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PubMed1983

recA protein promoted DNA strand exchange.

recA protein and circular single-stranded DNA form a stable complex in the presence of single-stranded DNA binding protein (SSB), in which one recA protein monomer is bound per two nucleotides of DNA. These complexes are kinetically significant intermediates in the exchange of strands between the single-stranded DNA and an homologous linear duplex. After completion of strand exchange, the recA protein remains tightly associated with the circular duplex product of the reaction and the SSB is bound to the displaced linear single strand. Upon addition of ADP, the recA protein-duplex DNA complex dissociates. RecA protein also interacts with single-stranded DNA in the absence of SSB; however, the amount of recA protein bound is substantially reduced. These findings provide direct physical evidence for the participation of SSB in the formation of the recA protein-single-stranded DNA complexes inferred earlier from kinetic analysis. Moreover, they confirm the ability of recA protein to equilibrate between bound and free forms in the absence of SSB.

Adenosine Diphosphate↗

PubMedDate not supplied

[Enzymatic mechanisms of degradation of DNA replication forks in vitro].

The present work provides experimental evidence of two ways of fermentative degradation of DNA replication forks in vivo. The first way proceeds under the influence of exonuclease V, which degradates DNA replication forks, uncovered by singlestrand binding (ssb) proteins. DNA replication forks protected against nucleases by ssb protein are degrated by a second way: by tandem action of DNA polymerase II with ssb protein complexes and exonuclease V. The default of normal ssb protein in cells of Escherichia coli is responsible for the first way of DNA replication forks degradation. The second way is occurs at excess of normal ssb protein.

Bacterial Proteins↗

PubMed1982

Detection of DNA single-strand breaks produced during the repair of damage by DNA-protein cross-linking agents.

In this investigation, the combination of 1-beta-D-arabinofuranosylcytosine and hydroxyurea was used to inhibit the polymerase step of DNA excision repair. The DNA single-strand breaks (SSB), which accumulated in the presence of these agents, were measured by alkaline elution. With this approach, DNA SSB were detected in normal human fibroblasts after exposure to trans-platinum(II)diamminedichloride, formaldehyde, or potassium chromate. These agents all share the common feature that they induce DNA-protein cross-links in mammalian cells. In the case of trans-platinum(II)diamminedichloride or formaldehyde, the frequency of these SSB was markedly less in excision-deficient xeroderma pigmentosum cells. With chromate, a high level of SSB was induced in both normal and xeroderma pigmentosum cells; these results indicate that chromate damage to DNA is repaired by a mechanism different than the classical excision pathway since xeroderma pigmentosum cells responded normally. Several other agents were investigated with this approach, and no SSB were detected with nickel sulfate, 12-O-tetradecanoylphorbol-13-acetate or asbestos fibers in the presence of the polymerase inhibitor. This approach was found to be a very sensitive method to detect DNA excision repair.

Cells, Cultured↗

PubMed1978

Effects of hyperthermia and drug in cultured mammalian cells.

Hyperthermia (42 degrees C) and peptichemio (PTC) applied simultaneously result in an increased killing effect and in a significant induction of single strand breaks (SSB) of DNA molecule. The enhanced killing effect was observed in all circumstances, whenever hyperthermia was applied before, during or after PTC treatment, but the most effective cell killing was obtained when hyperthermia and PTC were applied simultaneously. The results show that PTC concentrations used in these experiments do not induce SSB in DNA molecule during incubation for 2 hours at 37 degrees C. When the cells were exposed to PTC and hyperthermia the induction of SSB was observed. The number of SSB depends on the exposure time and PTC concentration. Cells with a greater number of SSB lost the capacity for repair during post-incubation at 42 degrees C.

Cell Survival↗

PubMed1993

Dual topoisomerase I and II inhibition by intoplicine (RP-60475), a new antitumor agent in early clinical trials.

