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Biomedical subjects

J K Setlow

Publications and source records attributed to J K Setlow.

At least 91 records · Page 5Linked to original sources
PubMed1970

Repair of ultraviolet-irradiated transforming deoxyribonucleic acid in Haemophilus influenzae.

Ultraviolet-sensitive and wild-type Haemophilus influenzae cells were exposed to irradiated and unirradiated transforming deoxyribonucleic acid (DNA) containing a marker which can be linked to another marker in the cells. Lysates were made after various times of incubation and assayed for transforming activity on an excisionless recipient. Repair can be noted as an increase in activity from the irradiated donor DNA after its linkage to the recipient DNA. No repair can be observed in a mutant which is unable to integrate transforming DNA. There is a little repair in another mutant which is unable to excise pyrimidine dimers. H. influenzae cells also repair nondimer damage, as judged by the increase in activity observed in lysates made with irradiated and maximally photoreactivated DNA.

DNA Replication↗
PubMed1970

Endonuclease from Micrococcus luteus which has activity toward ultraviolet-irradiated deoxyribonucleic acid: its action on transforming deoxyribonucleic acid.

An endonuclease purified from Micrococcus luteus makes single-strand breaks in ultraviolet (UV)-irradiated, native deoxyribonucleic acid (DNA). The purified endonuclease is able to reactivate UV-inactivated transforming DNA of Haemophilus influenzae, especially when the DNA is assayed on a UV-sensitive mutant of H. influenzae. After extensive endonuclease action, there is a loss of transforming DNA when assayed on both UV-sensitive and -resistant cells. The endonuclease does not affect unirradiated DNA. The results indicate that the endonuclease function is involved in the repair of biological damage resulting from UV irradiation and that the UV-sensitive mutant is deficient in this step. We interpret the data as indicating that the various steps in the repair of DNA must be well coordinated if repair is to be effective.

DNA, Bacterial↗
PubMed1970

Transformation between Haemophilus influenzae and Haemophilus parainfluenzae.

Heterospecific transformation between Haemophilus influenzae and H. parainfluenzae is from one to more than six orders of magnitude lower than homospecific transformation, depending on the marker assayed. However, the physical integration of deoxyribonucleic acid (DNA) in heterospecific compared with homospecific transformation is only slightly decreased. Measurement of integration of ultraviolet-irradiated heterospecific transforming DNA suggests that compared with homospecific DNA a longer piece of heterospecific transforming DNA must undergo pairing for integration to occur. Heterospecific transforming DNA behaves towards ultraviolet inactivation of biological activity as though it had undergone some previous inactivation. The efficiency of heterospecific transformation can be improved by light sonic treatment of the DNA or by the use of DNA containing markers which originated from the heterospecific recipient. The presence of an excision mechanism in the recipient cell does not affect killing or marker efficiency in heterospecific transformation. The data indicate that the low frequency of transformation between H. influenzae and H. parainfluenzae results mostly from lethality. It is proposed that integration of heterospecific transforming DNA results in alterations in the base sequence of the recipient genome which cannot be repaired. Transcription and translation of the altered DNA could result in synthesis of nonfunctional essential proteins.

DNA, Bacterial↗
PubMed1969

Ultraviolet inactivation and photoproducts of transforming DNA irradiated at low temperatures.

Solutions of Haemophilus influenzae transforming DNA were irradiated at temperatures ranging from 25 degrees C to - 196 degrees C. Temperature dependence of the formation of thymine-containing dimers was closely correlated with inactivation of transforming activity; in general, both dimerization and inactivation decreased with decreasing temperature. The fraction of nonphotoreactivable damage increased with increasing dose at low temperatures. The nonphotoreactivable spore-type photoproduct was formed at low temperatures with a maximum at - 100 degrees C, a temperature at which the nonphotoreactivable biological inactivation was also a maximum. Intrastrand cross-linking, like dimer formation, decreased with decreasing irradiation temperature.

Chromatography, Paper↗
PubMed1969

Killing of Haemophilus influenzae cells by integrated ultraviolet-induced lesions from transforming deoxyribonucleic acid.

Highly competent cultures of Haemophilus influenzae are inactivated by exposure to transforming deoxyribonucleic acid (DNA) irradiated with ultraviolet light (UV). As a function of UV dose to the DNA, the killing goes to a maximum and then decreases. The killing of H. influenzae by unirradiated H. parainfluenzae DNA, reported by other workers, is enhanced by low doses of UV, but drops off at high doses. Since there are no such lethal effects in a strain of H. influenzae that takes up DNA normally but does not integrate it, it is concluded that the killing is associated with integrated UV lesions. All the killing of wild-type cells due to irradiated DNA is eliminated by photoreactivation of the DNA. The killing of an excisionless strain of H. influenzae, however, is not eliminated by maximal photoreactivation of the irradiated transforming DNA. The nonphotoreactivable fraction of killing in the excisionless strain increases with increasing dose. The kinetics of the killing-dose curves may be explained only partially in terms of UV-induced loss of integration. It is postulated that the number of pyrimidine dimers relative to other DNA components integrated decreases at higher UV doses.

DNA, Bacterial↗
PubMed1969

Synthesis of deoxyribonucleic acid after ultraviolet irradiation of sensitive and resistant Haemophilus influenzae.

Synthesis of deoxyribonucleic acid (DNA) has been measured as a function of ultraviolet (UV) radiation dose in wild-type and seven UV-sensitive strains of Haemophilus influenzae. At the UV doses used, all strains were able to resume DNA synthesis, even those which are unable to excise pyrimidine dimers from their DNA. These excisionless strains showed longer UV-induced delays in DNA synthesis than all but one of the other strains. The longest delay was shown by DB117, a strain which can excise dimers but which is recombination deficient and unable to rejoin X ray-induced single-strand breaks. All strains showed a progressive decrease in sensitivity as they approached the stationary phase.

DNA, Bacterial↗
PubMed1968

Repair of deoxyribonucleic acid in Haemophilus influenzae. I. X-ray sensitivity of ultraviolet-sensitive mutants and their behavior as hosts to ultraviolet-irradiated bacteriophage and transforming deoxyribonucleic acid.

Seven mutants of Haemophilus influenzae were isolated by the criterion of sensitivity to ultraviolet (UV) inactivation of colony formation. These mutants and the wild type were characterized with regard to X-ray inactivation of colony formation, UV induction of division inhibition, the ability of the eight strains to act as recipients to UV-irradiated H. influenzae phage and transforming deoxyribonucleic acid (DNA), and the influence of acriflavine on the survival of UV-irradiated transforming DNA with these strains as recipients. The photoreactivable sector of transforming DNA with yeast photoreactivating enzyme was measured for the most UV-sensitive mutant and was found to be greater than that of wild type. Judged by the above criteria, the order of the strains' sensitivities shows some, but by no means complete, correlation from one type of sensitivity characterization to another, indicating that a minimum of two variables is needed to explain the differences in the strains. Acriflavine increases the UV sensitivity of transforming DNA except in the most sensitive mutant. This effect is usually, but not always, more pronounced in the case of the more UV-resistant marker. The acriflavine effect is postulated to be the result of at least two factors: (i) interference with repair of transforming DNA in the host cell, and (ii) interference with the probability of recombination between transforming DNA and host DNA.

Acridines↗