Abstract
Plant DNA is damaged by exposure to solar radiation, which includes ultraviolet (UV) rays. UV damaged DNA is repaired either by photolyases, using visible light energy, or by nucleotide excision repair (NER), also known as dark repair. NER consists of two subpathways: global genomic repair (GGR), which repairs untranscribed DNA throughout the genome, and transcription-coupled repair (TCR), which repairs transcribed DNA. In mammals, CSA, CSB, UVSSA, USP7, and TFIIS have been implicated in TCR. Arabidopsis homologs of CSA (AtCSA-1/2) and CSB (CHR8) have previously been shown to contribute to UV tolerance. Here we examine the role of Arabidopsis homologs of UVSSA, USP7 (UBP12/13), and TFIIS (RDO2) in UV tolerance. We find that loss of function alleles of UVSSA, UBP12, and RDO2 exhibit increased UV sensitivity in both seedlings and adults. UV sensitivity in atcsa-1, uvssa, and ubp12 mutants is specific to dark conditions, consistent with a role in NER. Interestingly, chr8 mutants exhibit UV sensitivity in both light and dark conditions, suggesting that the Arabidopsis CSB homolog may play a role in both NER and light repair. Overall our results indicate a conserved role for UVSSA, USP7 (UBP12), and TFIIS (RDO2) in TCR.
Highlights
IntroductionAn important and unavoidable component of a plant’s environment is solar radiation, which includes both beneficial visible light and damaging ultraviolet (UV) rays
Unable to move, plants must adapt to their surroundings
In this study we identify the Arabidopsis UV Stimulated Scaffold protein A (UVSSA) homolog and examine the roles of UVSSA, UBP12/13, and reduced dormancy 2 (RDO2) in UV tolerance
Summary
An important and unavoidable component of a plant’s environment is solar radiation, which includes both beneficial visible light and damaging ultraviolet (UV) rays. UV radiation harms a variety of cellular components including DNA. UV damaged DNA, primarily pyrimidine photodimers, is repaired by photolyases, using the energy from visible light (light repair), and by nucleotide excision repair (NER) (dark repair) (Pang and Hays, 1991; Molinier, 2017). Nucleotide excision repair is a conserved multistep pathway involving damage recognition, strand unwinding, excision, repair synthesis, and ligation. Damage recognition is via one of two NER sub-pathways. Global genomic repair (GGR) identifies UV damage in DNA throughout the genome, while transcription coupled repair (TCR) initiates repair of transcribed strands
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
