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Biomedical subjects

C Kerr

Publications and source records attributed to C Kerr.

54 records · Page 3Linked to original sources
PubMed1974

Packaging and maturation of DNA of bacteriophage T7 in vitro.

We have developed an in vitro complementation assay to demonstrate packaging and maturation of DNA of phage T7. Cells of Escherichia coli B infected with an appropriate T7 amber mutant are concentrated 200-fold and lysed by freezing and thawing. Two extracts from cells infected with different amber mutants are mixed and incubated at 30 degrees . Positive complementation results in a 100-fold increase in phage titer. Using this assay we have demonstrated the packaging of phage DNA from an extract that contains no phage heads (gene 9(-), 10(-)), within head structures present in an extract that contains no phage DNA (gene 5(-)). We have also demonstrated an activity in extracts that contain no phage DNA or heads (gene 5(-), 9(-), 10(-)), which complements gene 19(-)-infected cells. We have proven that this activity is due to the gene-19 product by showing that the activity is temperature-sensitive if the extract is made from cells infected with a mutant having a temperature-sensitive mutation in gene 19. This assay should be useful in elucidating the mechanism of packaging and maturation of DNA of phage T7.

Cell-Free System↗
PubMed1970

Degradation of Escherichia coli B deoxyribonucleic acid after infection with deoxyribonucleic acid-defective amber mutants of bacteriophage T7.

The degradation of bacterial deoxyribonucleic acid (DNA) was studied after infection of Escherichia coli B with DNA-negative amber mutants of bacteriophage T7. Degradation occurred in three stages. (i) Release of the DNA from a rapidly sedimenting cellular structure occurred between 5 and 6 min after infection. (ii) The DNA was cleaved endonucleolytically to fragments having a molecular weight of about 2 x 10(6) between 6 and 10 min after infection. (iii) These fragments of DNA were reduced to acid-soluble products between 7.5 and 15 min after infection. Stage 1 did not occur in the absence of the gene 1 product (ribonucleic acid polymerase sigma factor), stage 2 did not occur in the absence of the gene 3 product (phage T7-induced endonuclease), and stage 3 did not occur in the absence of the gene 6 product.

Carbon Isotopes↗
PubMedDate not supplied

Analysis of human T-lymphotrophic virus sequences in multiple sclerosis tissue.

Several observations suggest that retroviral infection is involved in the pathogenesis of the human demyelinating disease multiple sclerosis (MS). First, lymphadenopathy-associated virus/human T-lymphotropic virus type III (LAV/HTLV-III), the agent of acquired immune deficiency syndrome (AIDS), has been shown to be neurotropic in man. Second, the genetic organization of the lentivirus visna, which causes a chronic demyelinating disease of sheep, closely resembles that of LAV/HTLV-III. Recently, Koprowski and colleagues reported that MS is associated both with raised levels of circulating antibodies to HTLV-I and with the presence of HTLV-I-specific RNA within cell lines derived from the cerebrospinal fluid (CSF). Here we report that no HTLV-I-like or LAV/HTLV-III-like sequences can be detected, by in situ hybridization, in central nervous system (CNS) tissues from MS patients, and that nonspecific HTLV-I-like signal in peripheral blood mononuclear cells or in CSF cell lines is characteristic of MS. Furthermore, enzyme-linked immunosorbent assay (ELISA) analysis of circulating and CSF antibodies for HTLV-I reactivity fails to distinguish between MS and control groups.

Antibodies, Viral↗
PubMedDate not supplied

Heat-induced damage to HeLa-S3 cells: correlation of viability, permeability, osmosensitivity, phase-contrast light-, scanning electron- and transmission electron-microscopical findings.

The responses of HeLa S-3 to mild hyperthermia for relatively critical times at 43 and 45 degrees C were analysed in detail, including growth and colony-forming ability, permeability, osmotic sensitivity and microscopical appearances. For comparative purposes lower temperatures (e.g. 41 degrees C) and higher temperatures (50 and 55 degrees C) were used in some experiments. The evidence from many different aspects, including scanning and transmission electron microscopy, suggests that critical heat exposures do not per se cause severe membrane damage and loss of cell integrity, but changes quickly become manifest when cells are 'recovered' by returning to 37 degrees C. Attention is drawn to the ability of heat-treated cells to show osmotic-like swelling and restoration towards normal volume in medium of 30 per cent normal strength, which would not be expected on the hypothesis that hyperthermia primarily disrupts membrane structure and functioning. Ultrastructural changes during and after hyperthermia--including nucleolar changes, the appearance of perichromatin granules, the formation of electron-dense cytoplasmic clusters, and the development of intranuclear actin rods--corroborate and extend other findings. However, mitochondrial changes were found to be particularly significant, appearing early and correlating well with the loss of viability and metabolic functioning found after heat treatment. These include the early development of intramitochondrial dense granules, followed by vesicularization of the cristae, swelling of the intracristal spaces, myelin degeneration and the formation of bodies which could otherwise be mistaken for secondary lysosomes. The findings indicate the need for more intensive investigations of mitochondria and mitochondrial functioning in hyperthermia-induced cell damage, and their careful correlation with the 'recovery' of energy-dependent process in cells subsequently returned to 37 degrees C.

Cell Division↗