Role of retrotransposon-derived imprinted gene, Rtl1, in the feto-maternal interface of mouse placenta

Abstract

Eutherian placenta, an organ that emerged in the course of mammalian evolution, provides essential architecture, the so-called feto-maternal interface, for fetal development by exchanging nutrition, gas and waste between fetal and maternal blood. Functional defects of the placenta cause several developmental disorders, such as intrauterine growth retardation in humans and mice. A series of new inventions and/or adaptations must have been necessary to form and maintain eutherian chorioallantoic placenta, which consists of capillary endothelial cells and a surrounding trophoblast cell layer(s). Although many placental genes have been identified, it remains unknown how the feto-maternal interface is formed and maintained during development, and how this novel design evolved. Here we demonstrate that retrotransposon-derived Rtl1 (retrotransposon-like 1), also known as Peg11 (paternally expressed 11), is essential for maintenance of the fetal capillaries, and that both its loss and its overproduction cause late-fetal and/or neonatal lethality in mice.

MicroRNA-431 accelerates muscle regeneration and ameliorates muscular dystrophy by targeting Pax7 in mice

“…miR-431 is from the miRNA cluster that is processed from the antisense strand of maternally expressed imprinted gene Rtl1 (ref. 38). Rtl1 is a paternally expressed intronless protein-coding gene, and six miRNAs (miR-431, miR-433, miR-127, miR-434, miR-432 and miR-136) are maternally generated when the Rtl1 gene is transcribed in the opposite direction [39][40][41] .…”

Imprinted genes in mouse placental development and the regulation of fetal energy stores

“…Rtl1 null mice are growth retarded with reduced viability associated with inheritance of the mutation on a pure C57BL/6 background. Rtl1-deficient placentae are characterised by a severely disrupted labyrinth and impaired passive transport capacity (Sekita et al 2008). Overlapping the paternal expression of Rtl1 is maternal expression of an antisense Rtl1 transcript (Rtl1as) that is processed into multiple microRNAs that target degradation of the paternal Rtl1 transcript , Davis et al 2005.…”

“…Fetal endothelium of labyrinth layer Sekita et al (2008) Imprinted genes in mouse placental development…”

Selfish genetic elements, genetic conflict, and evolutionary innovation

“…One side effect of their very efficient repeat elimination is that the maintenance of gene duplications is difficult in Neurospora, thus affecting its evolutionary trajectory (17). DNA methylation suppression of TEs occurs in both animals and plants and has been invoked as a likely preadaptation for evolution of the placenta and genomic imprinting in mammals (35,36).…”