Species-specific regulation of XIST by the JPX/FTX orthologs.

X chromosome inactivation (XCI) is an essential process, yet it initiates with remarkable diversity in various mammalian species. XIST, the main trigger of XCI, is controlled in the mouse by an interplay of lncRNA genes (LRGs), some of which evolved concomitantly to XIST and have orthologues across all placental mammals. Here, we addressed the functional conservation of human orthologues of two such LRGs, FTX and JPX.

Success to reach 3cm of dilation with a Dinoprostone Vaginal Insert in primiparous women with a previous cesarean section versus nulliparous: A retrospective case-control study.

Background The best methods of labour induction have still been controversial because of an increased risk of uterine rupture, especially in exposed women of labour induction with prostaglandins. We here attempted to determine, after Dinoprostone Vaginal Insert, previous cesarean women (exposed women), compared with nulliparous women (non-exposed women), are more likely 1) to have the dilated cervix (up to 3 cm or more), and 2) to require cesarean after cervix being dilated 3 cm or more. Methods This retrospective observational study included 43 exposed women and 188 non exposed women .

A primate-specific retroviral enhancer wires the XACT lncRNA into the core pluripotency network in humans.

Transposable elements (TEs) have been proposed to play an important role in driving the expansion of gene regulatory networks during mammalian evolution, notably by contributing to the evolution and function of long non-coding RNAs (lncRNAs). XACT is a primate-specific TE-derived lncRNA that coats active X chromosomes in pluripotent cells and may contribute to species-specific regulation of X-chromosome inactivation. Here we explore how different families of TEs have contributed to shaping the XACT locus and coupling its expression to pluripotency.

The Ftx Noncoding Locus Controls X Chromosome Inactivation Independently of Its RNA Products.

Accumulation of the Xist long noncoding RNA (lncRNA) on one X chromosome is the trigger for X chromosome inactivation (XCI) in female mammals. Xist expression, which needs to be tightly controlled, involves a cis-acting region, the X-inactivation center (Xic), containing many lncRNA genes that evolved concomitantly to Xist from protein-coding ancestors through pseudogeneization and loss of coding potential. Here, we uncover an essential role for the Xic-linked noncoding gene Ftx in the regulation of Xist expression.