Some aspects of the SOS response system--a critical survey.

Janion, Celina

doi:10.18388/abp.2001_3894

Cited by 80 publications

(35 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[ 13 ] Here, the cell fi lamentation may serve as part of the bacterium's defence strategies to counteract cytotoxicity originating from the undissolved ZnO solids, by halting DNA replication while repairing DNA defects to prevent transmission of the potentially deleterious mutations to daughter cells. [ 17,18 ] The current observations of cell fi lamentation are in agreement with earlier studies which found DNA damage in E. coli upon exposure to ZnO NPs. [ 19,20 ] We further observed that the SOS-fi lamentation response is however independent of cellular oxidative stress.…”

Section: Figuresupporting

confidence: 92%

Zinc Oxide Nanoparticles Induce Cell Filamentation in Escherichia coli

Gunawan

Teoh

ricardo

et al. 2013

Part & Part Syst Charact

View full text Add to dashboard Cite

Zinc oxide nanoparticles (ZnO NPs) induce morphological transformation of Escherichia coli from its native rod‐shape of ≈2–4 μm to filamentous cells of 20–40 μm in length. The transient response can only be observed at up to 3.5 h proliferation, beyond which the cytotoxic effect is neutralized and the rod‐shape is restored. The filamentation is part of the bacterium SOS response to the Trojan horse‐type internalization of undissolved ZnO solids. In the absence of ZnO solids, no cell filamentation can be observed from the leached soluble zinc fraction or dissolved zinc salt.

show abstract

Section: Figuresupporting

confidence: 92%

Zinc Oxide Nanoparticles Induce Cell Filamentation in Escherichia coli

Gunawan

Teoh

ricardo

et al. 2013

Part & Part Syst Charact

View full text Add to dashboard Cite

show abstract

“…The proofreading function is ensured by the e subunit of Pol III and is inactivated by the mutD5 mutation in dnaQ gene (Takano et al, 1986). Deprivation of the proofreading activity leads to a large increase in spontaneous mutations, chronic induction of SOS response (Nowosielska et al, 2004a;2004b;Janion et al, 2002), and expression of over 40 genes, among them polB, dinB, and umuDC, encoding repair polymerases Pol II, Pol IV, and Pol V, respectively (Friedberg et al, 1995;Tang et al, 1999;Janion, 2001). A common feature of the SOS-inducible DNA polymerases is their ability to replicate past a non-instructive lesion (Szekeres et al, 1996;Napolitano et al, 2000).…”

mentioning

confidence: 99%

Effect of SOS-induced Pol II, Pol IV, and Pol V DNA polymerases on UV-induced mutagenesis and MFD repair in Escherichia coli cells.

et al. 2005

View full text Add to dashboard Cite

Irradiation of organisms with UV light produces genotoxic and mutagenic lesions in DNA. Replication through these lesions (translesion DNA synthesis, TSL) in Escherichia coli requires polymerase V (Pol V) and polymerase III (Pol III) holoenzyme. However, some evidence indicates that in the absence of Pol V, and with Pol III inactivated in its proofreading activity by the mutD5 mutation, efficient TSL takes place. The aim of this work was to estimate the involvement of SOS-inducible DNA polymerases, Pol II, Pol IV and Pol V, in UV mutagenesis and in mutation frequency decline (MFD), a mechanism of repair of UV-induced damage to DNA under conditions of arrested protein synthesis. Using the argE3®Arg + reversion to prototrophy system in E. coli AB1157, we found that the umuDC-encoded Pol V is the only SOS-inducible polymerase required for UV mutagenesis, since in its absence the level of Arg + revertants is extremely low and independent of Pol II and/or Pol IV. The low level of UV-induced Arg+ revertants observed in the AB1157mutD5DumuDC strain indicates that under conditions of disturbed proofreading activity of Pol III and lack of Pol V, UV-induced lesions are bypassed without inducing mutations. The presented results also indicate that Pol V may provide substrates for MFD repair; moreover, we suggest that only those DNA lesions which result from umuDC-directed UV mutagenesis are subject to MFD repair. Irradiation of organisms with UV light produces lesions in DNA that stop replication. The two primary UV induced lesions in DNA are cis,syn-cyclobutane pyrimidine dimers Vol. 52 No. 1/2005 139-147 QUARTERLY . 50th Anniversary

show abstract

“…De-repression occurs when the RecA protein binds to single-stranded DNA at replication forks that are blocked by DNA damage, forming RecA-ssDNA nucleoprotein filaments (Courcelle and Hanawalt, 2003;Janion, 2008). Once bound to DNA, the RecA protein changes conformation and acts as a co-protease in the cleavage of LexA, thus allowing transcription of the SOS genes (Little, 1991;Janion, 2001;Giese et al, 2008). Among these are genes such as uvrA, recA, recN or umuDC, responsible for DNA repair, and others such as sulA, that couple DNA damage to cell division (D'Ari, 1985;Janion, 2001).…”

Section: Sensing Elementsmentioning

confidence: 99%

“…Once bound to DNA, the RecA protein changes conformation and acts as a co-protease in the cleavage of LexA, thus allowing transcription of the SOS genes (Little, 1991;Janion, 2001;Giese et al, 2008). Among these are genes such as uvrA, recA, recN or umuDC, responsible for DNA repair, and others such as sulA, that couple DNA damage to cell division (D'Ari, 1985;Janion, 2001). Expression of a given SOS gene depends on the specific LexA-binding properties of its promoter, determined by the sequence of the LexA-binding sites (SOS boxes), their number and their arrangement (Lewis et al, 1994;Fernández de Henestrosa et al, 2000;Norman et al, 2005).…”

Section: Sensing Elementsmentioning

confidence: 99%

Bacterial genotoxicity bioreporters

Biran

Yagur‐Kroll

Pedahzur

et al. 2010

Microbial Biotechnology

View full text Add to dashboard Cite

SummaryEver since the introduction of the Salmonella typhimurium mammalian microsome mutagenicity assay (the ‘Ames test’) over three decades ago, there has been a constant development of additional genotoxicity assays based upon the use of genetically engineered microorganisms. Such assays rely either on reversion principles similar to those of the Ames test, or on promoter–reporter fusions that generate a quantifiable dose‐dependent signal in the presence of potential DNA damaging compounds and the induction of repair mechanisms; the latter group is the subject of the present review. Some of these assays were only briefly described in the scientific literature, whereas others have been developed all the way to commercial products. Out of these, only one, the umu‐test, has been fully validated and ISO‐ and OECD standardized. Here we review the main directions undertaken in the construction and testing of bacterial‐based genotoxicity bioassays, including the attempts to incorporate at least a partial metabolic activation capacity into the molecular design. We list the genetic modifications introduced into the tester strains, compare the performance of the different assays, and briefly describe the first attempts to incorporate such bacterial reporters into actual genotoxicity testing devices.

show abstract

Some aspects of the SOS response system--a critical survey.

Cited by 80 publications

References 75 publications

Zinc Oxide Nanoparticles Induce Cell Filamentation in Escherichia coli

Zinc Oxide Nanoparticles Induce Cell Filamentation in Escherichia coli

Effect of SOS-induced Pol II, Pol IV, and Pol V DNA polymerases on UV-induced mutagenesis and MFD repair in Escherichia coli cells.

Bacterial genotoxicity bioreporters

Contact Info

Product

Resources

About