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LOCALIZATION OF JAK2 IN MOUSE PREIMPLANTATION EMBRYOS.
Ito, Masahiko1, Nakasato, Makoto1, Suzuki, Tomonori2, Sakai, Senkiti2, Aoki, Fugaku1,2, 1 2
ABSTRACT- Protein Tyrosine Kinases (PTKs) play essential roles on cellular functions, i.e. differentiation, proliferation and morphogenesis, in various types of cells. In mouse embryo, various receptors for peptide growth foctors which have a intrinsic PTK activity have been shown to be involved in the regulation of early development after 4-cell stage. However, there is little knowledge about PTKs regulating the development before 4-cell stage. We previously reported that Jak2 was one of the dominantly expressed PTKs in the mouse unfertilized oocytes and that the amount of Jak2 mRNA was the highest in the unfertilized oocytes and gradually decreased until 4-cell stage. To reveal the function of Jak2 in the early development, temporal and spatial changes in the expression of Jak2 protein were examined for oocytes and embryos during meiotic maturation and preimplantation development by immunocytochemistry. Jak2 was localized in the germinal vesicles in the full-grown oocytes. Jak2 appeared to be localized on the chromosome but not in the nucleoplasm, since DNA is not evenly distributed in the germinal vesicles and the confocal images of the immunofluorescence with Jak2 could be superimposed on those of DNA staining in the oocytes double-stained with anti-Jak2 antibody and propidium iodide. During meiotic maturation, Jak2 was detected on the condensed chromosome. After fertilization, Jak2 was localized in the pronucleus. The intensity of fluorescence was always much higher in the female pronucleus than the male one. At the first M phase, Jak2 was localized again on the chromosome. After cleavage to the 2-cell stage, Jak2 was still localized in the nucleus. During the 2-cell stage, however, the intensity of immunofluorescence was decreased as it was weak at the late G2. It was not detected in the 4-cell embryos or morula. These results suggest that Jak2 regulates the early development by the novel mechanism.
KEY WORDS: mouse, embryo, jak2, protein tyrosine kinase
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