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C W Gibson

Publications and source records attributed to C W Gibson.

42 records · Page 3Linked to original sources
PubMed1984

Analysis of initiation of sites of cell wall growth in Streptococcus faecium during a nutritional shift.

Three-dimensional reconstruction methods were applied to electron micrographs of Streptococcus faecium to study the initiation of cell wall growth sites during a nutritional shift experiment. Upon lowering the mass doubling time from 76 to 33 min by the addition of excess glutamate, the formation of new cell wall growth sites accelerated above the old steady-state rate at about the same time (10 to 15 min) as did mass, RNA, protein, cell numbers, and autolytic capacity but considerably before DNA (30 min) and peptidoglycan (20 min) synthesis did. During the shift, the average range of cell volumes over which new wall growth sites were introduced did not change significantly. However, upon the shift there was an increase in the frequency of cells having new sites, which was due to the faster-growing cells initiating more new sites in peripheral locations before division. After a transition period, the number of new sites per milliliter of culture increased at a rate that paralleled that of the culture mass. These findings support a model in which new sites are introduced when cells grow to a relatively constant, growth rate-independent size, while the rate at which sites form and grow increases with the growth rate. In this model, chromosome synthesis does not regulate the formation of new sites of cell wall growth, but existing sites cannot be completed until rounds of chromosome synthesis are completed.

Bacterial Proteins↗
PubMed1983

Initiation of wall assembly sites in Streptococcus faecium.

In electron micrographs of replicas of Streptococcus faecium, sites of wall growth are located between pairs of raised equatorial bands. Analysis of cells taken from cultures with mass doubling times between 30 and 125 min indicates that rounds of wall synthesis are initiated at a time close to division, which is temporally unrelated to the initiation or termination of chromosome replication. Growth sites are initiated at a relatively constant volume independent of growth rate when the volume contained within the two segments of wall adjoining an equatorial band marker approaches ca. 0.26 micrometer 3.

Cell Division↗
PubMed1983

Cell wall assembly during inhibition of DNA synthesis in Streptococcus faecium.

Growth sites which are bounded by raised wall bands can be observed in electron micrographs of replicas of Streptococcus faecium. When mitomycin C was added to an exponential-phase culture doubling in mass every 64 min, DNA synthesis was inhibited, and eventually cell division stopped. The growth sites formed before and after inhibition of DNA synthesis enlarged until they contained about 0.25 micron3 of cell volume, at which point they ceased to increase in size. When these sites approached this 0.25-micron3 limit, new sites were initiated; this result had also been observed in untreated cells undergoing a large range of exponential-phase mass doubling times. Thus, regardless of whether chromosome replication is inhibited or uninhibited, sites have the same finite capacity to enlarge to about 0.25 micron3, and when this capacity is reached, new sites are initiated. Although initiation of new growth sites seems to be independent of normal chromosome replication, these results confirm previous studies showing that chromosome replication is necessary for the terminal events of growth site development which result in the division of a site into two separate poles. Two classes of models for the regulation of growth site initiation are discussed.

Cell Wall↗
PubMedDate not supplied

Analysis of nutritional shift-up of Streptococcus faecium.

Three-dimensional reconstruction methods were applied to electron micrographs of Streptococcus faecium to study the initiation of cell wall growth sites during a nutritional shift-up experiment. Upon lowering the mass doubling time from 76 to 33 min by the addition of excess glutamate, the formation of new cell wall growth sites was studied in relation to other growth parameters (autolytic capacity, cell number, mass, RNA, DNA and peptidoglycan). The findings from these studies, to be described below, support a model in which new sites are introduced when cells grow to a relatively constant, growth-rate-independent size, while the rate at which sites form and grow increases with growth rate. In this model, chromosome synthesis does not regulate the formation of new sites of cell wall growth, but existing sites cannot be completed until rounds of chromosome synthesis are completed.

Cell Wall↗
PubMedDate not supplied

p53 influences mice skeletal development.

The p53 tumor suppressor gene encodes a transcriptional activator whose targets include genes that regulate cell cycle progression and apoptosis. Since we have shown that a critical event in the life history of the chondrocyte is programmed cell death, we asked the question: does loss of the p53 gene influence skeletogenesis? Female p53(+/-) mice were mated with p53(+/-) male mice and 17-day-old fetal mice were studied. Exencephaly was the most profound skeletal defect of the p53 null mutation. This defect was due to failure of formation of the bones that comprise the mouse calvarium. There was also loss of the hyoid bone, and defective mineralization of the manubrium sternum and the terminal phalanges. In the homozygous state (-/-), in the absence of exencephaly, the number of skeletal deformities was markedly reduced. Aside from the gross changes associated with null status, the mutants exhibited alterations in bone length and width. Small differences in the size and orientation of the mineral crystals in embryonic bone, as evaluated by small-angle X-ray scattering, were found to disappear after birth. To explain these observations, we evaluated the extent of apoptosis in the tibial growth plates using the TUNEL stain. In the growth plate of the p53(-/-) homozygote, there was minimal labeling of the hypertrophic layer. Since the p53(-/-) TUNEL stain pattern at 17 days was very similar to the pattern of labeling of the p53(+/+) at 15 days, we concluded that the growth defect reflected a delay in cartilage maturation rather than a change in chondrocyte phenotype. On this basis, we predict that after birth, in mice that survive, differences in bone length would become minimal, and at maturity, the length of the long bones of (+/+) and (-/-) mice would be similar.

Animals↗