Integration and scaling of UV‐B radiation effects on plants: from DNA to leaf

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.