A method for linking fluorescent labels to polynucleotides: application to studies of ribosome-ribonucleic acid interactions.
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Biomedical subjects
Publications and source records attributed to L Gold.
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The gene 32 protein of the bacteriophage T4 plays an important role in genetic recombination, DNA repair, and DNA replication; the protein functions in these processes by virtue of a strong binding capacity for single-stranded DNA. During infections of Escherichia coli by bacteriophage carrying amber of temperature-sensitive mutations in gene 32, the altered gene 32 protein (that is, the amber fragment of the missense polypeptide) is synthesized at greatly elevated rates. During infections by phages that are mutant in other genes (and wild type in gene 32), gene 32 expression is coupled to the quantity of single-stranded DNA produced during the infection. The data are consistent with a model in which the gene 32 protein binds preferentially to all available single-stranded DNA. When all available single-stranded DNA is complexed with gene 32 protein, free gene 32 protein represses its own synthesis. The high level expression of altered gene 32 proteins (amber fragments or missense polypeptides) is a direct consequence of the proposed autoregulation.
Functional half-life measurements of the bacteriophage T4 gene 32 messenger RNA indicate that this mRNA is extremely stable. Regulation of gene 32 expression at the transcriptional level cannot account for the rapidity with which P32 synthesis can be repressed. Furthermore, derepression of P32 synthesis occurs in the presence of rifampicin, a drug which inhibits transcriptional initiation. In addition, T4-infected cultures in which P32 expression is repressed possess almost as much gene 32 mRNA as derepressed cultures. We conclude that expression of the T4 gene 32 protein is regulated at the level of translation.
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The affected teeth in this case of odontodysplasia exhibited abnormal hypoplastic enamel, abnormal dentin containing extensive interglobular regions and completely lacking a peritubular matrix, and an abnormal irregular tissue consisting of highly calcified and partially fused granules located within the dentin of the tooth tips. Electron micrographs of the irregular tissue showed that the granules consisted of crystallites densely and radically packed in a noncollagenous amorphous matrix. Granules were surrounded by a slightly calcified, irregularly arranged, collagenous matrix. The irregular tissue formed in the pulp of the tooth tip befofe and independently of the dentin. It was at least partially formed by pulpal calcification. Abnormal dentin matrix was formed by odontoblasts which were less differentiated than normal. Odontodysplastic teeth showed abnormal differentiation of odontoblasts and ameloblasts resulting in defective enamel and dentin and, in extreme cases, in extensive pulpal calcification.
T-even coliphages have 5-hydroxymethylcytosine in their DNA instead of cytosine. In some T4 mutants, the replicated DNA contains cytosine, but then no late gene products are made. We show that the inability to make late gene products with cytosine-containing T4 DNA is due to a T4 gene products. This gene product, while probably nonessential under normal conditions, interacts with an essential part of the transcription apparatus. Mutations in this gene allow viable T4 particles to be made whose DNA has been substituted almost 100% with cytosine.
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Selective internal carotid arteriography was performed on a patient subsequently shown at surgery to have a primary carcinoma of the sphenoid sinus. The arteriogram demonstrated supply to the tumor from numerous hypertrophied branches of the cavernous portion of the internal carotid artery and a dense tumor stain within the sphenoid sinus. This is the first such report found in the literature.
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