| Research Abstract |
Several points of interest emerged from the present study on factors related to Xchromosome inactivation in the mouse. (1) To our disappointment, MC12 specific cDNA clone 121a proved unrelated to X chromosome inactivation because of its almost equal expression in MC12 and C4, and cl. 10, derivatives of MC12 with two active X chromosomes, and in male and female mouse embryos. However, in situ hybridization revealed that 121a was expressed first in the newly formed mesoderm of 6.5dpc embryos, atid the mesoderm specificity of 121a did not change thereafter. It is likely that 121a is involved in mesodermal differentiation. (2) Brown et al. (1991) reported a unaqtie X-linked gelle XIST that is expressed only when it is on the inactivated X cliromosome. Unlike human XIST, the mouse mouse homologue. Xist apparently has an ORF. Cell fusion between MC12 which had a late replication X and which expressed Xist and C4 or MC12 cl. 10 which had two synchroaously replicating X chromosomes and did not express Xist never altered the behavior of the X chromosomes. Thus, the product of Xist, if present, may not act in trans at least in these hybrid cells. (3) Making use of Rb (X. 2) lAd translocation, we studied genomic imprinting on the murine X chromosome. An extra maternally derived X cliromosome (X^M) but not a paternally derived one (X^P) is detrimental to early embryogenesis resulting in failure to form the ectoplacental cone and extra-embryonic ectoderm. Cytogenetic studies suggested that two X^M remain active in the trophnectoderm and possibly also the primitive endoderm, in which X^P is preferentially inactivated in normal female embryos. The observation that X^P0 but not X^M0 occurred less frequently than expected suggests the presence, on the murine X chromosome, of the other type of imprinting than that prevents inactivation of X^M.
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