Disease relevance of SOS Response (Genetics)

• Induction of SOS functions: regulation of proteolytic activity of E. coli RecA protein by interaction with DNA and nucleoside triphosphate [1].
• From our results we conclude that antipain inhibits lambda prophage induction by blocking proteolytic inactivation of lambda repressor and that it inhibits the induction or expression of SOS repair and filamentous growth [2].
• Inactivation of transfecting molecules showed that one lethal hit corresponded to 1.5 to 2.1 thymine glycols per phage DNA in normal cells, whereas conditions of W-reactivation (SOS induction) reversed 60 to 80% of inactivating events [3].
• Induction of SOS response in Salmonella typhimurium TA4107/pSK1002 by peroxynitrite-generating agent, N-morpholino sydnonimine [4].
• Two lines of evidence suggest that a gene analogous to the recA gene of Escherichia coli exists in Vibrio cholerae and that its product serves a proteolytic function in the SOS response [5].

High impact information on SOS Response (Genetics)

• RecA is also a multifunctional protein, serving in different biochemical roles for recombinational processes, SOS induction, and mutagenic lesion bypass [6].
• Genetic analyses have shown that SOS induction in response to double-stranded DNA (dsDNA) breaks requires LexA repressor, and the RecA and RecBCD enzymes--proteins best known for their role as initiators of dsDNA break repair and homologous recombination [7].
• Chi is dispensable when cells are induced for the SOS response or contain a recD mutation. recBC sbcA mutant cells are also capable of RDR induction [8].
• During the SOS response, LexA repressor is inactivated by specific cleavage [9].
• RecA protein modified by tif mutations allows expression of SOS functions in the absence of inducing treatments [1].

Chemical compound and disease context of SOS Response (Genetics)

• This system is different from the error-prone 'SOS' repair system for DNA, known to be induced in E. coli by treatments which damage DNA and/or inhibit DNA replication, such as irradiation by far-UV (254 nm) light or X rays, thymine starvation or treatment with naladixic acid or mitomycin C [10].
• Each of these three groups will be considered in turn by focusing on the following systems: the Rec A-dependent intramolecular cleavage of the Escherichia coli SOS response protein, LexA; the intramolecular activation of the mammalian aspartic acid protease, pepsinogen; and the autocatalytic cleavage of polyproteins synthesized by picornaviruses [11].
• Recovery of respiration following the SOS response of Escherichia coli requires RecA-mediated induction of 2-keto-4-hydroxyglutarate aldolase [12].
• A model for the structure and expression of the colicin E1 operon is proposed in which the cea and lys genes are expressed from a single inducible promoter that is controlled by the lexA repressor in response to the SOS system of Escherichia coli [13].
• Two-thirds of the mutations in irradiated phage assayed in recA host cells (no induction of the SOS response) were G:C to A:T transitions; it is hypothesized that these may arise during DNA replication from adenine mispairing with a cytosine product deaminated by irradiation [14].

Biological context of SOS Response (Genetics)

• Minichromosomes (oriC plasmids) pOC23 and pOC81 were induced to replicate in the absence of DnaA protein and transcription after SOS induction [15].
• In this work, induction of the SOS response by the addition of mitomycin C was found to be prevented by overexpression of the dinI gene. dinI is an SOS gene which maps at 24.6 min of the E.coli chromosome and encodes a small protein of 81 amino acids [16].
• The induction by methylating agents of the SOS function sfiA was measured by means of a sfiA::lac operon fusion in Escherichia coli mutants defective in alkylation repair [17].
• The bacterial RecA protein plays a central role in the repair of stalled replication forks, double-strand break repair, general recombination, induction of the SOS response, and SOS mutagenesis [18].
• It is a colorimetric assay based on the induction by these agents of the SOS function sfiA, whose level of expression is monitored by means of a sfiA::lacZ operon fusion [19].

Anatomical context of SOS Response (Genetics)

• Antioxidant effects of hydroxybenzalacetones on peroxynitrite-induced lipid peroxidation in red blood cell membrane ghost and SOS response in Salmonella typhimurium TA4107/pSK1002 [20].
• The nucleotide sequence upstream of the Escherichia coli yebG gene presents features similar to those found in SOS system regulatory sites (putative SOS box, -10 and -35 promoter boxes and a ribosome binding site) [21].

Associations of SOS Response (Genetics) with chemical compounds

• 2-Keto-4-hydroxyglutarate aldolase also plays a role in respiratory metabolic pathways, which suggests a mechanism for respiration resumption during the termination of the SOS response [12].
• Induction of the SOS response causes an increase in TLS events through the AAF adduct (approximately 13%) [22].
• To test this hypothesis, we investigated the effect of a protease inhibitor, antipain [(1-carboxy-2-phenylethyl)carbamoyl-L-arginyl-L-valylargininal], on SOS induction [2].
• This high concentration of beta 2 may be responsible for the observation that very little (if any) bypass of pyrimidine photodimers occurred in vivo when the SOS system was not induced [23].
• When host cells were ultraviolet-irradiated to induce the SOS response, a slight increase (about 2-fold) in survival of transfecting f1-K12 DNA containing beta-ureidoisobutyric acid was observed [24].

Gene context of SOS Response (Genetics)

• It was not observed in lexA and recA mutants which abolish the induction of the SOS response [25].
• We found that a recA mutant that is defective in recombination but proficient in SOS induction could not elicit iSDR [26].
• We reported earlier that the SOS box of the neighbouring uvrA gene also controls the transcription of the ssb gene [27].
• These results indicate that the uvrD gene is induced during the SOS response, and that the expression of the gene may also be regulated by transcription attenuation [28].
• Moreover, despite the fact that both dinB and umuDC loci are controlled by the SOS response, their constitutive and induced levels of expression are dramatically different [29].

Analytical, diagnostic and therapeutic context of SOS Response (Genetics)

• On the basis of this sequence analysis, expression of the uvrD gene would be expected to increase after DNA damage or replication inhibition as part of the SOS response, as is reported in the preceding paper [Arthur and Eastlake, Gene 25 (1983) 309-316] [30].
• Production and crystallization of a selenomethionyl variant of UmuD', an Escherichia coli SOS response protein [31].
• Oxygen does not appear to be necessary in the activation of the SOS repair system by irradiation as tested with Escherichia coli since recA-deficient and recA-containing strains showed similar survival after treatment with UV and ionizing radiation in the presence or absence of oxygen [32].
• The BsoBI restriction endonuclease gene (bsoBIR) and part of the BsoBI methylase gene (bsoBIM) were cloned by the "endo-blue" method (SOS induction assay), and the remainder of bsoBIM was cloned by inverse PCR [33].

References