Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spermatogonial stem cells can be transplanted from a fertile donor mouse to the testis of an infertile recipient where they establish spermatogenesis and produce spermatozoa. In the present study we investigated whether treatment of recipient mice with the gonadotropin-releasing hormone (GnRH) agonist leuprolide acetate could alter the efficiency of colonization by donor spermatogonial stem cells in the recipient testis. Six recipient mice were treated with busulfan to destroy endogenous spermatogenesis followed by injection of leuprolide acetate to three of the mice. Testis cells from mice carrying the ZFlacZ transgene, which produces beta-galactosidase in spermatids, were used as donor cells for transplantation to allow for identification of donor spermatogenesis in the recipient testis by staining for enzyme activity. The extent of donor cell colonization was compared between leuprolide treated recipients and untreated control mice 3 months after transplantation. Efficiency of colonization by donor cells was markedly enhanced in recipient mice treated with the GnRH agonist leuprolide acetate, which makes the technique of spermatogonial transplantation applicable to a wide range of experimental situations. The present study also indicates that this technique can be used as a biological assay system to investigate factors controlling the establishment and progression of spermatogenesis.
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PMID:Leuprolide, a gonadotropin-releasing hormone agonist, enhances colonization after spermatogonial transplantation into mouse testes. 983 81

Testis-specific expression of tandemly repeated Stellate genes, located in eu- and heterochromatin regions of the X chromosome of Drosophila melanogaster, is suppressed by homologous Suppressor of Stellate repeats located on the Y chromosome. Using transgenic lines, we have demonstrated that three Su(Ste) copies failed to change the expression of the reporter construction carrying the bacterial beta-galactosidase gene under control of the Stellate gene regulatory sequence. Possible mechanisms of the Su(Ste) repeat suppressor activity are discussed.
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PMID:[The study of interaction between paralogous tandem repeats stellate and suppressor of stellate in the genome of Drosophila melanogaster]. 1082 25

Gonadotropin-releasing hormone (GnRH)-agonist or antagonist treatment supports recovery of spermatogenesis after irradiation damage in the rat and appears to be beneficial to colonization of recipient testes after spermatogonial transplantation from fertile donors to the testes of infertile recipients in rats and mice. In the present study, we quantified the effect of treatment of recipient mice with the GnRH-agonist leuprolide acetate on the extent of colonization by donor spermatogonial stem cells in the recipient testis. Testis cells from mice carrying transgenes, which produce beta-galactosidase in spermatogenic cells, were used as donor cells for transplantation to allow for quantification of donor spermatogenesis in the recipient testis by staining for enzyme activity. Donor cell colonization 3 months after transplantation was compared between recipients receiving leuprolide in different treatment protocols and untreated control mice. Two injections of leuprolide 4 weeks apart prior to transplantation with as little as 3.8 mg/kg resulted in a pronounced improvement in the number of donor-derived spermatogenic colonies as well as in the in the area of recipient seminiferous tubules occupied by donor cell spermatogenesis. Improved colonization efficiency by treatment with GnRH-agonist can make the technique of spermatogonial transplantation applicable to situations when only low numbers of donor cells are available.
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PMID:Effect of the GnRH-agonist leuprolide on colonization of recipient testes by donor spermatogonial stem cells after transplantation in mice. 1139 73

Phosphatidylserine synthase 1 (Pss1) and phosphatidylserine synthase 2 (Pss2) produce phosphatidylserine by exchanging serine for the head groups of other phospholipids. Pss1 and Pss2 are structurally similar (approximately 32% amino acid identity) but differ in their substrate specificities, with Pss1 using phosphatidylcholine for the serine exchange reaction and Pss2 using phosphatidylethanolamine. Whether Pss1 and Pss2 are both required for mammalian growth and development is not known, and no data exist on the relative contributions of the two enzymes to serine exchange activities in different tissues. To address those issues and also to define the cell type-specific expression of Pss2, we generated Pss2-deficient mice in which a beta-galactosidase marker is expressed from Pss2 regulatory sequences. Histologic studies of Pss2-deficient mice revealed very high levels of beta-galactosidase expression in Sertoli cells of the testis and high levels of expression in brown fat, neurons, and myometrium. The ability of testis extracts from Pss2-deficient mice to catalyze serine exchange was reduced by more than 95%; reductions of approximately 90% were noted in the brain and liver. However, we found no perturbations in the phospholipid content of any of these tissues. As judged by Northern blots, the expression of Pss1 was not up-regulated in Pss2-deficient cells and tissues. Testis weight was reduced in Pss2-deficient mice, and some of the male mice were infertile. We conclude that Pss2 is responsible for the majority of serine exchange activity in in vitro assays, but a deficiency in this enzyme does not cause perturbations in phospholipid content or severe developmental abnormalities.
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PMID:Defining the importance of phosphatidylserine synthase 2 in mice. 1236 52