Reactivation of the inactive X chromosome in development and reprogramming

In mammals, one of the two X chromosomes of female cells is inactivated for dosage compensation between the sexes. X chromosome inactivation is initiated in early embryos by the noncoding Xist RNA. Subsequent chromatin modifications on the inactive X chromosome (Xi) lead to a remarkable stability of gene repression in somatic cell lineages. In mice, reactivation of genes on the Xi accompanies the establishment of pluripotent cells of the female blastocyst and the development of primordial germ cells. Xi reactivation also occurs when pluripotency is established during the reprogramming of somatic cells to induced pluripotent stem cells. The mechanism of Xi reactivation has attracted increasing interest for studying changes in epigenetic patterns and for improving methods of cell reprogramming. Here, we review recent advances in the understanding of Xi reactivation during development and reprogramming and illustrate potential clinical applications.     

The protective effect of thiola against the genotoxic action of benzo(a)pyrene

Summary The protective effect of Thiola against the genotoxicity, induced by benzo(a)pyrene, in vitro and in vivo, was investigated. By association of Thiola to benzo(a)pyrene a significant decrease of the numerical and structural chromosome aberrations and a reduction of the incidence of c-mitoses has been obtained in human diploid cells, i.e. human embryonic lung fibroblasts of the cell-line ICP-23, and C₅₆Bl/6 mouse bone marrow cells.