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PubMed1975

Thermal enhancement of ultraviolet mutability in a dnaB uvrA derivative of Escherichia coli B/r: evidence for inducible error-prone repair.

DNA damage triggers coordinate expression of a cluster of diverse functions in Escherichia coli, including prophage induction, filamentous growth, and "aberrant" reintiation of DNA replication at the chromosomal origin. The "SOS repair" hypothesis proposes that one of these coordinately inducible functions is an error-prone system of DNA repair ("SOS repair") which is responsible for ultraviolet mutagenesis. In dnaB strains, incubation of 42 degrees C stops DNA synthesis and induces lambda prophage and should, therefore, also induce the postulated error-prone repair activity. Thermal posttreatment of a dnaB urvA derivative of E. coli B/r is found to enhance the yield of ultraviolet-light-induced mutations as much as 50-fold, while having no such effect in the dnaB+ parent strain. The results support the SOS repair hypothesis. The possibility is discussed that the inducible repair system is a mutagenic DNA polymerase.

Coliphages↗

PubMed1980

Transposition of IS1-lambdaBIO-IS1 from a bacteriophage lambda derivative carrying the IS1-cat-IS1 transposon (Tn9).

Tn9 is a transposable element in which a gene (cat) determining chloramphenicol resistance is flanked by directly repeated sequences that are homologous to the insertion sequence IS1. We show here that infection of Escherichia coli K12 (under Rec-Red-Int- conditions) with a lambda bio transducing phage carrying Tn9 results in the formation of lambda bio transductants as frequently as cat transductants as frequently as cat transductants (about 1 per 10(6) to 10(7) infected cells). Most of the lambda bio transductants do not carry cat, just as most of the cat transductants do not carry lambda bio. In spite of the absence of cat, the lambda bio prophage can transpose a second time, from the E. coli chromosome to different sites on an F'gal plasmid. Analysis of the structure of the transposed lambda bio element, by restriction nuclease digestion and by electron microscopy, demonstrates that the integrated lambda bio prophage is flanked by directly repeated IS1 elements. We conclude that there is no genetic information for the ability to transpose encoded in the non-repeated portion of Tn9, i.e. that the directly repeated IS1 elements alone are responsible for Tn9 transposition.

Bacteriophage lambda↗

PubMed1976

Expression of the guanine operon of Escherichia coli as analyzed by bacteriophage lambda induced mutations.

Studies were made on two guanine-requiring strains of Escherichia coli isolated independently as a result of insertion of prophage gamma into one of the structural genes of the guanine operon. These mutants do not exhibit any detectable guaB function but express the guaA function constitutively at a low level, presumably due to transcription from the pI promoter on the prophage. Various types of plaque-forming gua-transducing phages were generated from these lysogens. The approximate location and the mode of substitution of the gua genes in the phage genome were determined. These results clearly indicate that the gene guaB is located closer to the operator-promoter region of the gua operon than is guaA, and the gene order is "operator"-guaB-guaA.

Coliphages↗

PubMed1978

Mu-1 directed inhibition of DNA breakdown in Escherichia coli, recA cells.

The spontaneous DNA breakdown exhibited by recA strains, is reduced after heat induction of a thermoinducible Mu-1 prophage. This inhibition is dependent upon RNA synthesis, suggesting that Mu-1 directs synthesis of a recBC nuclease inhibitor, analogous to the product of the lambda gam gene. The genetic evidence presented here shows that Mu-1 enables a lambda red gam phage to grow on a recA host. The in vitro assay for ATP-dependent exonuclease activity reveals a complete inhibition of this activity 30 min after induction of the Mu-1 prophage.

Coliphages↗

PubMed1976

Genetic exchanges caused by ultraviolet photoproducts in phage lambda DNA molecules: the role of DNA replication.

