Plant tolerance mechanisms to DNA-damaging UV stress

Due to their sessile lifestyle, plants are continuously exposed to the UV component of sunlight, which threatens their genome stability. Although the Earth's ozone layer prevents a significant portion of the DNA-damaging UV radiation from reaching the surface, it still causes the formation of pyrimidine dimers in the genome that hinder transcription and DNA replication, and also causes the generation of reactive oxygen species (ROS), leading to oxidative DNA damage. To mitigate these effects, plants have evolved an elaborate, multilayered defense system to ensure genome stability under UV stress. Plants contain UV-shielding molecules that function as natural sunscreens to attenuate penetration into deeper tissues, and they also utilize the photoreactivation pathway, in which photolyase enzymes specifically recognize and repair pyrimidine dimers in a manner that is dependent on blue light. They perform light-independent nucleotide excision repairs that excise the pyrimidine dimer-containing oligonucleotides through dual incisions, followed by repair synthesis and ligation. They also maintain DNA replication under UV stress with the aid of translesion synthesis polymerases, which bypass damaged bases. Moreover, to sustain genome stability, DNA damage caused by UV-generated ROS and replication stress is eliminated through base excision repair, which corrects oxidative damage, as well as through pathways for double-strand-break repair, including classical non-homologous end joining, homologous recombination, alternative end joining, and single-strand annealing. Here we provide an overview of the molecular mechanisms that underlie plant UV tolerance. A deeper understanding of these pathways is essential for developing strategies to develop UV-resilient crop varieties.