle, and leaf expansion (Fig. 1). Supplemental model calibration, optimization, and testing can be readily performed as more comprehensive experimental data become available

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