Genetic recombination induced by structural damage in DNA molecules was investigated in E. coli K12 (lambda) lysogens infected with genetically marked phage lambda. Photoproducts were induced in the phage DNA before infection by exposing them either to 313 nm light in the presence of acetophenone or to 254 nm light. To test the role of the replication of the damaged phage DNA on the frequency of the induced recombination, both heteroimmune and homimmune crosses were performed. First, samples of a heteroimmune phage lambda imm434 P80 exposed to these treatments were allowed to infect cells lysogenic for prophage lambda cI857 P3. Phage DNA replication and maturation took place, and the resulting progeny phages were assayed for the frequency of P+ recombinants. Recombination was less frequent in infected cells exposed to visible light and in wild type cells able to perform excision repair than in excision-defective lysogens. Therefore, much of the induced recombination can be attributed to the pyrimidine dimers in the phage DNA, the only photoproducts known to be dissociated by photoreactivating enzyme. Second, in homoimmune crosses, samples of similarly treated homoimmune lambda P3 phages were allowed to infect lysogens carrying lambda cI857 P80. Replication of the phage DNA containing ultraviolet photoproducts was repressed by lambda immunity, and was further blocked by the lack of the P gene product needed for replication. The lysogens were purified and scored for both colony forming ability and for P+ recombinant prophages. The 254 nm photoproducts increased the frequency of recombination in these homimmune crosses, even though phage DNA replication was blocked. Irradiation with 313 nm light and acetophenone M, which produces dimers and unknown photoproducts, was not as effective per dimer as the 254 nm light. It is concluded from these results that certain unidentified 254 nm photoproducts can cause recombination even in the absence of DNA replication. They are not pyrimidine dimers, as they are not susceptible to excision repair or photoreactivation. In contrast, pyrimidine dimers appear to cause recombination only when the DNA containing them undergoes replication.

Coliphages↗

PubMed1978

Superinfection exclusion and changes in cellular transport processes in phage infected Salmonella typhimurium.

The changes induced by bacteriophage P22 in the cellular transport process(es) of the host Salmonella typhimurium (Taneja et al., 1975; Khandekar et al., 1975; Bandyopadhyay and Chakravorty, 1976) involve interactions between the superinfection exclusion system of the resident prophage and the C immunity region of the superinfecting phage. The sie A gene of the prophage interferes with the changes in the cellular transport process induced by the superinfecting phage. However, if the superinfecting phage carries active C1 and C2 genes there is no such interference. Thus the C1 and C2 genes of the superinfecting phage seem to be expressed in the sieA+ lysogen.

Biological Transport↗

PubMed1974

Transcription of bacteriophage mu. An analysis of the transcription pattern in the early phase of phage development.

It has previously been shown that the transcription of Mu is asymmetric and takes place on the heavy DNA strand (Bade, 1972; Wijffelman et al., 1974). The direction of transcription of Mu has now been determined by RNA-DNA hybridizations between purified Mu-RNA and the separated strands of lambda-Mu hybrid phages. The direction of transcription is from the c-gene (immunity gene) end of the heavy strand to the beta-end (immunity distal end) (Fig. 1). Thermo-inducible, defective Mu lysogens, in which the prophage is deleted from the beta-end, have a normal early transcription pattern, but the increase of RNA at later times is absent. A defective lysogen, which contains only the immunity gene c and the genes A and B, still has an early transcription pattern similar to that of the wild-type. Therefore, we conclude that the early RNA is transcribed from that region of the Mu genome. The early Mu-RNA synthesis is negatively regulated with a minimum rate of transcription at 9 minutes after induction. Before the onset of the late RNA synthesis, at about 22 minutes there is a rather long period in which the rate of Mu-RNA synthesis slowly increases. Using DNA strands of lambda-Mu hybrids which contain only that part of the Mu-DNA on which the early RNA synthesis takes place, we have determined that during the first half in the intermediate phase only early genes are transcribed. The amount of Mu-RNA synthesized by a Mu prophage carrying the X-mutation, which influences the excision of Mu, is greatly reduced. Negative regulation of early transcription occurs normally in this mutant.

