Publisher Correction: Female mice lacking Ftx lncRNA exhibit impaired X-chromosome inactivation and a microphthalmia-like phenotype.

In the original HTML version of this Article, the affiliation details for Hirosuke Shiura, Hidetoshi Hasuwa and Takashi Kohda were incorrect, as detailed in the associated Publisher Correction. These errors have been corrected in both the HTML version of the Article.

Female mice lacking Ftx lncRNA exhibit impaired X-chromosome inactivation and a microphthalmia-like phenotype.

X-chromosome inactivation (XCI) is an essential epigenetic process in female mammalian development. Although cell-based studies suggest the potential importance of the Ftx long non-protein-coding RNA (lncRNA) in XCI, its physiological roles in vivo remain unclear. Here we show that targeted deletion of X-linked mouse Ftx lncRNA causes eye abnormalities resembling human microphthalmia in a subset of females but rarely in males.

Ftx is dispensable for imprinted X-chromosome inactivation in preimplantation mouse embryos.

X-chromosome inactivation (XCI) equalizes gene expression between the sexes by inactivating one of the two X chromosomes in female mammals. Xist has been considered as a major cis-acting factor that inactivates the paternally derived X chromosome (Xp) in preimplantation mouse embryos (imprinted XCI). Ftx has been proposed as a positive regulator of Xist.

Identification of an imprinted gene cluster in the X-inactivation center.

Mammalian development is strongly influenced by the epigenetic phenomenon called genomic imprinting, in which either the paternal or the maternal allele of imprinted genes is expressed. Paternally expressed Xist, an imprinted gene, has been considered as a single cis-acting factor to inactivate the paternally inherited X chromosome (Xp) in preimplantation mouse embryos. This means that X-chromosome inactivation also entails gene imprinting at a very early developmental stage.

Severe inhibition of in vitro cardiomyogenesis in mouse embryonic stem cells ectopically expressing EGAM1C homeoprotein.

Embryoid bodies were prepared from mouse embryonic stem cells expressing exogenous EGAM1C to analyze their ability to differentiate toward terminally differentiated cell types. The generation of cardiomyocytes was severely suppressed in Egam1c transfectants without upregulation of Nkx2-5, a crucial gene for cardiomyogenesis. These results indicate that EGAM1C is capable of affecting terminal differentiation in mouse embryonic stem cells.

Preferential emergence of cell types expressing markers for primitive endoderm lineages in mouse embryonic stem cells expressing exogenous EGAM1 homeoprotein.

Embryonic stem (ES) cells have been considered as a valuable renewable source of materials in regenerative medicine. Recently, we identified the homeoprotein EGAM1 both in preimplantation mouse embryos and mouse ES cells. Expression of the Egam1 transcript and its encoded protein was detectable in differentiating mouse ES cells, while it was almost undetectable in undifferentiated cells.

Effect of ectopic expression of homeoprotein EGAM1C on the cell morphology, growth, and differentiation in a mouse embryonic stem cell line, MG1.19 cells.

The homeoprotein EGAM1C was identified in preimplantation mouse embryos and embryonic stem (ES) cells. To explore the impact of EGAM1C on the hallmarks of mouse ES cells, MG1.19 cells stably expressing EGAM1C at levels similar to those in blastocysts were established using an episomal expression system.

Relationships between homeoprotein EGAM1C and the expression of the placental prolactin gene family in mouse placentae and trophoblast stem cells.

The mouse Crxos gene encodes three structurally related homeoproteins, EGAM1, EGAM1N, and EGAM1C, as transcription and splicing variants. Recently, we identified the functions of EGAM1 and EGAM1N in the regulation of differentiation in mouse embryonic stem cells. However, the function of EGAM1C remains unknown.

Cloning of complementary DNAs encoding structurally related homeoproteins from preimplantation mouse embryos: their involvement in the differentiation of embryonic stem cells.

During the preimplantation development of mouse embryos between the 4-cell to 8-cell stage and the morula stage, when the first irreversible segregation of cell fates proceeds into the pluripotent inner cell mass (progenitor cells to form the fetus) and the trophectoderm (to form the placenta) of blastocysts, pluripotency-maintaining and differentiation-inducing genes are expressed to coordinately regulate cell fates. Three structurally related cDNAs (Crxos1, Crxos1 sv2, and Crxos1 tv3) that exhibited concomitant elevated expression during this critical period were identified by subtractive cDNA cloning. CRXOS1 contains two homeodomains, while CRXOS1 sv2 and CRXOS1 tv3 each contain one of the homeodomains included in CRXOS1.