Abstract
In their life cycle, plants are exposed to various unfavorable environmental factors including ultraviolet (UV) radiation emitted by the Sun. UV-A and UV-B, which are partially absorbed by the ozone layer, reach the surface of the Earth causing harmful effects among the others on plant genetic material. The energy of UV light is sufficient to induce mutations in DNA. Some examples of DNA damage induced by UV are pyrimidine dimers, oxidized nucleotides as well as single and double-strand breaks. When exposed to light, plants can repair major UV-induced DNA lesions, i.e., pyrimidine dimers using photoreactivation. However, this highly efficient light-dependent DNA repair system is ineffective in dim light or at night. Moreover, it is helpless when it comes to the repair of DNA lesions other than pyrimidine dimers. In this review, we have focused on how plants cope with deleterious DNA damage that cannot be repaired by photoreactivation. The current understanding of light-independent mechanisms, classified as dark DNA repair, indispensable for the maintenance of plant genetic material integrity has been presented.
Highlights
Solar light is indispensable for life on Earth
The surface of the Earth is protected against UV irradiation by the ozone layer which is present in the upper part of the atmosphere
These proteins belong to different pathways which are responsible for the maintenance of genomic stability including NER, BER, MMR, NHEJ, HR and translesion synthesis (TLS)
Summary
The blue and red light absorbed by photosynthetic machinery serves as a source of energy used for biomass production. The exposure of living organisms to UV radiation leads to the formation of different types of DNA lesions (Figure 1). UV irradiation causes formation of pyrimidine dimers (a) that can be repaired. Alternatively,either pyrimidine dimers can beUV-A/blue bypassed during byexcision. Mismatches are repaired by MMR (mismatch (d), which leads to production of mismatched bases (e). UV-induced oxidative stress may lead to formation of 8-oxo-dG (g) that are repaired via BER repair) (f). UV-induced oxidative stress may lead to formation of 8-oxo-dG (g) that are repaired via (base excision repair). Arrows represent represent the mechanisms of dark repair, while photoreactivation is marked in blue. The mechanisms of dark repair, while photoreactivation is marked in blue
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