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J S Colter

Publications and source records attributed to J S Colter.

At least 19 recordsLinked to original sources
PubMed1985

Transformation of hamster embryo cells by chymotrypsin-treated and untreated polyoma virus: characterization of transformants.

The ability of chymotrypsin-treated (chymo+) and untreated (chymo-) polyoma virus to transform cultured hamster embryo fibroblasts was examined. The data show that exposure to this protease reduces the ability of the virus to transform non-permissive cells to essentially the same extent as it reduces its ability to replicate in permissive cells. Twenty-five lines of transformed cells were established from colonies growing in soft agar, and after 20 in vitro passages, cells of all lines were characterized with respect to their ability to form colonies in soft agar and their tumorigenicity in hamsters. While the studies showed that there are striking differences among the lines with respect to colony-forming ability, and real, though less striking differences in tumorigenicity, they failed to reveal any obvious differences between the groups of cell lines transformed by chymo- and chymo+ polyoma virus. Of 13 lines examined, all were found to express both middle and small polyoma T antigens, none express significant levels of large T antigen, and 11 express some form of what is probably a truncated large T antigen, the most common species having a molecular weight of 67000.

Animals↗
PubMed1984

Rescue of BKV from BKV-transformed hamster, rat, and mouse cells: correlation with levels of nonintegrated viral DNA.

Infectious BKV was rescued from 39 of 40 lines of virus-free, BKV-transformed hamster, rat, and mouse cells, which had been either maintained continuously in culture or reestablished in culture after one or more passage in the appropriate host, by Sendai virus-catalyzed fusion with permissive cells. Striking differences were observed among the 39 lines with respect to the efficiency of virus rescue. Fourteen of the lines were examined for the presence of nonintegrated viral DNA by dot-blot hybridization. The values obtained, which ranged from less than 1 to 2880 viral genome equivalents/cell, reveal a strong correlation between the efficiencies with which BKV can be rescued from these lines and the amounts of free viral DNA that they contain.

Animals↗
PubMed1984

Evidence that polyoma polypeptide VP1 is a serine protease.

It has been shown that when purified polyoma (Py) virions are dissociated by incubation in 150 mM NaCl-50 mM Tris-HCl (pH 8.5) containing 1 mM EGTA and 3 mM DTT, two new polypeptides (MW 43.5K and 40K) are produced by proteolysis of virion polypeptide VP1. Proteolysis is blocked by diisopropyl fluorophosphonate (DFP) and phenylmethyl sulfonyl fluoride (PMSF), suggesting that the virion-associated enzyme is a serine protease. When Py virions were dissociated in the presence of radiolabeled DFP, only VP1 became labeled to any significant extent, which suggests that the protease activity is a property of this viral polypeptide and that the 43.5K and 40K species are produced by autodigestion.

Electrophoresis, Polyacrylamide Gel↗
PubMed1979

Isolation and characterization of BK virus-transformed rat and mouse cells.

The isolation and characterization of four groups of BK virus (BKV)-transformed rat embryo fibroblast (RE) and mouse kidney (MK) cells are described. They consist of (1) seven RE lines transformed with a BKV pool containing a high proportion of defective virions, and (2) 16 RE, (3) 14 Balb/c-MK and (4) 2 Swiss ICR-MK lines, all transformed, at different input multiplicities, with a pool of BKV free of defective virions. None of the lines produces BKV, all contain BKV T antigen and all grow to higher saturation densities and have higher plating efficiencies than do the corresponding control cells. Cells of the RE lines, transformed with the BKV pool containing defective virions, form colonies in soft agar and produce tumours in irradiated weanling rats, while those of the RE lines transformed with the defective virion-free pool do neither. Cells of the Balb/c-MK, but not of the ICR-MK lines are tumorigenic, although cells of both groups form colonies in soft agar. In general, those lines transformed at higher multiplicities express the biological properties associated with transformation more strongly than do those transformed at lower multiplicities.

Animals↗
PubMed1979

Studies of two temperature-sensitive mutants of Mengo virus.

Studies of the synthesis of viral ribonucleates and polypeptides in cells infected with two RNA- ts mutants of Mengo virus (ts 135 and ts 520) have shown that when ts 135 infected cells are shifted from the permissive (33 degrees C) to the nonpermissive (39 degrees C) temperature: (i) the synthesis of all three species of viral RNA (single stranded, replicative form, and replicative intermediate) is inhibited to about the same extent, and (ii) the posttranslational cleavage of structural polypeptide precursors A and B is partially blocked. Investigations of the in vivo and in vitro stability of the viral RNA replicase suggest that the RNA- phentotype reflects a temperature-sensitive defect in the enzyme. The second defect does not appear to result from the inhibition of viral RNA synthesis at 39 degrees C, since normal cleavage of polypeptides A and B occurs in wt Mengo-infected cells in which viral RNA synthesis is blocked by cordycepin, and at the nonpermissive temperature in ts 520 infected cells. Considered in toto, the evidence suggests that ts 135 is a double mutant. Subviral (53S) particles have been shown to accumulate in ts 520 (but not ts 135) infected cells when cultures are shifted from 33 to 39 degrees C. This observation provides supporting evidence for the proposal that this recently discovered particle is an intermediate in the assembly pathway of Mengo virions.

Animals↗
PubMed1978

Observations on the growth and plaque assay of BK virus in cultured human and monkey cells.

Although human embryo kidney (HEK), muscle (HEM) and lung (HEL) cells are capable of supporting the replication of BK virus (BKV) through passage levels 9, 12 and 12 respectively, only third, fourth and fifth passage level HEK cells were found to be satisfactory for the plaque assay of the virus. BSC-I and VERO cells can also be used for the plaque assay of BKV. However, in HEK cells plaques can be visualized in 20 days (compared to 28 days in BSC-I cells), and since in VERO cells the plaques are poorly defined and the titre about I log10 lower than in either HEK or BSC-I cells, HEK cells were the ones chosen for use.

Animals↗