Survival and SOS response induction in ultraviolet B irradiatedEscherichia colicells with defective repair mechanisms

Abstract

Purpose In this paper, the contribution of different genes involved in DNA repair for both survival and SOS induction in Escherichia coli mutants exposed to ultraviolet B radiation (UVB, [wavelength range 280-315 nm]) was evaluated. Materials and methods E. coli strains defective in uvrA, oxyR, recO, recN, recJ, exoX, recB, recD or xonA genes were used to determine cell survival. All strains also had the genetic sulA::lacZ fusion, which allowed for the quantification of SOS induction through the SOS Chromotest. Results Five gene products were particularly important for survival, as follows: UvrA > RecB > RecO > RecJ > XonA. Strains defective in uvrA and recJ genes showed elevated SOS induction compared with the wild type, which remained stable for up to 240 min after UVB-irradiation. In addition, E. coli strains carrying the recO or recN mutation showed no SOS induction. Conclusions The nucleotide excision and DNA recombination pathways were equally used to repair UVB-induced DNA damage in E. coli cells. The sulA gene was not turned off in strains defective in UvrA and RecJ. RecO protein was essential for processing DNA damage prior to SOS induction. In this study, the roles of DNA repair proteins and their contributions to the mechanisms that induce SOS genes in E. coli are proposed.

Transcriptomic analysis of the response of Pseudomonas fluorescens to epigallocatechin gallate by RNA-seq

“…The recO gene encodes a gap repair protein and is essential for processing DNA damage prior to SOS induction in E . coli [58]. Consistent with the present results, previous research has demonstrated that green tea polyphenols also induced two DNA repair-related genes, lexA and recN , in P .…”

Antigenotoxic Effect Against Ultraviolet Radiation‐induced DNA Damage of the Essential Oils from Lippia Species

“…Overall, the antigenotoxic and antioxidant activities of these compounds were not related, suggesting that an antioxidant mechanism was not involved in their antigenotoxicity. We have previously shown that E. coli strain defective for OxyR regulon exposure to UV was as sensitive as wild-type phenotype (59). This supports previous findings that indicate cyclobutane pyrimidine dimers (CPD) and 6-4-pyrimidine pyrimidone photoproducts (6-4PP), instead of oxidative DNA damage, as mainly responsible for the genotoxic effects caused by all types of UV radiation (60).…”

“…The PQ37 strain used the expression of β‐galactosidase to assay the functional transcription of the sulA gene, whose product is responsible for cellular division blocked in E. coli . Since photoproducts are an obstacle for E. coli chromosome replication, a postirradiation reduction of sulA gene expression in the presence of genoprotective compounds can be considered indicative of DNA photoproduct repair and cellular division recovery . Therefore, we assume that the antigenotoxic effect detected for Lippia EO against UV occurs by reducing photoproducts formation or stimulating their repair on the DNA molecule.…”

Photoprotective and Antigenotoxic Effects of the Flavonoids Apigenin, Naringenin and Pinocembrin

“…Since CPD are an obstacle for chromosome replication, compound antigenotoxicity detected with SOS chromotest could be linked to inhibition of CPD formation or photoproducts DNA repair with cell division restoration events . Our study used the E. coli PQ37 strain ( uvr A), which is defective for nucleotide excision repair and its sul A gene was not turned off after UV treatment . Therefore, CPD repair can be excluded as potential antigenotoxic mechanism.…”

“…This radiation controller continuously measured the irradiance, calculated the irradiation dose and switched the lamps after reaching the target dose. The UVB radiation dose used was 10 J m −2 , which induced SOS functions in E. coli PQ37 cells .…”