The mechanisms of action of intoplicine (RP-60475), a 7H-benzo[e]pyrido[4,3-b]indole derivative that is presently in early clinical trials, have been investigated. Intoplicine induced both topoisomerase I- and II-mediated DNA strand breaks, using purified topoisomerases. The topoisomerase cleavage site patterns induced by intoplicine were unique, relative to those of camptothecin, 4'-(9-acridinylamino)methanesulfon-m-anisidide (m-AMSA), and other known topoisomerase inhibitors. Both topoisomerase I- and II-induced DNA breaks decreased at drug concentrations higher than 1 microM, which is consistent with the DNA-intercalating activity of intoplicine. DNA damage was investigated in KB cells in culture by using alkaline elution. Intoplicine induced single-strand breaks (SSB) in a bell-shaped manner with respect to drug concentration (maximum frequency at 1 microM approximately 220 rad-equivalents). SSB formation was fast, whereas reversal after drug removal was slow. Similar bell-shaped curves were obtained for DNA double-strand breaks (DSB) and DNA-protein cross-links. SSB and DNA-protein cross-link frequencies were approximately equal, and no protein-free breaks were detectable, indicating the protein concealment of the breaks, as expected for topoisomerase inhibition. Comparison of SSB and DSB frequencies indicated that intoplicine produced a significant amount of SSB not related to DSB, which is consistent with concomitant inhibition of both DNA topoisomerases I and II in cells. Data derived from resistant cell lines indicated that multidrug-resistant cells were cross-resistant to intoplicine but that m-AMSA- and camptothecin-resistant cells were sensitive to intoplicine. Hence, intoplicine might circumvent topoisomerase I-mediated and topoisomerase II-mediated resistance by poisoning both enzymes simultaneously.

Animals↗

PubMed1993

Variation of single-strand break yield with scavenger concentration for the SV40 minichromosome irradiated in aqueous solution.

We have measured the yield of single-strand breaks (SSBs) induced in aerobic aqueous solution by 137Cs gamma irradiation for the SV40 minichromosome as measured by agarose gel electrophoresis. Under these conditions, DNA SSBs are caused mainly by the hydroxyl radical. To characterize the reactivity of the SV40 minichromosome with the hydroxyl radical and to compare its behavior with that of naked DNA, we examined the variation of the G value for SSB formation, G(SSB), with the concentration of added hydroxyl radical scavengers. We find that simple competition kinetics is not applicable, but that a nonhomogeneous kinetics model is in much better agreement. Estimates of the efficiency of SSB induction per OH radical interaction with the SV40 minichromosome (0.04-0.05) indicate that this substrate is about five times more radioresistant than naked DNA at scavenging capacities < 10(8) s-1. At a DNA concentration of 50 micrograms ml-1, G(SSB) for the direct effect in the minichromosome is about 1 x 10(-5) mumol J-1 (2 x 10(-10) SSB Gy-1 Da-1), essentially equal to that for naked DNA.

Cesium Radioisotopes↗

PubMed1993

Isolation of helicase alpha, a DNA helicase from HeLa cells stimulated by a fork structure and signal-stranded DNA-binding proteins.

A DNA helicase, called DNA helicase alpha, was purified from HeLa cells to apparent homogeneity. The helicase and its single-stranded DNA-dependent ATPase activities cosedimented in glycerol gradients with two polypeptides of 110 and 90 kDa with a sedimentation coefficient of 7.4 S. The DNA helicase was markedly stimulated by DNA substrates with a 5'-tailed fork. A DNA substrate with a 3'-tailed fork structure was less stimulatory, although it was more active than substrates without a fork. The directionality of unwinding is 3'-->5' with respect to the single-stranded DNA to which the enzyme was bound. The helicase activity also required a single-stranded DNA-binding protein (SSB) for unwinding activity. The stimulation by SSBs was nonspecific; all SSBs tested, such as human SSB, bacteriophage T4 gene 32, and Escherichia coli SSB, stimulated the DNA helicase activity to a varying extent in the presence of a fork structure. With long duplex substrates (> 500 base pairs), the presence of a fork substantially stimulated the DNA helicase activity in the presence of E. coli SSB. Human SSB stimulated the DNA helicase activity to the greatest extent (> 10-fold) with a substrate containing a fork compared with substrates without a fork. DNA helicase activity required ATP hydrolysis and could be supported by all eight nucleoside triphosphates. The Km values for ATP and dATP in unwinding were 28 and 48 microM, respectively. In general, ribonucleoside triphosphates were better effectors than deoxyribonucleoside triphosphates. The properties of this DNA helicase make it a candidate for a DNA replicative helicase in human cells.

