spontaneous hydrolysis of the N-glycosidic bond, alkyl- ations, and damage by reactive oxygen or nitrogen species and lipid peroxidation products (9–13). Lesions are also caused by errors in DNA metabolic processes, including the formation of single- and double-strand breaks, the collapse of replication forks, and the introduc- tion of modiﬁed nucleic acid bases during DNA replica- tion. Counting all together, daily 1016–1018 repair events occur in a healthy adult man (1012 cells) (14). Despite the protection provided by these mechanisms some of the damage escapes repair, and in consequence leads to muta- tions, ageing and various diseases, including carcinogen- esis and neurodegeneration (15–19). DNA repair is a very complicated process, involving many factors. For instance to date, 168 genes that encode proteins involved in DNA repair have been identiﬁed in the human genome (18–20). They are involved in diverse processes, starting from detection of a damage site in the DNA, through several steps of en- zymatic transformation of the damaged DNA, to recom- bination and signaling to stop the cell cycle or initiate apoptosis. Another form of dealing with the DNA damage is lesion bypass, which facilitates continuation of replication even when irremovable modiﬁcations occur, but does not guarantee proper recreation of the original sequence and frequently leads to mutation generated by translesion synthesis (TLS) polymerases. The numerous chemical and structural transformations leading from damaged DNA to repaired DNA can be described as pathways, comprising series of reaction steps. Currently known DNA damage signaling (DDS), repair and damage tolerance pathways can be divided into eight categories: . DDS: induced in response to the DNA damage caused by some endogenous and environmental agents; . Direct reversal repair (DDR): directly restores the native nucleotide residue by removing the non-native chemical modiﬁcation; . Base-excision repair (BER): initiated by excision of modiﬁed base from the DNA. Depending on the length of DNA resynthesis, the pathway is subdivided into two sub-pathways: short-path (SP-BER) or long-path (LP-BER); . Nucleotide excision repair (NER): removes bulky damage from the DNA. The damage from the active strand of transcribed genes is removed by transcription coupled repair (TCR)–NER, while global genome repair (GGR)–NER removes damage present else- where in the genome; . Mismatch repair (MMR): postreplicational DNA repair that removes errors introduced during the rep- lication (misinserted nucleotides, small loops, inser- tions, deletions); . Homologous recombination repair (HRR): repair of DNA double-strand breaks using the homologous DNA strand as a template for resynthesis; . Non-homologous end joining repair (NHEJ): ligation of ends resulting from DNA double-strand breaks (including the more error-prone microhomology end joining (MMEJ) mechanism; Nucleic Acids Research, 2011, Vol. 39, Database issue D789 . Translesion synthesis (TLS): damage-tolerance pathway that employs specialized polymerases to replicate across lesions in order to ﬁnish replication despite DNA damage. Each of these pathways can be represented as a series of enzymatic transformations between different DNA struc- tures, catalyzed by a dedicated system of proteins. It must be emphasized that DNA repair pathways are connected to each other, i.e. they can share some steps and/or proteins involved (14). As a consequence, DNA repair proteins rarely work in isolation in the cell, and their activity is dependent on other components of DNA repair systems. Therefore, knowledge of both the entire DNA repair systems and their components is critical to our understanding of how cells controls and repairs the constantly occurring damage of their genomes. Many of the proteins involved in DNA repair are very well-described (including substrate speciﬁcity, kinetics, mechanisms of action and 3D structure in complex with the substrate and/or the product of its activity). Information about different factors involved in DNA repair is, however, scattered in the literature and thus far there has been no resource to organize information on DNA repair at the systems level. Moreover, there are still processes, for which an enzymatic activity is known or suspected to exist, but the genes/proteins/ enzymes proteins have not been characterized yet. As an example an enzyme that is capable of removing 5-hydroxymethyluridine, a product of thymine oxidation in human cells must exist, but to date has not been identiﬁed yet (21). We have developed the REPAIRtoire database as a single online resource to store and organize information about DNA repair at the systems level. The purpose of REPAIRtoire is to gather together information about all DNA repair systems and proteins from model organisms, and to facilitate the access to knowledge about correlation of human diseases with mutation in genes responsible for DNA integrity and stability as well as information about the toxic and mutagenic agents causing DNA damage. DATABASE CONTENT Based on a comprehensive literature survey, we have compiled the following data sets: . A list of DNA lesions linked to environmental muta- genic and cytotoxic agents; . DDS, repair and tolerance pathways comprising struc- tures of damaged DNAs and intermediates of the repair processes, connected by known transformations, usually reactions catalyzed by enzymes; . Proteins involved in the aforementioned transform- ation and . Information about diseases connected with defects in DNA repair proteins. All data items have been curated manually and whenever possible and reasonable, we provided references to the published experimental reports and/or to other databases.