Coliphages↗

PubMed1978

Cloning of a restriction fragment of phage mu DNA coding for early functions.

The DNA of an E. coli K12 strain harboring ten wildtype Mu prophages was restricted with endonuclease EcoRI, and the fragments ligated into the plasmid vector pMB9. Upon transformation of a strain carrying a heat inducible (Mu cts62) prophage, one temperature-resistant transformant was isolated. This transformant strain harbors the hybrid plasmid pKN001, containing the EcoRI.C fragment of Mu DNA as shown by restriction and heteroduplex analysis. Stable transformants of pKN001 are immune to superinfection with phage Mu. Transformation of Mu sensitive bacteria with pKN001 results in killing of the recipients (10(-4) surviving bacteria). The killing function is not expressed upon transformation of Mu-immune (lysogenic) bacteria.

Cell Transformation, Viral↗

PubMed1979

Map position of the replication terminus on the Escherichia coli chromosome.

The directions of replication of several prophages integrated with a known orientation in the vicinity of the terminus (tre) of chromosome replication (trp::Mu, min 27; lambda rev integrated within rac, min 31, man::Mu, min 35), have been established by determining the molecular polarity of Okazaki pieces specific to these prophages. The results obtained strongly suggest that the site tre is located between rac and man, an otherwise genetically silent region.

Chromosome Mapping↗

PubMed1987

The glucose kinase gene of Streptomyces coelicolor and its use in selecting spontaneous deletions for desired regions of the genome.

A number of deletions in the glucose kinase (glk) region of the Streptomyces coelicolor chromosome were found among spontaneous glk mutants. The deletions were identified by probing Southern blots of chromosomal DNA from glk mutants with cloned glk DNA. The deletions ranged in size from 0.3 kb to greater than 2.9 kb. When cloned glk DNA was introduced on a phi C31 phage vector into a glk mutant that contained a deletion of the entire homologous chromosomal glk region, glucose kinase activity was detected in extracts of these cells. The entire coding information for at least a subunit of glucose kinase is therefore present on the cloned glk DNA. The 0.3 kb glk chromosomal deletion was used to demonstrate that transfer of chromosomal glk mutations on to the phi C31::glk phage could occur by recombination in vivo. Since glk mutations frequently arise from deletion events, a method was devised for inserting the cloned glk DNA at sites in the chromosome for which cloned DNA is available, and thus facilitating the isolation of deletions in those DNA regions. phi C31::glk vectors containing a deletion of the phage att site cannot lysogenize S. coelicolor recipients containing a deletion of the glk chromosomal gene unless these phages contain S. coelicolor chromosomal DNA. In such lysogens, the glk gene becomes integrated into the chromosome by homologous recombination directed by the chromosomal insert on the phage DNA. In appropriate selective conditions, mutants which contain deletions of the glk gene that extend into the adjacent host DNA can be easily isolated. This method was used to insert glk into the methylenomycin biosynthetic genes, and isolate derivatives with deletions of host DNA from within the prophage into the adjacent host DNA. Phenotypic and Southern blot analysis of the deletions showed that there are no genes essential for methylenomycin biosynthesis for at least 13 kb to the left of a region concerned with negative regulation of methylenomycin biosynthesis. Many of the deletions also removed part of the phi C31 prophage.

Chromosome Deletion↗

PubMed1984

Near-ultraviolet radiation blocks SOS responses to DNA damage in Escherichia coli.