Adenosine Triphosphatases↗

PubMed1996

Protein-protein interactions between the Escherichia coli single-stranded DNA-binding protein and exonuclease I.

It was demonstrated previously that a deoxyribophosphodiesterase (dRpase) activity is associated with the DNA repair enzyme exonuclease I, and that this activity is stimulated by the addition of the E. coli single-stranded DNA-binding protein (Ssb). This activity catalyzes the release of deoxyribose-phosphate groups at apurinic/apyrimidinic (AP) sites in the DNA that have been cleared by the action of an AP endonuclease. We have now used the yeast two-hybrid system to demonstrate that a protein-protein interaction occurs between exonuclease I and Ssb. When the E. coli ssb gene was fused in frame to the DNA-activating domain of the GAL4 transcriptional activator and the exonuclease I gene was fused in frame to the DNA-binding domain, a functional GAL4 transcriptional activator was produced as determined by growth of yeast on selective medium and the measurement of beta-galactosidase activity. We have also demonstrated that Ssb can stimulate the dRpase activity of exonuclease I using double-stranded bacteriophage M13 DNA containing several strand interruptions at incised AP sites. These results suggest that Ssb may be required for efficient base-excision repair in bacteria.

Bacteriophage M13↗

PubMed1997

Effect of polyamine-induced compaction and aggregation of DNA on the formation of radiation-induced strand breaks: quantitative models for cellular radiation damage.

The yield of DNA single-strand breaks, G(SSB), upon gamma irradiation of SV40 DNA and SV40 minichromosomes in aqueous solution under aerobic conditions was determined at physiological ionic strength in the presence of various potential radioprotective agents. Putrescine (PUT), spermidine (SPD), glutathione, trans-4,5-dihydroxy-1,2-dithiane, 2-mercaptoethyl disulfide and cystamine, all at 0.1-10 mM, spermine (SPM, 0.1-1 mM) and WR-33278 (WRSSWR, 0.1-2 mM) lowered G(SSB) of SV40 DNA. These results were expected from the ability of these agents to scavenge OH radical in the bulk solution. However, SPD, above 10 mM, and SPM and WRSSWR, each above 2 mM, produced dramatic radioprotection attributed to polyamine-induced compaction and aggregation of the DNA (PICA effect). The DNA of SV40 minichromosomes was inherently less radiosensitive and was subject to a PICA effect at lower polyamine concentrations, i.e. approximately 5 mM SPD, approximately 0.6 mM SPM and approximately 0.5 mM WRSSWR. The PICA effect decreased G(SSB) for SV40 DNA and minichromosomes by one to two orders of magnitude, depending upon the scavenging capacity of the medium. The final yields were similar for SV40 DNA and minichromosomes and were comparable to the corresponding yield determined for cells. Results for the yield of double-strand breaks indicated that the yield of double-strand breaks, G(DSB), for DNA and minichromosomes is subject to a PICA effect by SPM and SPD comparable to that measured for G(SSB). Values of G(SSB) for SV40 DNA and minichromosomes subjected to the PICA effect were well approximated by calculations based upon a 30-nm cylinder assumed to model their condensed states. The results indicate that a major fraction of the formation of SSBs in condensed DNA and minichromosomes results from nonscavengeable radical intermediates. Minichromosomes subjected to the PICA effect of 2 mM SPM were protected against formation of radiation-induced SSBs 1.5-fold by 20 mM DTT but 5-fold by 10 mM DTT plus 10 mM WR-1065 relative to 2 mM SPM alone. Thus WR-1065 is capable of providing marked protection of compacted and aggregated minichromosomes, a protection ascribed to the chemical repair of DNA radicals by WR-1065.

Cystamine↗

PubMed2001

Stimulation of DNA repair by the spermatidal TP1 protein.

The chromatin remodeling process that takes place during spermiogenesis in mammals is characterized by a transient increase in DNA single-strand breaks (SSB). The mammalian transition proteins (TPs) are expressed at a high level at mid-spermiogenesis steps coincident with chromatin remodeling and could be involved in the repair of these lesions since SSB are no longer detected in terminally differentiated spermatids. We report that TP1 can stimulate the repair of SSB in vitro and demonstrate that in vivo repair of UV-induced DNA lesions is enhanced in mammalian cells stably expressing TP1. These results suggest that, aside from its role in DNA compaction, this major transition protein may contribute to the yet unidentified enzymatic activity responsible for the repair of SSB at mid-spermiogenesis steps. These results also suggest that the TP1 proteins have the potential to participate in the repair process following genotoxic insults and therefore may play an active role in the maintenance of the integrity of the male haploid genome during spermiogenesis.

