**3.1.1.1 DDB1 & DDB2**

In mammalian systems, damage detection in the GG-NER pathway involves UV-Damaged DNA Binding protein 1 and 2 (DDB1 and DDB2) followed by the XPC-HR23B-CEN2 complex. In humans DDB2 complements the *XPE* mutation and plays a role in recognition of the UV-induced lesion, while DDB1 is required for high affinity interaction of the DDB1- DDB2 complex (Groisman et al., 2003; Luijsterburg et al., 2007; Rapic-Otrin et al., 2002). *S. pombe* Ddb1 knockouts result in chromosomal segregation defects, UV sensitivity and slow S phase progression leading to defects in meiosis (Holmberg et al., 2005). DDB1 and DDB2 homologues have been identified in rice, where they are UV-induced in proliferating tissues (Ishibashi et al., 2003). *Arabidopsis thaliana* encodes two homologs of DDB1 – DDB1A and DDB1B. These proteins are 91% identical with redundant function. Although *ddb1b* null alleles appear lethal, a viable partial loss of function allele exhibits no developmental or UV sensitive phenotypes (Bernhardt et al., 2010; Schroeder et al., 2002). Overexpression of DDB1A in *Arabidopsis* confers enhanced UV resistance and *ddb1a* knockouts exhibit mild UV sensitivity (Al Khateeb & Schroeder, 2009; Molinier et al., 2008). *AtDDB2* encodes a 48 kDa nuclear localized protein with upregulated expression upon UV-induction. *AtDDB2* loss of function results in UV sensitivity while overexpression increases UV tolerance (Biedermann & Hellmann, 2010; Koga et al., 2006; Molinier et al., 2008).
