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M Blanco

Publications and source records attributed to M Blanco.

At least 235 records · Page 13Linked to original sources
PubMed1984

Restoration of RecA protein activity by genetic complementation.

Bacteria carrying either recA430 or recA453-441 mutations are sensitive to UV-irradiation since they amplify the synthesis of RecA protein either poorly or not at all. We show here that, in a recA453-441 (recA430) heterodiploid, UV-resistance and amplification of RecA430 protein were restored, indicating that the cellular level of RecA-associated protease activity was high enough to inactivate LexA repressor. Prophage 434 repressor was also extensively inactivated, whereas RecA430 protein alone cannot cleave this substrate. On the other hand, during growth of the recA453-441(recA430) heterodiploid at 42 degrees C in the presence of adenine, a treatment activating only RecA441 protein, RecA441 protease activity was as high as in a recA441 haploid. In contrast, following this inducing treatment, there was no complementation between RecA441 and RecA+ proteins in a recA453-441(recA+) heterodiploid. These results indicate that multimerization of RecA protein molecules results in a functional interaction that, in some combination between RecA protein subunits, may enhance RecA-associated protease activity.

Alleles↗
PubMed1982

Evidence for the existence of a monovalent cation-stimulated, magnesium-dependent adenosine triphosphatase activity in the isolated plasma membranes of amoebas of the slime mold dictyostelium discoideum.

Evidence for a magnesium-dependent ATPase activity that can be stimulated by Na+ and K+, or equally by Na+ or K+ alone, has been found in the plasma membranes isolated from amoebas of the slime mold Dictyostelium discoideum when the membranes are isolated from cultures grown up to the stationary phase. This ATPase activity is scarcely inhibitable by ouabain or phlorizin, but is very sensitive to low concentrations of azide or thimerosal. When the plasma membranes are isolated from amoebas growing in logarithmic phase, this monovalent cation-stimulated Mg2+-dependent activity is barely detectable.

Adenosine Triphosphatases↗
PubMed1981

Plasmid pKM101-dependent repair and mutagenesis in Escherichia coli cells with mutations lexB30 tif and zab-53 in the recA gene.

Bacterial survival after UV irradiation was increased in E. coli K12 lexB30 and tif zab-53 mutants harboring plasmid pKM101. Mutagenesis in response to UV was observed in these bacteria which, in absence of pKM101, are not UV-mutable. The mutator effect observed in unirradiated wild-type cells containing pKM101 was higher than incubation at 30 degrees C with adenine than at 37 degrees C. This effect was still enhanced by tif mutation, even in the tif zab-53 strain, but it was abolished by lexB30 mutation. In the tif zab-53 (pKM101) strain, repair and mutagenesis of UV-irradiated phage lambda was observed, but not in the lexB30 mutant carrying pKM101. The pKM101 mutant, pGW1, was unable to protect tif zab-53 bacteria against killing by UV, whereas the protection of lexB30 was intermediate; moreover, it did not promote the mutator effect at 30 degrees C or enhance phage repair and mutagenesis in tif zab-53 cells. All UV-induced bacterial mutations in lexB30 (pKM101) strain were suppressors; in contrast, true revertants were found after UV irradiation of the tif zab-53 (pKM101) cells. We suggest that the constitutive activity of RecA protein is enough for the production of UV-promoted suppressor mutations, whereas true reversions require a more active form of this protein which could exert its effects directly or by acting at a regulatory level on other cellular functions.

DNA Repair↗
PubMed1978

Influence of the recF143 mutation of Escherichia coli K12 on prophage lambda induction.

Prophage lambda induction in a recF143 mutant of E. coli K12 was studied. The recF143 (lambda) lysogen was inducible by UV irradiation or treatment with mitomycin C. However, the time required for the onset of derepression brought about by these treatments was longer in the recF143 mutant than in rec+ strains, suggesting that the induction pathway was altered in the recF143 mutant. The recF143 (lambda) lysogen was induced at very low doses of UV irradiation or mitomycin C treatment. Moreover, the presence of the recF143 mutation increased the sensitivity to thermal induction of a tif strain.

Coliphages↗
PubMed1977

Prophage induction in Escherichia coli K12 cells deficient in DNA polymerase I.

The induction of prophage lambda by ultraviolet light has been measured in E. coli K12 lysogenic cells deficient in DNA polymerase I. The efficiency of the induction process was greater in polA1 polC(dnaE) double mutants incubated at the temperature that blocks DNA replication than in polA+ polC single mutants. Similarly, the polA1 mutation sensitized tif-promoted lysogenic induction in a polA1 tif strain at 42 degrees. In strains bearing the polA12 mutation, which growth normally at 30 degrees, induction of the prophage occurred after the shift to 42 degrees. It is concluded that dissapearance of the DNA polymerase I activity leads to changes in DNA replication that are able, per se, trigger the prophage induction process.

Coliphages↗
PubMed1977

Characterization of lexB mutations in Escherichia coli K-12.