Animals↗

PubMed2006

Family-based association study of TPH1 and TPH2 polymorphisms in autism.

The TPH1 and TPH2 genes encode the rate-limiting enzymes that control serotonin biosynthesis, and serotonin is clearly altered in autism. In the current study, eight SNPs in the TPH1 gene region and eight SNPs within the TPH2 gene were examined by family-based association tests in a large cohort of 352 families with autism and in clinically defined subsets of these families with either severe obsessive-compulsive behaviors (sOCB) or self-stimulatory behaviors (SSB). We found no evidence for association between autism and single SNPs or haplotypes of the TPH1 and TPH2 genes in the cohort of all families or in the sOCB and SSB subsets. In particular, we failed to replicate the association between autism and variants of the TPH2 gene, rs4341581 (TRANSMIT P = 1; PDT P = 0.323; FBAT P = 0.446) and rs11179000 (TRANSMIT P = 0.174; PDT P = 0.293; FBAT P = 0.374). Furthermore, no evidence for linkage was observed between autism and SNPs in the TPH1 and TPH2 genes (although linkage at the TPH2 locus was observed in the SSB subset). Thus, it appears unlikely that the TPH1 and TPH2 genes play a significant role in the susceptibility to autism or to autism endophenotypes including sOCB and SSB.

Autistic Disorder↗

PubMed2004

Bacillus thuringiensis delta-endotoxin binding to brush border membrane vesicles of rice stem borers.

The receptor binding step in the molecular mode of action of five delta-endotoxins (Cry1Ab, Cry1Ac, Cry1C, Cry2A, and Cry9C) from Bacillus thuringiensis was examined to find toxins with different receptor sites in the midgut of the striped stem borer (SSB) Chilo suppressalis (Walker) and yellow stem borer (YSB) Scirpophaga incertulas (Walker) (Lepidoptera: Pyralidae). Homologous competition assays were used to estimate binding affinities (K(com)) of (125)I-labelled toxins to brush border membrane vesicles (BBMV). The SSB BBMV affinities in decreasing order was: Cry1Ab = Cry1Ac > Cry9C > Cry2A > Cry1C. In YSB, the order of decreasing affinities was: Cry1Ac > Cry1Ab > Cry9C = Cry2A > Cry1C. The number of binding sites (B(max)) estimated by homologous competition binding among the Cry toxins did not affect toxin binding affinity (K(com)) to both insect midgut BBMVs. Results of the heterologous competition binding assays suggest that Cry1Ab and Cry1Ac compete for the same binding sites in SSB and YSB. Other toxins bind with weak (Cry1C, Cry2A) or no affinity (Cry9C) to Cry1Ab and Cry1Ac binding sites in both species. Cry2A had the lowest toxicity to 10-day-old SSB and Cry1Ab and Cry1Ac were the most toxic. Taken together, the results of this study show that Cry1Ab or Cry1Ac could be combined with either Cry1C, Cry2A, or Cry9C for more durable resistance in transgenic rice. Cry1Ab should not be used together with Cry1Ac because a mutation in one receptor site could diminish binding of both toxins.

Animals↗

PubMed2003

In primary Sjögren's syndrome, HLA class II is associated exclusively with autoantibody production and spreading of the autoimmune response.

