Oncogenic viruses: the last twelve years.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R Dulbecco.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The fate of polyoma form IDNA generated during replication was investigated in resting BALB-3T3 cells. The experiments showed that there was extensive re-entry of such molecules into replication. This process took place over a period of several hours and appeared to be random. Progeny form I molecules must, therefore, spend some time in a nonreplicating pool before reinitiating replication. We propose that two factors affect the fate of progeny form IDNA. (i) The rate of reinitiation of progeny molecules is determined by the capacity of the initiation machinery. (ii) The extent of re-entry is determined by the availability of maturation proteins which divert form I from replication.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A kinetic study of the early changes in uridine- and phosphate-transport rates and 3':5'-cyclic AMP levels induced by the addition of serum to quiescent 3T3 cells revealed that the increase in phosphate uptake and the decrease in the intracellular concentration of 3':5'-cyclic AMP immediately follow the addition of serum. In contrast, the increase in uridine transport occurred after a lag of several minutes and was clearly preceded by the other changes. The activation of phosphate transport involved an increase in V(max), while a more complex pattern was observed for uridine transport. A possible role of phosphate in connection with the other early events was also studied. The addition of phosphate to quiescent cells produced a time-dependent decrease in 3':5'-cyclic AMP levels and this ion was required for full activation of uridine transport by serum. The results show that the increase in phosphate transport is a primary event in the reinitiation of growth and suggest that the increase in phosphate transport may be connected with subsequent metabolic steps.
The T antigen of simian virus 40, which may play a role in the control of viral DNA replication, is recovered from nuclei of cells transformed by simian virus 40 in several forms sedimenting at different rates. The large molecular weight forms are converted to the smallest (5 S) form by high salt, suggesting that they differ in the degree of aggregation. All the forms of the antigen bind efficiently to double-stranded DNA-cellulose columns at pH 6.2 and low salt, and elute in two fractions: one at pH 8.0 and low salt, the other at pH 8.0 and high salt. The antigen has little affinity for single-stranded DNA.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Nuclei from secondary mouse-embryo cells contain an activity capable of untwisting closed-circular DNAs containing either negative or positive superhelical turns. The activity has no apparent effect on a closed-circular DNA containing no superhelical turns, and is not due to the combined action of an endonuclease and polynucleotide ligase. The enzyme apparently acts by introducing a single-strand nick into the DNA, forming a DNA-enzyme complex that allows the strands to rotate relative to the helix axis before reversing the reaction and sealing the break. The enzyme might possibly serve as a swivel during DNA replication.
The proteins of purified Simian virus 40 (SV40) were examined by sodium dodecyl sulfate-acrylamide gel electrophoresis and compared with the polypeptides synthesized in SV40-infected monkey cells. Purified virions contain two major components, with molecular weights of 44,000 and 31,000. Together they make up 83% of the total virion proteins. In addition, the virus contains 12 minor polypeptides, which are believed to be cellular proteins, or peptides derived from proteolytic degradation of the 44,000 molecular weight polypeptide. Pulse-label experiments show that about 90% of the polypeptides synthesized after SV40 infection are host-cell proteins; 10% represent the two major structural components of the virion. A small fraction (about 0.5%) consists of three polypeptides (molecular weights 70,000, 60,000, and 8,000) that are neither part of the virion nor detectable in uninfected cells. They are either virus-induced cellular proteins or, more likely, proteins coded for by the SV40 genome.
Strand orientation of transcription in BSC-1 cells infected by simian virus 40 (SV40) was investigated by annealing RNAs extracted from infected cells with asymmetric complementary RNA from SV40 DNA synthesized in vitro by RNA polymerase from Escherichia coli. The results suggest that the early viral RNA sequences (those made before replication of viral DNA) and the late RNA sequences (those synthesized concurrently with replication of viral DNA) are transcribed from opposite strands of the SV40 DNA. The RNA synthesized in vitro is of the same polarity as the early in vivo RNA and is complementary to the late in vivo RNA. Knowledge of strand selection in lytic infection is a step towards understanding the regulation of transcription of this viral DNA.
Complete hybrids of simian virus 40 (SV40)DNA and its complementary RNA (cRNA) are not retained on nitrocellulose membranes. At saturating cRNA concentrations, retention of the hybrids indicates incomplete homology between DNA and RNA, probably due to incorporation of host DNA in the viral DNA; this effect is most pronounced when DNA is produced in cells infected at high multiplicity. Hybrids between DNA of Chinese hamster cells transformed by SV40 and cRNA are retained if the DNA fragments are long, but they are lost if the DNA is sheared to less than the length of an SV40 DNA molecule. Hence, in cells examined with about six SV40 genomes per cell, each genome is individually integrated. The results may explain previous discrepancies in the estimation of the number of viral genomes in transformed cells.
Explore the source record for details and available documents.
Infection of BALB/3T3 cells by polyoma virus causes an alteration in the cell surface, characterized by enhanced agglutination of the cells by wheat germ agglutinin or concanavalin A. Infection by the thermosensitive mutant of polyoma, ts-3, causes the cell surface alteration at the permissive temperature, but not at the nonpermissive temperature. The cell surface alteration requires cellular DNA synthesis, but not viral DNA synthesis. BHK cells transformed by ts-3 show the surface alteration when grown at the permissive temperature, but not when grown at the nonpermissive temperature. It is concluded that the surface alteration in transformed cells is under the control of a viral gene.