## 1 Introduction  
The genetic programs of organisms require robust mechanisms to maintain integrity of information carried in the base sequence of double stranded DNA (dsDNA). Surprisingly, the intrinsic stability of dsDNA in water is low and alone does not match the imperative to preserve its information-bearing sequence intact [1, 2, 3, 4]. In addition, the structure of dsDNA is readily compromised by products of cellular processes, such as reactive oxygen species, which can introduce nearly two dozen characterized nucleobase lesions [5]; as well, exogenous agents, such as UV radiation and environmentally-derived agents can react with and disrupt the structure of dsDNA [6]. It is estimated that each mammalian cell absorbs tens of thousands of damaging events each day [2]; since bacterial DNA inhabits a similar chemical environment, the rates for bacterial cells are anticipated to be similar. Left underdressed, constant decoration with lesions has the potential to disrupt replication and transcription, and, crucially, to corrupt information contained within dsDNA. To prevent this, bacterial and eukaryotic cells have evolved at least six distinct pathways to protect information in genomic DNA: direct reversal, base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), homologous recombination (HR) and nonhomologousend joining (NHEJ) [7]. Here, we review one of these pathways, bacterial NER; the other pathways have also been reviewed recently [6; 8; 9; 10; 11; 12; 13; 14; 15]. NER operates in two modes (Figure 1): (1) global-genome repair (GGR) characterized by general patrol and repair of lesions within the genome and (2) transcription-coupled repair (TCR), a specialized NER process that interfaces with RNA polymerase to repair lesions on the transcribed strand. During repair of damaged DNA, the two modes of NER, GGR and TCR, operate via several distinct stages: damage detection, damage verification, inc  
Figure 1: The nucleotide excision repair (NER) pathways. Nucleotide excision repair can occur via different sub-pathways. In global genome repair (GGR), the DNA damage is recognized by the UvrA\({}_{2}\)B\({}_{2}\) damage sensor. Transcription couple repair (TCR), which removes lesions form the DNA strand that is being transcribed, is mediated by the Mfd protein. Mfd binds to RNA polymerase (RNAP) that is stalled by the lesion, pushes it forward to expose the lesion and recruits the nucleotide excision repair (NER) machinery. Recently, an alternative pathway has been proposed for TCR that is dependent on UvrD. In this newly proposed sub-pathway, UvrD binds to the stalled RNAP in the presence of the transcription elongation factor NusA and ppGpp and induces backtracking to expose the lesion; this is followed by lesion recognition by NER proteins. All three sub-pathways culminate in the formation of UvrB\(\bullet\)DNA pre-incision complex, which commits the bound DNA for incision and subsequent repair. repair synthesis and ligation to restore the original DNA sequence; the main difference between the branches of NER centers on the initial detection of the lesion. In bacteria, the UvrA\({}_{2}\) protein dimer, alone or in complex with the UvrB protein (UvrA\({}_{2}\)B\({}_{2}\)), uses the energy of ATP binding and hydrolysis to search the genome for lesions [16; 17]. In the damage sensing complex, UvrA\({}_{2}\) dimer alone contacts DNA [18], as it discriminates native from damaged DNA. Several hypotheses have been advanced to explain mechanisms that underlie damage sensing, however, a great deal remains to be understood [19; 20; 21; 22]. Identification of a lesion and verification of the damage by UvrB trigger eviction of UvrA from the complex on DNA, with UvrB taking its place at the lesion to form the pre-incision complex [18]. The mechanisms associated with the handoff of damaged DNA from UvrA to UvrB, however, remain to be firmly established. UvrB subsequently recruits the UvrC endonuclease to form the incision complex. Within this complex, UvrC introduces two incisions.