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Biomedical subjects

J Bonner

Publications and source records attributed to J Bonner.

At least 127 records · Page 7Linked to original sources
PubMed1971

Fractionation of liver chromatin.

Rat liver chromatin has been fractionated into two fractions on the basis of precipitability in standard saline after mild treatment with DNase II. The major portion of liver chromatin contains little nonhistone protein and is enriched in histones, while a minor portion of such chromatin, with which RNA polymerase is associated, is highly enriched in proteins other than histone and impoverished in histones. Although the relative concentrations of the several histone species present in two chromatin fractions are identical, binding of histones to DNA in the minor fractions appears to be modified, presumably by the presence of proteins other than histones.

Animals↗
PubMed1971

Association of chromosomal RNA with repetitive DNA.

Chromosomal RNA, which is a component of the chromosomes of higher organisms, and whose participation is required for sequence-specific interaction of chromosomal proteins with chromosomal DNA, occurs in chromosomes bound to DNA. We have found that the DNA sequences to which chromosomal RNA binds are repetitive ones.

Chromosomes↗
PubMed1970

Template activity of liver chromatin increased by in vivo administration of insulin.

The hypothesis that insulin may serve as a derepressor of genetic information in the liver of diabetic rats has been tested by comparing the template activity for RNA synthesis of chromatin from liver of insulin-treated diabetic rats to that of chromatin from liver of insulin-deficient diabetic rats. The template activity of the chromatins of insulin-treated diabetic rats is found to be 28 per cent greater than that of chromatin from liver of diabetic rats not treated with insulin. Time course studies show that the template activity of liver chromatin of rats injected with a single dose of insulin reaches a peak at two hours, which is some hours before the appearance of a typical insulin-induced liver enzyme, glucokinase. We conclude that insulin derepresses genetic material of the diabetic liver genome that is repressed in the absence of insulin.

Animals↗