MechanisMs of the dna repair in bacterial and yeast cells

Malfunctioning of some dna repair pathways predisposes to certain types of cancer. impaired base excision repair, nucleotide excision repair, mismatch repair and recombination are implied in human tissues. these repair pathways are engaged very quickly in the cell when the external (chemical carcinogens) and internal (lipid peroxidation products) compounds react directly with dna. this reaction may either lead to different modifications (damages) in dna and genes. this damages may lead finally to mutation and cancer progression and induce different dna repair mechanisms such as. ber, ner, hr and MMr. in the ber mechanisms repair is initiated by the action of a damage-specific dna n-glycosylase that is responsible for the recognition and removal of an altered base through cleavage of the n-glycosylic bond and action of ap-endonuclease. nucleotide excision repair (ner) is the most versatile and flexible dna repair pathway of living cells as it deals with a wide range of structurally unrelated dna lesions. ner corrects a wide array of dna lesions that distort the dna double helix, interfere in base pairing and block dna duplication and transcription. the most common examples of these lesions are the cyclobutane pyrimidine dimers (cpds) and 6-4 photoproducts (6-4 pps) induced by ultraviolet radiation (UV) and bases with large substitutes derived from chemicals such as polycyclic aromatic hydrocarbons or exocyclic adducts. homologous recombination, utilize large regions of dna homology, usually the homological chromosome, to exchange damaged dna for the intact one. dna mismatch-repair system (MMr) is involved in the repair of mispaired bases formed during replication, genetic recombination and as a result of dna damage.