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Over the past decade, advances in strategies to tag cells have opened new avenues for examining the development of myelin-forming glial cells and for monitoring transplanted cells in animal models of myelin insufficiency. The strategies for labelling glial cells have encompassed a range of genetic modifications as well as methods for directly attaching labels to cells. Genetically modified oligodendrocytes have been engineered to express enzymatic (e.g., beta-galactosidase, alkaline phosphatase), naturally fluorescent (e.g., green fluorescent protein), and antibiotic resistance (e.g., neomycin, zeomycin) reporters. Genes have been introduced in vivo and in vitro with viral or plasmid vectors to somatically label glial cells. To generate germ-line transmission of tagged oligodendrocytes, transgenic mice have been created both by direct injection into mouse fertilized eggs and by "knock-in" of reporters targetted to myelin gene loci in embryonic stem cells. Each experimental approach has advantages and limitations that need to be considered for individual applications. The availability of tagged glial cells has expanded our basic understanding of how oligodendrocytes are specified from stem cells and should continue to fill in the gaps in our understanding of how oligodendrocytes differentiate, myelinate, and maintain their myelin sheaths. Moreover, the ability to select oligodendrocytes by virtue of their acquired antibiotic resistance has provided an important new tool for isolating and purifying oligodendrocytes. Tagged glial cells have also been invaluable in evaluating cell transplant therapies in the nervous system. The tracking technologies that have driven these advances in glial cell biology are continuing to evolve and present new opportunities for examining oligodendrocytes in living systems. Microsc. Res. Tech. 52:766-777, 2001. Published 2001 Wiley-Liss, Inc.

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Mouse prostatic hyperplasia can be induced experimentally by the direct implantation of fetal urogenital sinus (UGS) or its mesenchyme (UGM) tissue in situ. This study characterized the time course, the requirement of sex steroids, and the optimal ages of donor and host tissues necessary to induce the maximal overgrowth of the adult mouse prostate gland in this model system. To test the potential uses of these fetal inductors as general growth-promoting substances for other adult organs, we have also tested directly the activity of fetal UGS in several non-UGS-derived adult organs. These results were compared with the growth-promoting effect achieved by fetal UGM in order to gain further insight into the relative contribution of UGS/UGM in the overall growth responses. Peak DNA synthesis in the implanted prostate occurred at three time periods-Days 4, 7-16, and 35. At Day 4, DNA synthesis may have reflected tissue repair following surgical trauma, but the DNA synthesis on Days 7-16 and 35 is attributable to growth of the chimeric (enlarged) prostate gland. Initiation and maintenance of hyperplasia required testicular androgens. Exogenous testosterone propionate (175 micrograms/day) did not induce additional prostatic overgrowth in intact, sexually mature hosts, but promoted additional overgrowth in immature and pubertal hosts. Exogenous estrogen (17 beta-estradiol dipropionate, 20 micrograms/day) inhibited fetal UGS-induced prostatic overgrowth by inhibiting the hypothalamic-pituitary-testicular axis. UGS derived from fetuses of Days 14, 16, or 18 of gestation had similar growth-inductive capability in intact adult hosts, but this capability was restricted soon after birth.(ABSTRACT TRUNCATED AT 250 WORDS)

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