Summary of the repair systems 

All cells contain systems that maintain the integrity of their DNA sequences in the face of damage or errors of replication and that  distinguish the DNA from sequences of a foreign source.
Repair systems can recognize mispaired, altered, or missing bases in DNA, as well as other structural distortions of the double helix. Excision repair systems cleave DNA near a site of damage, remove one strand, and synthesize a new sequence to replace the excised material. The uvr system provides the main excision repair pathway in E. coli. The mut and dam systems are involved in correcting mismatches generated by incorporation of incorrect bases during replication and function by preferentially removing the base on the strand of DNA that is not methylated at a dam target sequence.
Eukaryotic homologs of the E. coli MutS/L system are involved in repairing mismatches that result from replication slippage; mutations in this pathway are common in certain types of cancer.

Repair systems can be connected with transcription in both prokaryotes and eukaryotes. Eukaryotes have two major nucleotide excision repair pathways: one that repairs damage anywhere in the genome, and another that specializes in the repair to transcribed strands of DNA. Both pathways depend on subunits of the transcription factor TF_II H. Human diseases are caused by mutations in genes coding for nucleotide excision repair activities, including the TF_IIH subunits. They have homologs in the conserved RAD genes of yeast.
Recombination-repair systems retrieve information from a DNA duplex and use it to repair a sequence that has been damaged on both strands. The prokaryotic RecBC and RecF pathways both act prior to RecA, whose strand-transfer function is involved in all bacterial recombination. A major use of recombination-repair may be to recover from the situation created when a replication fork stalls. Genes in the RAD52 group are involved in homologous recombination in eukaryotes.
Nonhomologous end joining (NHEJ) is a general mechanism for repairing broken ends in eukaryotic DNA when homologous recombination is not possible. The Ku heterodimer brings the broken ends together so they can be ligated. Several human diseases are caused by mutations in enzymes of both the homologous recombination and nonhomologous end-joining
pathways.
All repair occurs in the context of chromatin. Histone modifications and chromatin-remodeling enzymes are required to facilitate repair, and histone chaperones are needed to reset chromatin structure after repair is completed.
RecA has the ability to induce the SOS response. RecA is activated by damaged DNA in an unknown manner. It triggers cleavage of the LexA repressor protein, thus releasing repression of many loci and inducing synthesis of the enzymes of both excision repair and recombination-repair pathways. Genes under LexA control possess an operator SOS box. RecA also directly activates some repair activities. Cleavage of repressors of lysogenic phages may induce the phages to enter the lytic cycle.