947 resultados para 300602 Tree Improvement (Selection, Breeding and Genetic Engineering)


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To feed a world population growing by up to 160 people per minute, with >90% of them in developing countries, will require an astonishing increase in food production. Forecasts call for wheat to become the most important cereal in the world, with maize close behind; together, these crops will account for ≈80% of developing countries’ cereal import requirements. Access to a range of genetic diversity is critical to the success of breeding programs. The global effort to assemble, document, and utilize these resources is enormous, and the genetic diversity in the collections is critical to the world’s fight against hunger. The introgression of genes that reduced plant height and increased disease and viral resistance in wheat provided the foundation for the “Green Revolution” and demonstrated the tremendous impact that genetic resources can have on production. Wheat hybrids and synthetics may provide the yield increases needed in the future. A wild relative of maize, Tripsacum, represents an untapped genetic resource for abiotic and biotic stress resistance and for apomixis, a trait that could provide developing world farmers access to hybrid technology. Ownership of genetic resources and genes must be resolved to ensure global access to these critical resources. The application of molecular and genetic engineering technologies enhances the use of genetic resources. The effective and complementary use of all of our technological tools and resources will be required for meeting the challenge posed by the world’s expanding demand for food.

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Herpes simplex virus vectors are being developed for delivery and expression of human genes to the central nervous system, selective destruction of cancer cells, and as carriers for genes encoding antigens that induce protective immunity against infectious agents. Vectors constructed to meet these objectives must differ from wild-type virus with respect to host range, reactivation from latency, and expression of viral genes. The vectors currently being developed are (i) helper free amplicons, (ii) replication defective viruses, and (iii) genetically engineered replication competent viruses with restricted host range. Whereas the former two types of vectors require stable, continuous cell lines expressing viral genes for their replication, the replication competent viruses will replicate on approved primary human cell strains.

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Proliferation, migration-associated differentiation, and cell death occur continuously and in a spatially well-organized fashion along the crypt-villus axis of the mouse small intestine, making it an attractive system for studying how these processes are regulated and interrelated. A pathway for producing glycoconjugates was engineered in adult FVB/N transgenic mice by expressing a human alpha 1,3/4-fucosyltransferase (alpha 1,3/4-FT; EC 2.4.1.65) along the length of this crypt-villus axis. The alpha 1,3/4-FT can use lacto-N-tetraose or lacto-neo-N-tetraose core chains to generate Lewis (Le) blood group antigens Le(a) or Le(x), respectively, and H type 1 or H type 2 core chains to produce Leb and Le(y). Single- and multilabel immunohistochemical studies revealed that expression of the alpha 1,3/4-FT results in production of Le(a) and Leb antigens in both undifferentiated proliferated crypt cells and in differentiated postmitotic villus-associated epithelial cells. In contrast, Le(x) antigens were restricted to crypt cells. Villus enterocytes can be induced to reenter the cell cycle by expression of simian virus 40 tumor antigen under the control of a promoter that only functions in differentiated members of this lineage. Bitransgenic animals, generated from a cross of FVB/N alpha 1,3/4-FT with FVB/N simian virus 40 tumor antigen mice, expand the range of Le(x) expression to include villus-associated enterocytes that have reentered the cell cycle. Thus, the fucosylations unveil a proliferation-dependent switch in oligosaccharide production, as defined by a monoclonal antibody specific for the Le(x) epitope. These findings show that genetic engineering of oligosaccharide biosynthetic pathways can be used to define markers for entry into, or progression through, the cell cycle and to identify changes in endogenous carbohydrate metabolism that occur when proliferative status is altered in a manner that is not deleterious to the system under study.

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Previously, researchers have speculated that genetic engineering can improve the long-term function of vascular grafts which are prone to atherosclerosis and occlusion. In this study, we demonstrated that an intraoperative gene therapy approach using antisense oligodeoxynucleotide blockage of medial smooth muscle cell proliferation can prevent the accelerated atherosclerosis that is responsible for autologous vein graft failure. Selective blockade of the expression of genes for two cell cycle regulatory proteins, proliferating cell nuclear antigen and cell division cycle 2 kinase, was achieved in the smooth muscle cells of rabbit jugular veins grafted into the carotid arteries. This alteration of gene expression successfully redirected vein graft biology away from neointimal hyperplasia and toward medial hypertrophy, yielding conduits that more closely resembled normal arteries. More importantly, these genetically engineered grafts proved resistant to diet-induced atherosclerosis. These findings establish the feasibility of developing genetically engineered bioprostheses that are resistant to failure and better suited to the long-term treatment of occlusive vascular disease.

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Mode of access: Internet.

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Mode of access: Internet.

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We conducted a demographic and genetic study to investigate the effects of fragmentation due to the establishment of an exotic softwood plantation on populations of a small marsupial carnivore, the agile antechinus (Antechinus agilis), and the factors influencing the persistence of those populations in the fragmented habitat. The first aspect of the study was a descriptive analysis of patch occupancy and population size, in which we found a patch occupancy rate of 70% among 23 sites in the fragmented habitat compared to 100% among 48 sites with the same habitat characteristics in unfragmented habitat. Mark-recapture analyses yielded most-likely population size estimates of between 3 and 85 among the 16 occupied patches in the fragmented habitat. Hierarchical partitioning and model selection were used to identify geographic and habitat-related characteristics that influence patch occupancy and population size. Patch occupancy was primarily influenced by geographic isolation and habitat quality (vegetation basal area). The variance in population size among occupied sites was influenced primarily by forest type (dominant Eucalyptus species) and, to a lesser extent, by patch area and topographic context (gully sites had larger populations). A comparison of the sex ratios between the samples from the two habitat contexts revealed a significant deficiency of males in the fragmented habitat. We hypothesise that this is due to male-biased dispersal in an environment with increased dispersal-associated mortality. The population size and sex ratio data were incorporated into a simulation study to estimate the proportion of genetic diversity that would have been lost over the known timescale since fragmentation if the patch populations had been totally isolated. The observed difference in genetic diversity (gene diversity and allelic richness at microsatellite and mitochondrial markers) between 16 fragmented and 12 unfragmented sites was extremely low and inconsistent with the isolation of the patch populations. Our results show that although the remnant habitat patches comprise approximately 2% of the study area, they can support non-isolated populations. However, the distribution of agile antechinus populations in the fragmented system is dependent on habitat quality and patch connectivity. (C) 2004 Elsevier Ltd. All rights reserved.