Two mutations have been located at the recA locus and phenotypically characterized along with a third one, previously called rec-34. The three mutants behaved similarly to lexA mutants. They were sensitive to ultraviolet (UV) light and X rays, and lambdaFec- phages were able to plate on them. The three mutations were called lexB because they could be distinguished from recA mutations by the last property. lexB mutants were less sensitive to UV and X irradiations than were recA mutants and were, to various degrees, recombination proficient. UV light failed to induce prophage lambda in all three lexB lysogens. In contrast, thymine starvation induced lexB31 and lexB34 lysogens. In lexB34 mutants, but not in lexB30 and lexB31 mutants, UV reactivation occurred at a low level. In Escherichia coli K-12, the recA gene has basic functions in the repair of deoxyribonucleic acid lesions, deoxyribonucleic acid recombination, and prophage induction. The three lexB mutations alter unequally and independently the three functions. This suggests that the recA and lexB mutations affect the same gene.

Chromosome Mapping↗
PubMed1976

Role of the bacterial and phage recombination systems and of DNA replication in genetic recombination of UV-irradiated phage Lambda.

In this paper are studied in E. coli K12 the influence of the bacterial Rec and phage mu Red recombination systems on the rescue of the O plus gene from the prophage by a superinfecting O minus phage, UV irradiated or not. In the absence of UV irradiation the Red system produces more recombinants than does the Rec system, and its action requires DNA replication. The presence of UV lesions in the mu DNA facilitates the action of the Rec system, which is more efficient in this instance than the Red system and can act in the absence of DNA replication. In all cases, there is a cooperation between the two generalized recombination systems.

Coliphages↗
PubMed1976

Effects and specificity of anticancer agents on the respiration and energy metabolism of tumor cells.

Using 35 new anticancer agents from the screening program of the National Cancer Institute we have performed a biochemical study of the effects on the respiration and oxidative phosphorylation of rat liver mitochondria and on the respiration of leukocyte, liver, L1210 leukemia, and Ehrlich ascites cell suspensions. Fifteen of the 35 compounds were found to be potent respiratory inhibitors as defined by 50% inhibition of mitochondrial respiration at concentrations of 110 mu mol/liter or less. The mechanism of respiratory inhibition by the drugs was either a rotenone-, antimycin-, or oligomycin-like effect. One triazine derivative showed some specificity for inhibiting tumor cell respiration in comparison with normal cell respiration. Two naphthoquinone derivatives showed inhibition of respiration in in vivo treatments at chemotherapeutic doses. It was concluded that data on respiratory effects may assist in the interpretation of the results of in vivo and in vitro screening tests of the drugs, and that in some cases, as with the naphthoquinone derivatives, the effects on respiration could be related to the mechanism of action or the mechanism of toxicity of the drugs.

Animals↗
PubMed1975

Recovery of phage lambda from ultraviolet damage.

Recovery of phage lambda from ultraviolet damage can occur, in the dark, through three types of repair processes as defined by microbiological tests: (1) host-cell reactivation, (2) prophage reactivation, and (3) UV reactivation. This paper reviews the properties of the three repair processes, analyzes their dependence on the functioning of bacterial and phase genes, and discusses their relationship. Progress in the understanding of the molecular mechanisms underlying the three repair processes has been relatively slow, particularly for UV reactivation. It has been shown that host-cell reactivation is due to pyrimidine dimer excision and that prophage reactivation is due to genetic recombination (prereplicative). We provide evidence showing that neither of these mechanisms accounts for UV reactivation of phage lambda. Furthermore, UV reactivation differs from the other repair processes in that it is inducible and error-prone. Whether UV-damaged bacterial DNA is subject to a similar repair process is still an open question.

Cell Survival↗
PubMed1975

E. coli K12 inf: a mutant deficient in prophage lambda induction and cell filamentation.

The bacterial mutant inf-3 (lambda) is not inducible and does not form filaments following thymine starvation. Lysogenic induction is neither produced by ultraviolet light (UV) nor promoted by tif-1. This phenotype is due to a mutation infA3 located between 60 and 73 min on the E. coli K12 map. The inf mutant is resistant to X-ray and UV irradiation, in contrast to all other known non-inducible bacterial mutants. It is Rec+ and able to perform host cell reactivation as well as UV-reactivation of phage lambda. After exposure to UV light, its DNA is degraded more than that of the parent and the resumption of DNA synthesis is delayed by 30 min; nevertheless, the cell survival is analogous to that of the parent. The inf mutant is also resistant to thymine starvation, for at least 3 hours. Wild type phage lambda forms clear plaques on a lawn of non-lysogenic inf bacteria; a corresponding low level of lysogenization is found. The capacity of inf bacteria to reproduce phages lambda, T4 or T6 is impaired. No gross defect in DNA transcription has been detected. Nevertheless, this mutant might have a slight alteration in the transcription process or in any other process involved in gene expression. This alteration might affect the regulation of DNA replication and cell division as well as prophage lambda induction.

Bacteriophage lambda↗
PubMed1973

Mitochondrial functions in five cases of human neuromuscular disorders.

We determined the respiration, respiratory control, and Pi:O ratios with different substrates in mitochondria isolated from five cases of human neuromuscular disorders (two cases of central core disease, two cases of neuropathy of Dejerine-Sottas, and one case of Kugelberg-Welander's disease) and compared them with normal human muscle. In all the myopathies studied, a severe derangement of the respiratory control with variable derangement of oxidative phosphorylation was found. This supports the idea that a group of neuromyopathies shares the same biochemical lesion as the so-called mitochondrial myopathies, forming with them a group of myopathies which may be related through a similar biochemical lesion of varying degree. Alternatively, disturbance of mitochondrial functions in a number of myopathies could be considered as a non-specific finding.

Adenosine Diphosphate↗