**3. Nucleotide excision repair**

Nucleotide excision repair (NER) is a light independent repair process involving a series of reactions: initial damaged DNA recognition, DNA unwinding, dual incision bracketing the lesion, repair synthesis and final ligation to seal the repaired site. NER initiates with specific sub-pathways for transcriptionally active (Transcription Coupled Repair (TC-NER)) or silent (Global Genomic Repair (GG-NER)) DNA. TC-NER and GG-NER exhibit different damage recognition strategies followed by a common repair pathway (Gillet & Scharer, 2006) (Fig. 2). Defects in human NER genes result in the photosensitive syndromes Xeroderma pigmentosum (XP) or Cockayne syndrome (CS). Eight genetic complementation groups for XP have been identified (XPA-G, V) as well as two for CS (CSA and CSB). While XP-V mutation uniquely results in defects in translesion synthesis, XP -A, -B, -D, -F, and -G mutation results in both TC-NER and GG-NER defects, while XP –C and -E mutation results in GG-NER defects only. CSA and CSB mutation results exclusively in TC-NER defects (Hoeijmakers, 2001; Svejstrup, 2002). Bioinformatic analysis of the plant NER protein machinery suggests the molecular mechanisms are largely but not entirely conserved with that of the extensively studied yeast *S. cerevisiae* and mammalian cells (Kimura & Sakaguchi, 2006; Kunz et al., 2005, 2006). NER in plants has been studied primarily in rice and *Arabidopsis* (Singh et al., 2010). Many *Arabidopsis* NER related genes were initially isolated by analysis of UV hypersensitive (*uvh*) and UV repair defective (*uvr*) mutants which were subsequently mapped to homologues of the human XP genes (Table 1).
