No abstract

No abstract

No abstract

Synovial cysts of the ligamentum flavum, measuring 1 cm in diameter, caused compression of the lumbar nerve roots in four patients. The authors discuss the association of these cysts with advanced focal spondylosis, and speculate on their etiology.

Using site-specific mutagenesis, we have examined the mutagenic activity in vivo of O-methylguanine or 06-n-butylguanine located at a preselected site in gene G of bacteriophage OX174. The experiments were designed so that the phage mutant produced by a targeted transition from either of these alkylated derivatives would be recognizable by a simple plaque assay. Spheroplasts derived from normal and repairdeficient cells were transfected, and the lysates were screened for mutant virus. In cells with normal repair, DNA carrying the methylguanine produced the expected transition in 15% of the total phage; DNA carrying the butylguanine produced the same mutation in 0.3% of the phage4 In cells deficient in excision repair (uvrA) the transition frequency went up by a factor of 8 for O6-butylguanine and down by a factor of 40 for 06' methylguanine. In cells deficient in recombination (recA), the transition frequency increased 1.5-fold for butylguanine and decreased by a factor of 8 for methylguanine. The data show that (i) both methyl-and butylguanine produce site-directed transitions in OX174; (ii) the transition occurs in recA cells; (iii) the frequency of the transition is influenced by both recA and uvrA mutations; (iv) the recA and uvrA mutations alter the transition frequency for methylguanine and butylguanine in opposite directions.The gene products of uvrA, -B, and -C play a key role in removing a variety of damaged purine or pyrimidine nucleotide residues that deform the DNA helix (1-7). The ada gene product, on the other hand, appears to operate only on 06-methyl-or 06-ethylguanine in DNA, in an alkyl-transfer reaction that regenerates the guanine (8-12). In this paper we report our initial studies dealing with effects of DNA repair on the frequency of site-directed mutations produced in vivo by alkylated purine or pyrimidine residues located at preselected positions in an essential gene of bacteriophage OX174. The results show an unexpected effect of uvrA and recA mutations on the production of a specific transition from an 06-methylguanine or 06-n-butylguanine in the first position of the third codon in gene G of qX174.MATERIALS AND METHODS Bacterial Strains. Escherichia coli AB1157 and its isogeneic derivatives AB1886 (uvrA6), AB2463 (recA13), and AB2480 (uvrA6 recA13) were obtained from B.

No abstract

No abstract

As part of our studies on the molecular mechanisms of mutation by carcinogens we have synthesized 12 oligonucleotides (15-mers) containing an O6-alkylguanine residue at a preselected position for use as primers in the enzymatic synthesis of biologically active DNA. Ten of these oligonucleotides are derived from a minus strand sequence carrying the modified nucleotide in the third codon of gene G of bacteriophage phi X174 DNA. Two others are derived from plus strand sequences carrying the modification in the 12th codon of the human Ha-ras protooncogene. During this work several potentially serious side reactions, which could complicate interpretation of mutagenesis data, were observed. This paper describes a detailed study of these reactions. Since we were unable to avoid undesirable side products, we developed simple chromatographic methods for detecting and removing them.