OBJECTIVE: To reevaluate, in a large series of patients with Sjögren's syndrome (SS) recruited from 2 French centers, the question of whether HLA is associated with SS itself or with a pattern of secretion of autoantibodies. METHODS: One hundred forty-nine white patients fulfilling the American-European Consensus Group criteria for SS were divided into 3 subgroups, according to their anti-Ro/SSA and anti-La/SSB status, as follows: group 1 (n = 53), no antibody; group 2 (n = 46), anti-SSA only; group 3 (n = 50), both anti-SSA and anti-SSB. Patients were compared with 222 unrelated healthy subjects representative of the white population in France. RESULTS: Comparisons between the 149 SS patients and 222 controls confirmed the association of SS with DRB1*03 (the frequency was 25% in patients versus 10% in controls) and DQB1*02 (32% versus 22%). The association between HLA and SS was restricted to patients with anti-SSA and/or anti-SSB; no association with HLA was observed in patients in group 1 (no antibody). The frequency of HLA-DRB1*15 was highest in group 2 (24%), compared with 11% in group 1 and 11% in controls, whereas the frequency of HLA-DRB1*03 was highest in group 3 (44%), compared with 12% in group 1, 19% in group 2, and 10% in controls. Group 2 and group 3 had more clinical and biologic markers of activity than did group 1 but were not clinically different. HLA alleles were not associated with clinical features of the disease, and were associated with only some biologic features: rheumatoid factor positivity, increased serum IgG, and thrombocytopenia were associated with HLA-DRB1*03, and neutropenia was associated with DQB1*01. CONCLUSION: HLA class II markers confer genetic susceptibility to Sjögren's syndrome. The association between HLA and SS is restricted to patients with anti-SSA and/or anti-SSB antibodies; HLA is not associated with SS in patients without these autoantibodies. The absence of a difference in disease severity between groups 2 and 3, as well as the restricted association of HLA-DRB1*03 in group 3, strongly suggest that HLA alleles predispose to autoantibody secretion, without being associated with clinical outcome. HLA class II phenotype might support epitope spreading: HLA-DR15 favors anti-SSA synthesis, whereas HLA-DR3 is associated with both anti-SSA and anti-SSB production.

Adult↗

PubMed1989

DNA strand breakage in normal and solar ultraviolet-sensitive ICR 2A frog cell lines exposed to solar ultraviolet wavelengths.

ICR 2A frog cells and two solar ultraviolet (UV)-sensitive cell lines, DRP 36 and DRP 153, were irradiated with 150 kJ/m2 of the UV radiation produced by a fluorescent sun lamp, the radiation from which was passed through a sheet of 48A Mylar (DuPont, Wilmington, DE) to eliminate wavelengths shorter than approximately 315 nm. The irradiated cultures were also exposed to photoreactivating light (PRL), resulting in the removal of most of the pyrimidine dimers induced by the sun lamp UV irradiation, and then incubated 0-4 hr. At the end of the incubations, the cells were subjected to the alkaline elution assay. In these elutions, the cell lysates were either treated with proteinase K (proK) to eliminate any DNA-protein crosslinks (DPC) that may be present in the cells, or left untreated with proK. For the ICR 2A cells, the level of apparent DNA single-strand breaks (ssb) detected in elutions using proK increased with the incubation time after irradiation and remained high. However, when the DNA was eluted without proK pretreatment, the number of ssb fell rapidly. In contrast, the levels of ssb decreased in the DRP 36 and DRP 153 cells regardless of the use of proK in the elutions. Hence, this differential response in ssb induction may be indicative of a system involved with recovery following irradiation with solar UV wavelengths.

Animals↗

PubMed2007

Bonding characteristics of newly developed all-in-one adhesives.

This study evaluated the microtensile bond strength and the interfacial morphology of newer adhesives. The occlusal surfaces of extracted teeth were ground flat for random allocation to four equal groups. Resin composite was bonded to each surface using either Clearfil SE Bond [SEB], Clearfil Protect Bond [PB], G-Bond [GB], or an experimental adhesive, SSB-200 [SSB]. After storage for 24 h in water at 37 degrees C, they were sectioned into beams (cross-sectional area 1 mm(2)) for microtensile bond strength testing (muTBS) at a crosshead speed of 1 mm/min. The load at failure of each was recorded; the data were analyzed by one-way ANOVA and Games Howell tests. The surfaces of the fractured specimens were observed using SEM. For the ultra-morphology of the interface, the occlusal surfaces of four more teeth were prepared as before and a thin layer of flowable resin composite was bonded to each surface using one of the four adhesives. The mean muTBS ranged from 39.68 MPa (GB) to 64.97 MPa (SEB). There were no statistical differences between SEB and SSB, or between PB and GB (p > 0.05). The muTBS of SEB and SSB were significantly greater than that of PB and GB (p < 0.05). SEMs of the fractured surfaces revealed a mixed (cohesive/interfacial) failure. TEM examination highlighted differences in the hybrid layer; SEB had a thicker layer than the others. In conclusion, the newer all-in-one adhesives produced a thin hybrid layer but varied in their bond strengths. The 2-step self-etching adhesives do not necessarily produce higher bond strengths than that of the all-in-one systems.

