Mechanical transmission of galinsoga mosaic virus in soil

Galinsoga mosaic virus (GMV) was isolated from Galinsoga parviflora plants growing near Gympie in south-eastern Queensland. Although the virus was always recovered from the roots of naturally infected G. parviflora plants, the tops sometimes contained no detectable virus. When soil collected near naturally infected plilnts was kept moist in a glasshouse for 15 months and periodically planted with seed or seedlings of G. parviflora, the plants continued to become infected. Addition of captafol or ethazol fungicides to the soil had no effect on transmission of GMV in a glasshouse. Air-drying the soil for 20 days abolished its infectivity to G. parvi/lora plants and also decreased the amount of virus directly extractable from it. Pasteurized or autoclaved potting mix became infective to G. pariJif/ora when mixed with GMVcontaining plant roots, tops, leaf extracts or drainage water of infected G. parvif/ora. When leafinoculated and healthy G. parviflora plants were grown together in the same autoclaved potting mix with their tops separated by a glass partition, transmission between roots occurred. When there was foliage but not root contact, transmission was also obtained. The virus was transmitted neither by seed of infected G. parviftora plants, nor by the fungus OIpidium brassicae which, with tobacco necrosis virus, usually coexisted with GMV in the field

Prospects for a small molecule able to induce somatic growth through the growth hormone receptor

This article reviews the prospects for a small-molecule agonist of the growth hormone receptor in the light of current successes in identifying small agonist molecules for other homomeric class 1 cytokine receptors. A variety of mutagenic analyses on both hormone and receptor, studies with monoclonal antibody agonists of the GH receptor, and the use of a constitutively dimerized GH receptor chimera which displays constitutive activity lead us to believe that such a development is possible. However, it is likely that a precise alignment of the lower cytokine receptor homology domains will be necessary in order to facilitate cross-activation of cytoplasmic Janus kinases bound to Box 1

Protein trans-Splicing To Produce Herbicide-Resistant Acetolactate Synthase

Protein splicing in trans has been demonstrated both in vivo and in vitro by biochemical and immunological analyses, but in vivo production of a functional protein by trans-splicing has not been reported previously. In this study, we used the DnaE intein from Synechocystis sp. strain PCC6803, which presumably reconstitutes functional DnaE protein by trans-splicing in vivo, to produce functional herbicide-resistant acetolactate synthase II (ALSII) from two unlinked gene fragments in Escherichia coli. The gene for herbicide-resistant ALSII was fused in frame to DnaE intein segments capable of promoting protein splicing in trans and was expressed from two compatible plasmids as two unlinked fragments. Cotransformation of E. coli with the two plasmids led to production of a functional enzyme that conferred herbicide resistance to the host E. coli cells. These results demonstrate the feasibility of expressing functional genes from two unlinked DNA loci and provide a model for the design of nontransferable transgenes in plants

Nuclear targeting of the growth hormone receptor results in dysregulation of cell proliferation and tumorigenesis

Growth hormone receptor (GHR) has been demonstrated to be nuclear localized both in vivo and in vitro, but the significance of this observation has remained elusive. Here we show that nuclear GHR is strongly correlated with proliferative status in vivo by using a liver regeneration model. In vitro, nuclear translocation of the GH receptor is GH-dependent and appears to be mediated by the Importin system. Constitutive nuclear targeting of GHR in murine pro-B cells is associated with constitutive activation of STAT5, a transforming agent in lymphoma and other cell types. This activation is abrogated by inhibition of JAK2 and appears to be driven by autocrine murine GH action coupled with enhanced nuclear uptake of phospho-STAT5. Nuclear targeting induces dysregulated cell cycle progression in the pro-B cell line, associated with constitutive up-regulation of the proliferation inducers Survivin and Mybbp, the metastasis related Dysadherin, and other tumor markers. GHR nuclear-targeted cells generate aggressive metastatic tumors when injected into nude mice, which display nuclear localized GHR strikingly similar to that seen in human lymphomas. We conclude that aberrant nuclear localization of GHR is a marker of high proliferative status and is sufficient to induce tumorigenesis and tumor progression