Escherichia coli cells in which the recA promoter is fused to a lac structural gene, (Mu) Mud(Ap,lac)::rec, were irradiated with two far-ultraviolet light wavelengths (254 and 290 nm), selected monochromatic near-ultraviolet (NUV) wavelengths 313 nm, 334 nm, 365 nm, or broad band solar-UV (290-420 nm) from a solar simulator. Irradiation with the two far-ultraviolet wavelengths was followed by high yields of beta-galactosidase, lambda prophage induction, and Weigle reactivation. These end points were not observed after irradiation with the selected NUV wavelengths or the broad spectrum solar-UV. Thus, neither broad spectrum solar-UV nor monochromatic NUV wavelengths resulted in the derepression of the recA promoter. Further, prior exposure of the cells either to the selected monochromatic NUV wavelengths or to solar-UV inhibited (a) the induction of beta-galactosidase by subsequent 254-nm radiation, (b) subsequent 254-nm induction of lambda prophage, (c) Weigle reactivation, and (d) mutation frequency. These observations are consistent with the hypothesis that NUV blocks subsequent recA protease action.

Bacteriophage lambda↗

PubMed1983

Replication-control functions block the induction of an SOS response by a damaged P1 bacteriophage.

UV-damaged bacteriophage P1 causes an SOS response in infected bacteria that can be measured colorimetrically with the aid of a lambda pL-lacZ fusion strain of Escherichia coli. This response is blocked by a P1 prophage. Evidence is offered that the blockage is caused by the concerted action of the incompatibility determinant incA and the immunity (c1 and c4) repressors of the prophage. We suggest that indirect induction of lambda by damaged P1 is caused by the abortive initiation of replication in either of two modes, one under incA control, the other under c1 control and indirectly (via ant, the determinant of a repression antagonist) under c4 control.

Bacteriophage lambda↗

PubMed1983

DNA repair properties of Escherichia coli tif-1, recAo281 and lexA1 strains deficient in single-strand DNA binding protein.

Mutations affecting single-strand DNA binding protein (SSB) impair induction of mutagenic (SOS) repair. To further investigate the role of SSB in SOS induction and DNA repair, isogenic strains were constructed combining the ssb+, ssb-1 or ssb-113 alleles with one or more mutations known to alter regulation of damage inducible functions. As is true in ssb+ strains tif-1 (recA441) was found to allow thermal induction of prophage lambda + and Weigle reactivation in ssb-1 and ssb-113 strains. Furthermore, tif-1 decreased the UV sensitivity of the ssb-113 strain slightly and permitted UV induction of prophage lambda + at 30 degrees C. Strains carrying the recAo281 allele were also constructed. This mutation causes high constitutive levels of RecA protein synthesis and relieves much of the UV sensitivity conferred by lexA- alleles without restoring SOS (error-prone) repair. In contrast, the recAo281 allele failed to alleviate the UV sensitivity associated with either ssb- mutation. In a lexA1 recAo281 background the ssb-1 mutation increased the extent of postirradiation DNA degradation and concommitantly increased UV sensitivity 20-fold to the level exhibited by a recA1 strain. The ssb-113 mutation also increased UV sensitivity markedly in this background but did so without greatly increasing postirradiation DNA degradation. These results suggest a direct role for SSB in recombinational repair apart from and in addition to its role in facilitating induction of the recA-lexA regulon.

Bacterial Proteins↗

PubMed1985

Isolation of transfer-negative nif-plasmids (pCE1) and their integration into the chromosome of Escherichia coli with the help of phage Mu.

Strain JC5466 of Escherichia coli K12 harbouring the nitrogen fixation plasmid pCE1 was lysogenized with bacteriophage Mu cts, followed by partial induction and infection with bacteriophage PRD1. This made it possible to obtain transfer-defective derivatives of pCE1, carrying Mu prophage. These derivatives could be mobilized by using the helper plasmid pME400 and it was possible to segregate the helper plasmid from the donor plasmid in the transconjugants. By incubating the strains 302 and 328 at 42 degrees C, for induction of Mu prophage, derivatives with different plasmid contents could be obtained such as strains without plasmids, some with smaller or larger plasmids and others possessing plasmids without any visible alteration in size. Integration of the nitrogen-fixation (nif) genes into the chromosomes of the strains without plasmids and those containing a smaller plasmid, was confirmed by Southern hybridization using radioactive nifKDH DNA. Conjugation assays have shown that the plasmid is integrated into the chromosome as a unit but that it can also be excised.