Composite Resins↗

PubMed1995

A mechanism for induction of the SOS response in E. coli: insights into the regulation of reversible protein polymerization in vivo.

During normal DNA replication, RecA, the principal recombinational repair enzyme of E. coli, cannot assemble its filament on SSB-bound single-stranded DNA at the replication forks. This behavior is paralleled in vitro, where at low Mg2+ concentrations RecA can not polymerize on SSB-bound single-stranded DNA. Inhibition of DNA replication in vivo renders RecA able to polymerize on SSB-bound single-stranded DNA and to activate the SOS response. Although the mechanism of SOS induction is still obscure, abundant in vitro observations indicate that RecA filament formation on SSB-bound single-stranded DNA is facilitated at elevated concentrations of ATP, Mg2+ and spermidine. It is proposed here that inhibition of DNA synthesis in vivo leads to a similar accumulation of ATP and its counter-ions, Mg2+ and spermidine, resulting ultimately in SOS induction. When DNA synthesis is restored, the concentration of ATP, Mg2+ and spermidine returns to normal levels, favoring RecA depolymerization. On the basis of the known structure of RecA, a mechanism for reversible RecA polymerization is presented. In a RecA polymer, the monomers are known to interact with each other primarily through hydrophobic, oppositely charged surfaces. In conditions suboptimal for polymerization, these hydrophobic surfaces of the monomers are possibly masked by electrostatic interactions with other, oppositely charged domains of the monomers. There are known recombinational repair proteins whose specific functions are likely to assist in RecA polymerization or depolymerization. Features of reversible polymerization of eukaryotic proteins tubulin and actin are consistent with the possibility that RecA exploits a general principle for the regulation of reversible protein polymerization.

Actins↗

PubMed1996

Study on simian virus 40 DNA synthesis in herpes simplex virus-infected cells.

Replication of simian virus 40 (SV40) DNA occurs in SV40 nonpermissive hamster cells upon infection with herpes simplex virus (HSV), leading to concatemeric replication products characteristic for HSV DNA replication. This SV40 origin (ori)-dependent process is governed by SV40 large T antigen and HSV-encoded DNA replication factors; e.g., DNA polymerase, single-strand binding protein (SSB), and helicase-primase. In this study, we show that specific interaction of SV40 T antigen with SV40 ori is crucial for HSV-directed SV40 DNA synthesis and that the property of T antigen to bind and unwind the ori is not sufficient for this process. A T antigen with the mutation T217S, affecting a hypothetical novel DNA replication subfunction, is able to support DNA synthesis in vitro but not in cultured primate cells. This subfunction is also necessary in HSV-infected hamster cells. Using temperature-sensitive mutants, we demonstrate that the T antigen acts at early stages of DNA synthesis while HSV helicase is required continuously as has been shown for HSV DNA polymerase. HSV SSB is also continuously involved in heterologous SV40 DNA synthesis. However, a HSV mutant, temperature-sensitive in SSB function, showed residual synthesis of SV40 DNA but not of HSV DNA at the nonpermissive temperature. The nature of this dichotomy between HSV SSB function on SV40 DNA and HSV DNA will be discussed.

Animals↗

PubMed1981

A T7 amber mutant defective in DNA-binding protein.

A T7 amber mutant, UP-2, in the gene for T7 DNA-binding protein was isolated from mutants that could not grow on sup+ ssb-1 bacteria but could grow on glnU ssb-1 and sup+ ssb+ bacteria. The mutant phage synthesized a smaller amber polypeptide (28,000 daltons) than T7 wild-type DNA-binding protein (32,000 daltons). DNA synthesis of the UP-2 mutant in sup+ ssb-1 cells was severely inhibited and the first round of replication was found to be repressed. The abilities for genetic recombination and DNA repair were also low even in permissive hosts compared with those of wild-type phage. Moreover, recombination intermediate T7 DNA molecules were not formed in UP-2 infected nonpermissive cells. The gene that codes for DNA-binding protein is referred to as gene 2.5 since the mutation was mapped between gene 2 and gene 3.

Carrier Proteins↗