| First Author | Ogura H | Year | 1998 |
| Journal | Cytogenet Cell Genet | Volume | 80 |
| Issue | 1-4 | Pages | 173-8 |
| PubMed ID | 9678353 | Mgi Jnum | J:48822 |
| Mgi Id | MGI:1275855 | Doi | 10.1159/000014975 |
| Citation | Ogura H, et al. (1998) Translocation breakpoint possibly predisposes to nonrandom X-chromosome inactivation in mouse embryos bearing Searle's T(X;16)16H translocation. Cytogenet Cell Genet 80(1-4):173-8 |
| abstractText | To clarify the sequence of events that ultimately achieves the nonrandom inactivation of the paternally inherited X chromosome in postpartum female mice heterozygous for T(X;16)16H, we set out to examine the expression of Xist alleles and the X-linked HMG-lacZ transgene in embryos recovered at the egg cylinder stage. Lack of expression of the Xist(b) allele on the 16(x) translocation chromosome in the embryonic region of 7.5 d postcoitum (dpc) X- 16/X(n)Xist(a);16(x)Xist(b)/ 16 embryos strongly suggested the occurrence of nonrandom inactivation in favor of the normal X chromosome, The simplest explanation would be biased choice, followed by postinactivation selection against genetically unbalanced cells. However, the frequency and distribution of beta-galactosidase-positive cells in X-16/X(n)lacZ; 16(x)/16 embryos at 6.5 and 7.5 dpc, together with earlier cytogenetic data, raised an intriguing possibility that :he majority of 16(x) chromosomes were prevented from completing the inactivation process, when they had been chosen to be silenced. Phenotypes of female mice carrying a spontaneous recombination between X-n and 16(x) in the segment defined by the T16H breakpoint and the X-linked Ta locus suggested that the nonrandomness was brought about by disruption of an X-chromosomal sequence or structure at the translocation breakpoint. |
