Preferential DNA damage prevention by the E. coli AidB gene: A new mechanism for the protection of specific genes

Rippa, Valentina; Duilio, Angela; Pasquale, Pamela di; Amoresano, Angela; Landini, Paolo; Volkert, Michael R.

doi:10.1016/j.dnarep.2011.06.001

Cited by 21 publications

(36 citation statements)

References 35 publications

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“…AlkA is a glycosylase conserved from bacterium to human (Wyatt et al 1999;Hollis et al 2000). The exact functional role of AidB is still unknown (Rohankhedkar et al 2006;Bowles et al 2008;Rippa et al 2011).…”

Section: Direct Reversal Of Alkylation Damage By Alkyltransferasesmentioning

confidence: 99%

DNA Repair by Reversal of DNA Damage

2013

Cold Spring Harbor Perspectives in Biology

137

115

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Endogenous and exogenous factors constantly challenge cellular DNA, generating cytotoxic and/or mutagenic DNA adducts. As a result, organisms have evolved different mechanisms to defend against the deleterious effects of DNA damage. Among these diverse repair pathways, direct DNA-repair systems provide cells with simple yet efficient solutions to reverse covalent DNA adducts. In this review, we focus on recent advances in the field of direct DNA repair, namely, photolyase-, alkyltransferase-, and dioxygenase-mediated repair processes. We present specific examples to describe new findings of known enzymes and appealing discoveries of new proteins. At the end of this article, we also briefly discuss the influence of direct DNA repair on other fields of biology and its implication on the discovery of new biology. E ndogenous and environmental agents continuously threaten the genomic integrity of all living organisms. Replication of damaged DNA can lead to mutations that are tumorigenic, whereas DNA lesions that block replication or transcription can result in senescence and cell death. Therefore, cellular DNA must be promptly repaired. Well-known mechanisms include base-excision repair, nucleotide excision repair, mismatch repair, homologous recombination, and nonhomologous end joining. In addition, nature has also evolved several mechanisms in which the damage is directly reversed most often by a single repair protein without the incision of DNA backbone. Although such "direct repair" processes mediate the reversal of a relatively small set of DNA lesions, the simplicity and essentially error-free property of the direct reversal processes make them particularly attractive for a cell. Three major mechanisms of direct DNA repair have been identified to date: (i) photolyases reverse UV light-induced photolesions; (ii) O 6 -alkylguanine-DNA alkyltransferases (AGTs) reverse a set of O-alkylated DNA damage; and (iii) the AlkB family dioxygenases reverse N-alkylated base adducts (Fig. 1). This concise article intends to update knowledge since the publication of the second edition of DNA Repair and Mutagenesis (ASM) (Friedberg et al. 2006).

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Section: Direct Reversal Of Alkylation Damage By Alkyltransferasesmentioning

confidence: 99%

DNA Repair by Reversal of DNA Damage

2013

Cold Spring Harbor Perspectives in Biology

137

115

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“…AidB was characterized as a locus-specific detoxification protein (Rippa et al 2011; also see Rippa et al 2010). AidB protein binds, via the carboxy-terminal domain, to UP elements located at strong promoters, promoting efficient transcription of various genes including DNA repair and housekeeping genes.…”

Section: Dna Damage Responses In Prokaryotesmentioning

confidence: 99%

DNA Damage Responses in Prokaryotes: Regulating Gene Expression, Modulating Growth Patterns, and Manipulating Replication Forks

Kreuzer

2013

Cold Spring Harbor Perspectives in Biology

208

185

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Recent advances in the area of bacterial DNA damage responses are reviewed here. The SOS pathway is still the major paradigm of bacterial DNA damage response, and recent studies have clarified the mechanisms of SOS induction and key physiological roles of SOS including a very major role in genetic exchange and variation. When considering diverse bacteria, it is clear that SOS is not a uniform pathway with one purpose, but rather a platform that has evolved for differing functions in different bacteria. Relating in part to the SOS response, the field has uncovered multiple apparent cell-cycle checkpoints that assist cell survival after DNA damage and remarkable pathways that induce programmed cell death in bacteria. Bacterial DNA damage responses are also much broader than SOS, and several important examples of LexA-independent regulation will be reviewed. Finally, some recent advances that relate to the replication and repair of damaged DNA will be summarized. Since the publication of DNA Repair and Mutagenesis in 2006 (Friedberg et al. 2006), our understanding of bacterial DNA damage responses has progressed significantly. Some studies have refined known pathways and filled in important details, whereas other studies have uncovered surprising new pathways such as bacterial programmed cell death and a form of replicative repair that reconstitutes severely shattered genomes. This review will focus on these recent advances, with only limited discussion and citation to work that precedes the 2006 tome. THE SOS RESPONSEAs scientists have studied the SOS response in Escherichia coli and other bacteria over the last decade, our understanding of SOS has changed in unexpected ways and the pathway has been found integrated in diverse cellular processes. Our understanding of the mechanism of SOS induction has also advanced in recent years, including a view of induction at the single-cell level. A surprising finding is that the functions of the SOS pathway are not uniform between bacterial species, and so the view of SOS as

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“…Likewise, current research into the E. coli AidB protein (annotated in EcoCyc as an isovaleryl-CoA dehydrogenase - E.C.1.3.8.4 – and associated with the DEMs isovaleryl-CoA and methylcrotonyl-CoA) is uncovering a role in the protection from alkylating agents [22]. …”

Section: Resultsmentioning

confidence: 99%

Dead End Metabolites - Defining the Known Unknowns of the E. coli Metabolic Network

et al. 2013

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The EcoCyc database is an online scientific database which provides an integrated view of the metabolic and regulatory network of the bacterium Escherichia coli K-12 and facilitates computational exploration of this important model organism. We have analysed the occurrence of dead end metabolites within the database – these are metabolites which lack the requisite reactions (either metabolic or transport) that would account for their production or consumption within the metabolic network. 127 dead end metabolites were identified from the 995 compounds that are contained within the EcoCyc metabolic network. Their presence reflects either a deficit in our representation of the network or in our knowledge of E. coli metabolism. Extensive literature searches resulted in the addition of 38 transport reactions and 3 metabolic reactions to the database and led to an improved representation of the pathway for Vitamin B12 salvage. 39 dead end metabolites were identified as components of reactions that are not physiologically relevant to E. coli K-12 – these reactions are properties of purified enzymes in vitro that would not be expected to occur in vivo. Our analysis led to improvements in the software that underpins the database and to the program that finds dead end metabolites within EcoCyc. The remaining dead end metabolites in the EcoCyc database likely represent deficiencies in our knowledge of E. coli metabolism.

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Preferential DNA damage prevention by the E. coli AidB gene: A new mechanism for the protection of specific genes

Cited by 21 publications

References 35 publications

DNA Repair by Reversal of DNA Damage

DNA Repair by Reversal of DNA Damage

DNA Damage Responses in Prokaryotes: Regulating Gene Expression, Modulating Growth Patterns, and Manipulating Replication Forks

Dead End Metabolites - Defining the Known Unknowns of the E. coli Metabolic Network

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