Chromosomes, Bacterial↗

PubMed1986

Direct evidence for autogenous regulation of the Escherichia coli genes rpoBC in vivo.

We have fused the rpoBC genes to the strong controllable promoter PL in phage lambda while deleting most of the intercistronic regulatory DNA and ribosomal protein genes upstream of rpoB. Induction of a lysogen carrying the recombinant prophage gave rise to a 2-3-fold oversynthesis of beta beta' in the cell whereas rpoBC-mRNA levels rose by at least 10-fold. Similar observations were made when these sequences were present in the prophage, indicating that the removal of DNA sequences up to 26 base pairs before rpoB does not affect post-transcriptional autogenous regulation of beta beta' synthesis. Overexpression of beta beta' also autogenously regulated the synthesis of the beta polypeptide from the chromosome in two strains carrying electrophoretic mobility mutations in rpoB. S1 nuclease mapping experiments indicated that this regulation was also post-transcriptional, and confirmed that phage beta-mRNA synthesis exceeded chromosomal beta-mRNA synthesis by 20-fold. The provision of excess beta alone in the cell caused autoregulation of chromosomal beta, but not beta' synthesis, indicating that beta and beta' are regulated independently.

DNA-Directed RNA Polymerases↗

PubMed1981

Lysogenic induction of lambdoid phages in lexA mutants of Escherichia coli.

UV irradiation of lexA3 mutants of E. coli caused lysogenic induction of prophage lambda, lambda i21, lambda i434 and phi 80. Maximal induction in lexA3 lysogens needed less UV than in lexA+ bacteria and gave 25-100% of the normal levels of infective centres induced. Assays of gene expression arising from derepression of a defective lambda prophage showed at least 40% of the normal levels of induction by mitomycin C in lexA3 bacteria. The need for post-irradiation protein synthesis for lysogenic induction in lexA3 lysogens was reduced by increasing the basal level of recA protein with a recA+ plasmid. It is concluded that in lexA E. coli some recA protein synthesis, too small to be detected by physical means, is needed for UV induced lysogenic induction.

Bacteriophage lambda↗

PubMed1982

Expression of recA-gene dependent SOS functions in Salmonella typhimurium.

Thymine starvation of RecA+ Thy- strains of Salmonella typhimurium does not induce the inhibition of cellular respiration, one of the recA-gene dependent SOS functions. Nevertheless, thymine deprivation is able to produce a normal induction of prophage and thymineless death in these same strains However, when these mutants are treated, in the presence of thymine, with UV-irradiation or bleomycin, they show a normal inhibition of cellular respiration and other SOS functions. Thus, one injurious treatment (thymine deprivation) may trigger prophage induction but not cessation of respiration, whereas another agent (UV-irradiation) may induce both. Together, these results suggest a possible discrimination in the pathways and conditions of expression of various SOS functions.

Bleomycin↗

PubMed1982

Bacteriophage Mu DNA replication is stimulated by non-essential early functions.

The replication of a spontaneous Kil- mutant of bacteriophage Mu has been investigated. The Kil- mutation (Mucts62-13/4), which was introduced into a defective prophage, is pleiotrophic, leading to the loss of also the Gam, Cim and Sot functions. The mutation is caused by an insertion with the characteristics of IS1, located just outside the B gene. Mucts62-1 3/4 phages form extremely small plaques on wildtype indicator strains. The replication of the insertion mutant as compared to Mucts62 is strongly reduced. Normal replication could be restored by relieving the polarity of the insertion or by complementation with defective prophages which express all early functions. Apparently, early genes other than A and B are involved in normal Mu DNA replication.

Coliphages↗