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Biomedical subjects

P D Cooper

Publications and source records attributed to P D Cooper.

9 recordsLinked to original sources
PubMed1978

Acetylenics. 2. Synthesis and pharmacology of certain N,N-diakyl-3-phenylpropyn-2-amines. Some analogues with tryptamine-like behavioral effects in mice.

A number of N,N-dialkyl-3-phenylpropyn-2-amines 7 have been prepared and tested for their biological action. Certain analogues show tryptamine-like behavior effects in mice. The tryptamine-like activity of these compounds appears to be controlled by their lipophilicity. These compounds show only weak inhibition of rat liver monoamine oxidase. Although these compounds exhibit tryptamine-like action, experiments seem to indicate that there is no interaction with the tryptamine receptors.

Alkynes↗
PubMed1976

Poliovirus proteins associated with the replication complex in infected cells.

Viral polypeptides associated with the membrane-free replication complex of poliovirus RNA were multiple in nature. The structural protein precursors [VP0, VP1, VP3] predominated, and because they were found in a cytoplasmic component with the same S value and density as the replication complex are likely to be attached to it in vivo. They were not present in the form of empty capsids. The electrophoretic polypeptide pattern of the membrane-bound replication complex was similar but showed a predominance of NCVPX or VP1, unless the cells were slightly depleted in amino acids when the non-structural polypeptide NCVP2 became important. Cystine was the only amino acid capable of reversing this depletion effect on its own.

Amino Acids↗
PubMed1975

Poliovirus temperature-sensitivie mutants defective in cytopathic effects are also defective in synthesis of double-stranded RNA.

The proportion of cells absorbing trypan blue (tb-+ character) can be used to measure the late c.p.e. of wild-type poliovirus (ts-+. tb-+), which was the same at restrictive (39-2 to 39-6 degrees C) or permissive (37 degrees C) temperatures. Of twenty ts mutants, seven showed normal c.p.e. at 37 degrees C but were defective in C.P.E. (TB) AT 39-5 degrees C; all seven tb mutants have previously been shown (Cooper et al. 1971) to give evidence of a primary defect in replicase 1 activity (to make the complementary or minus strand of virus RNA). The remainder (tb-+) have all previously been shown to give evidence of a primary defect either in replicase II activity (to make progeny plus strands) or in structural protein. Thus, the late c.p.e. is dependent on a product of the replicase I gene, of which the in vivo effector is probably double-stranded RNA. Late c.p.e. is not caused by prevention of host protein, RNA or DNA synthesis and is not necessarily correlated with lysosomal enzyme release. The tb mutants were also defective in inducing early changes in chromatin (chr) and in prevention of thymidine incorporation (pti), but the tb and pti/chr characters are probably independent expressions of replicase I activity. Virus growth does not depend on repression of DNA synthesis. Poliovirus represses the activities of host DNA-dependent RNA polymerase I and II to an equal extent. There is no evidence that repression of DNA or RNA synthesis results from direct interaction of virus protein with the DNA.

Acridines↗
PubMed1975

Attempts to extend the genetic map of poliovirus temperature-sensitive mutants.

Eighteen new ts mutants of poliovirus have been isolated after a variety of mutagenic treatments, and their loci identified in relation to the previous genetic map. The map was only extended by 25%, and the physiological characters of the new isolates corresponded in all aspects tested with those of the previous isolates. Apparently single mutants at the extreme left of the map were defective in synthesis of both double- and single-stranded RNA, functions that do not co-vary in other mutants. Two procedures respectively predicted to induce mutations preferentially in the 5' and 3' regions of the genome gave isolates which all indicated that the structural protein region was nearest the 5' end. The loci fro resistance to dextran sulphate and to ethyl-2-methylthio-4-methyl-5-pyrimidine carboxylate both lie in the structural protein region.

Chromosome Mapping↗
PubMed1975

Poliovirus polypeptides examined in more detail.

The pattern of viral polypeptide synthesis and cleavage in poliovirus-infected cells was shown by autoradiography to be considerably more complex than previously thought. In normal growth, at least 26 distinct polypeptides were found, and various modifications of the cleavage process revealed a total of at least 34. Most of the new polypeptides were minor components that were unstable during a chase. Different cultural modifications led to different polypeptide ratios, and it appeared likely that several cleavage activities were involved . Minor differences were found in the polypeptide contents of cytoplasmic extracts and whole infected cells. The complexity of the cleavage pattern necessitated a new nomenclature based on mol. wt. (e.g. Pp110, "poliovirus protein" of 110000). Particular attention was paid to mol. wt. determinations, notably in the use of internal protein standards and more fully denaturing gel conditions. The size of the "primary translation product" of poliovirus RNA was found to be 210000 daltons, so that either 20% of the viral genome is not translated in vivo, or some is read as a smaller independent translation unit.

Cell Line↗
PubMed1975

Relations between poliovirus polypeptides as shown by tryptic peptide analysis.

Poliovirus proteins were labelled in vivo with [35S]-methionine, and the major products of translation and cleavage were separated by electrophoresis and compared in terms of two-dimensional tryptic peptide maps visualized by autoradiography. The main intermediates p110 and p90 had few or no methionine-labelled sequences in common, but were both contained in, and therefore almost fully account for, the presumed primary translation product p210. The sequences of p79, a major stable product of cleavage and a non-structural protein, were almost completely contained in p90, which in turn is the major component of the larger intermediates p168 and p155. P110 is confirmed as the precursor of virus particle protein, and VP0 as the precursor of VP2. However, the sequences of p31, the other major product of translation that is not a stuctural protein, were not contained in any of the viral polypeptides mentioned above.

Autoradiography↗
PubMed1975

The genome of RNA tumor viruses: a functional requirement for a polyploid structure?

This paper points out certain theoretical problems in DNA synthesis associated with antiprimer transcription and with circularization that could oblige RNA tumor viruses to rely on a polyploid genome. It is suggested that each completed act of reverse transcription may be coupled with an act of genetic recombination aimed at recovering the antiprimer information from an adjacent genome subunit in a polyploid train. A partially double-stranded DNA transcript could then be formed with sufficient terminal redundancy to permit circularization. The model provides satisfactory explanations for observed genetic interactions (particularly recombination and heterozygote formation), for inactivation data and for selective subunit transcription.

DNA, Viral↗