Ultraviolet-B Damage and Repair Mechanisms

DNA has a broad absorption peak between 235 and 315 nm and thus is photoactivated by UV. Since the effects of UV-B radiation on DNA affect all kinds of organisms, they have been particularly well studied. Several types of UV-triggered damage are known: strand breaks and cross-linking, as well as modifications of pyrimidine bases.

In plants, dimerisation of thymine—resulting in cyclobutane pyrimidine dimers (CPDs) and, to a smaller extent, in pyrimidinone dimers (known as 6-4 photoproducts)— is a common reaction to irradiation with UV-B. Less packaged DNA of mitochondria and probably also of chloroplasts is particularly sensitive. UV irradiation of yeast cells caused a 10% loss of nuclear DNA, but at the same time a 50-60% loss of mitochondrial DNA.

There are several mechanisms to repair such damage (for details, see biochemistry textbooks, e.g. Berg et al. (2015)), of which two are mentioned here: the DNA photolyase reaction, whichrequires blue light/UV-A; and light-independent reactions such as base excision and recombination. Repair usually takes only a few hours. Interestingly, UV-activated photolyases represent the evolutionary origin of the blue light receptor cryptochrome (Fig. 3.20). Strong UV stress leads directly to irreparable chromosome breakage and deletions resulting in the death of the organism. This is the basis for sterilisation of rooms and instruments with intense UV light.

Fig. 3.20. Cryptochromes are evolutionarily derived from ultraviolet (UV)-activated photolyases involved in DNA damage repair. Photolyases (type I: Escherichia coli; type II and 6-4 photolyase: Arabidopsis thaliana), their substrates and co-substrates. A blue-light-triggered intrinsic energy transfer from pteridine to reduced flavin adenine dinucleotide (FADH) leads to an energisation of the pyrimidine residues of the dimers (in a DNA strand) and to a rearrangement of the carbon bonds, resulting in the cleavage of the dimers and restoration of the original DNA helix. Structures of pterin (MTHF), deazaflavin (8-HDF) and the intermediate flavin radical (FADH^-). (Modified from Cashmore et al. (1999))

Irrespective of the repair mechanisms, DNA damage signalling involves a UV-damaged DNA-binding protein complex (UV-DDB complex), which recognises UV-induced DNA damage and recruits proteins of the nucleotide excision repair pathway. It also induces several other UV-B responses, such as the formation of protective pigments.

In addition to UV damage to DNA, photooxidation of UV-absorbing pigments is known: yellowing and complete bleaching of leaves of indoor plants after abrupt transfer to the open air are frequent phenomena. Here the protective effect of the chloroplast pigments (energy dissipation) on their protein environment can be seen. Photodestruction of the thylakoid pigments leads to a significant decline in the amount of ribulose-1,5-bisphosphate carboxylase/oxygenase (RubisCO).