Disease relevance of polA

• We have applied this method to purify DNA polymerase both from wild type E. coli cells and from cells bearing a lambda prophage carrying the polA gene (Kelley, W.S., Chalmers, K., and Murray, N.E. (1977) Proc. Natl. Acad. Sci. U.S.A. 74, 5632-5636) [1].
• Transduction with phage P1 indicates at least 70% linkage between glnA and polA [2].
• The Streptococcus pneumoniae polA gene was altered at various positions by deletions and insertions [3].
• Many wild type Salmonella strains are 4-5 times more sensitive than wild type E. coli and their inactivation curves is similar to that for E. coli with a mutation in the polA gene [4].
• (3) There was a 78% correspondence between results obtained with E. coli polA and Bacillus subtilis (H17/M45, 17A/45T) rec assay and between E. coli polA and Proteus mirabilis [5].

High impact information on polA

• A central Hae III fragment, Hae III-G, containing the nucleotide sequence coding for the RNA primer for the complementary strand and the nicking site for gene II protein, is sufficient for plasmid replication in M13-infected polA- cells but not for high frequency transformation [6].
• Screening of the mutations in vivo for the classical polA-defective phenotype (sensitivity to DNA damage) demonstrated that a genetic screen of this type may be a reasonable predictor or kcat or of DNA binding affinity in future mutational studies [7].
• Ferrate oxidation of Escherichia coli DNA polymerase-I. Identification of a methionine residue that is essential for DNA binding [8].
• Treatment of Escherichia coli DNA polymerase-I with potassium ferrate (K2FeO4), a site-specific oxidizing agent for the phosphate group-binding sites of proteins, results in the irreversible inactivation of enzyme activity as judged by the loss of polymerization as well as 3'-5' exonuclease activity [8].
• A further difference noted in infected polA strains was a 10-fold reduction in the frequency of Mu-mediated transposition of chromosomal genes to an F plasmid [9].

Chemical compound and disease context of polA

• In Escherichia coli polA lig-4 bacteria, the moles percent 6-methyladenine content of 10S deoxyribonucleic acid (Okazaki fragments) is 0.96 compared with 1.4 for bulk desoxyribonucleic acid [10].
• Excision of pyrimidine dimers in normal and T4-infected Escherichia coli: effect of polA and other mutations [11].
• A mutagenic effect of allylisothiocyanate (AITC) on E. coli WP 67 (trp uvrA polA) was only found in a test with metabolic activation in vitro [12].
• Since effects of the polA and the x or y mutations are additive, it is supposed that there are at least two pathways for the repair of methyl meth-anesulfonate-damaged T4 DNA, one controlled by the x and the y genes and the other in which E. coli DNA olymerase I is involved [13].
• Inhibition of Escherichia coli DNA polymerase-I by the anti-cancer drug cis-diaminedichloroplatinum(II): what roles do polymerases play in cis-platin-induced cytotoxicity [14]?

Biological context of polA

• These results suggest that lexA(Def) activates a RecA-independent, RecF-dependent recombination repair pathway that suppresses the defect in DNA replication in recA polA double mutants [15].
• Recently, a relationship was found between their antitumor properties and their cytotoxic effect on the polA Escherichia coli mutant strain, suggesting that 7H-pyrido[4,3-c]carbazole dimers might induce a DNA deformation that could be recognized by the E. coli SOS repair system [16].
• DNA was integrated into the S. typhimurium chromosome at aroC by transferring the vectors into S. typhimurium polA mutants and allowing homologous recombination to occur between the cloned and chromosomal aroC genes [17].
• Two different DNA damage-sensitive strains generated by chemical mutagenesis were found to be defective in a gene that has extended DNA and protein sequence homology with polA of Escherichia coli [18].
• Polypeptide chain-terminating mutations within the predicted open reading frame for the 27-kDa polypeptide abolished the synthesis of this polypeptide and also the Escherichia coli polA-independence phenotype of the pCU1 replicon [19].

Associations of polA with chemical compounds

• The adaptive response of E.coli to low levels of alkylating agent: the role of polA in killing adaptation [20].
• Several MMS-resistant revertants isolated from one of the S. sonnei polA mutants regained 3-120% of the DNA polymerase activity found in the extracts of the wild-type parent strain [21].
• Cells pretreated with nonlethal doses of plumbagin showed enhanced survival upon exposure to high concentrations of plumbagin, but were unchanged in their susceptibility to far-UV irradiation. polA and recA mutants were not significantly more sensitive than wild type to killing by plumbagin [22].
• The medium had no effect on the number of mutants expressed in an excision deficient uvrA- strain (WP2 uvrA trp-) or a polymerase I mutant (P3478 polA thy-) [23].
• This was interpreted to mean that the loss of streptomycin resistant mutants on PBA involves the excision repair pathway and is dependent on the polA gene product, polymerase I [23].

Analytical, diagnostic and therapeutic context of polA

• The breaks observed after treatment with metal chelators and H2O2 were repaired 60 min after H2O2 elimination in xthA but not polA mutant cells [24].

References