J/Psi and Psi' total cross sections and formation times from data for charmonium suppression in pApA collisions

The recent data for E866 experiment on the x_F dependence for charmonium suppression in pA collisions at 800 GeV are analyzed using a time- and energy-dependent preformed charmonium absorption cross section \sigma_{abs}^\psi(\tau,\sqrt{s}). For \sqrt{s}=10 GeV the initially (\tau=0) produced premeson has an absorption cross section of \sigma_{pr}~3mb. At the same energy but for \tau -> \infty one deduces for the total cross sections \sigma_{tot}^{J/Psi N}=(2.8\pm 0.3)mb, \sigma_{tot}^{J/Psi N}= (10.5\pm 3.6)mb. The date are compatible with a formation time \tau_{1/2}=0.6 fm/c.Comment: 13 pages of Latex including 2 figures; typos in the abstract are correcte

Induction of mouse type-C virus by translational inhibitors: evidence for transcriptional derepression of a specific class of endogenous virus.

Several biologically distinguishable type-C RNA viruses are genetically transmitted in mouse cells. In the present report, chemicals that inhibit several different steps in protein synthesis are shown to cause marked increases in the cellular concentration of virus-specific RNA and the subsequent induction of virus. Analysis of the effect of translational inhibitors on mouse embryo cells of different genotypes indicates that activation of viral RNA is specific for one endogenous virus class and is a dominant genetic characteristic. Two lines of evidence favor the hypothesis that the induction of viral RNA involves transcriptional derepression rather than an alteration in its post-transcriptional processing. First, nuclear and cytoplasmic fractions of induced cells are shown to demonstrate similar increases in their concentrations of virus-specific RNA. Second, the decay of induced viral RNA following inhibition of further RNA synthesis by actinomycin D is not prevented by continued exposure to the inducer. These findings weigh heavily against the possibility that translational inhibitors act to stabilize viral RNA post-transcriptionally. The results are consistent with a model in which the expression of one class of endogenous virus is regulated by a labile repressor protein acting at a transcriptional level

Segregation of genetic information for a B-tropic leukemia virus with the structural locus for BALB:virus-1.

A B-tropic type-C RNA virus isolatable from lymphoreticular tumors of the inbred BALB/c mouse strain has previously been shown to be leukemogenic in its natural host. This virus is not chemically inducible from BALB/c embryo cells or from embryo lines containing segregating inducibility loci for two known endogenous type-C viruses of BALB/c cells. Molecular hybridization and type-specific immunologic assays demonstrate a high degree of genetic homology between the B-tropic leukemia virus and BALB:virus-1, an N-tropic endogenous virus of BALB/c cells. Genetic sequences specific for BALB:virus-1 are shown to segregate with the locus for BALB:virus-1 induction in genetic crosses between BALB/c and the noninducible NIH Swiss strain. Thus, if the information of the B-tropic virus is encoded in the genome of the animal, it must be closely linked to the structural locus for BALB:virus-1. The evidence is consistent with a mechanism by which a small genetic alteration in BALB:virus-1 leads to a virus, whose growth is unrestricted, and subsequently to the development of neoplasia