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Publication : Expression of an X-linked HMG-lacZ transgene in mouse embryos: implication of chromosomal imprinting and lineage-specific X-chromosome activity.

First Author  Tam PP Year  1994
Journal  Dev Genet Volume  15
Issue  6 Pages  491-503
PubMed ID  7834909 Mgi Jnum  J:23724
Mgi Id  MGI:71415 Doi  10.1002/dvg.1020150608
Citation  Tam PP, et al. (1994) Expression of an X-linked HMG-lacZ transgene in mouse embryos: implication of chromosomal imprinting and lineage-specific X-chromosome activity. Dev Genet 15(6):491-503
abstractText  X-chromosome activity in female mouse embryos was studied at the cellular level using an X-linked lacZ transgene which encodes beta-galactosidase (beta-Gal). Translation of maternal RNA in oocytes is seen as beta-Gal activity that persists into early cleavage-stages. Zygotic transcription of the transgene from the maternal X chromosome (Xm) is first found at about the 8-cell stage. By contrast, expression of the lacZ transgene on the paternal X chromosome (Xp) is not seen until later at the 16-32-cell stage. Preferential inactivation of Xp occurs in the mural trophectoderm, the primitive endoderm, and derivatives of the polar trophectoderm, but a small number of cells in these lineages may still retain an active paternal X chromosome. X inactivation begins at 3.5 days in the inner cell mass but contrary to previous findings the process is not completed in the embryonic ectoderm by 5.5 to 6.0 days. Regional variation in beta-Gal activity is also observed in the embryonic ectoderm during gastrulation which may be related to the specification of cell fates. Random inactivation of Xp and Xm ensues in all somatic tissues but the process is completed at different times in different tissues. The slower progression of X inactivation in tissues such as the notochord, the heart, and the embryonic gut is primarily due to the persistent maintenance of two active X chromosomes in a significant fraction of cells in these tissues. Recent findings on the methylation of endogenous X-linked genes suggest that the prolonged expression of beta-Gal might also be due to the different rate of spreading of inactivation along the X chromosome to the lacZ transgene locus in different tissues.
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