Oct1 regulates trophoblast development during early mouse embryogenesis

Vittorio Sebastiano, Mathieu Dalvai, Luca Gentile, Karin Schubart, Julien Sutter, Guang-Ming Wu, Natalia Tapia, Daniel Esch, Jin-Young Ju, Karin Huebner, Marcos Jesus Arauzo-Bravo, Hans Robert Schoeler, Fatima Cavaleri, Patrick Matthias

Research output: Contribution to journalArticlepeer-review


Oct1 (Pou2f1) is a transcription factor of the POU-homeodomain family that is unique in being ubiquitously expressed in both embryonic and adult mouse tissues. Although its expression profile suggests a crucial role in multiple regions of the developing organism, the only essential function demonstrated so far has been the regulation of cellular response to oxidative and metabolic stress. Here, we describe a loss-of-function mouse model for Oct1 that causes early embryonic lethality, with Oct1-null embryos failing to develop beyond the early streak stage. Molecular and morphological analyses of Oct1 mutant embryos revealed a failure in the establishment of a normal maternal-embryonic interface due to reduced extra-embryonic ectoderm formation and lack of the ectoplacental cone. Oct1(-/-) blastocysts display proper segregation of trophectoderm and inner cell mass lineages. However, Oct1 loss is not compatible with trophoblast stem cell derivation. Importantly, the early gastrulation defect caused by Oct1 disruption can be rescued in a tetraploid complementation assay. Oct1 is therefore primarily required for the maintenance and differentiation of the trophoblast stem cell compartment during early post-implantation development. We present evidence that Cdx2, which is expressed at high levels in trophoblast stem cells, is a direct transcriptional target of Oct1. Our data also suggest that Oct1 is required in the embryo proper from late gastrulation stages onwards.

Original languageEnglish
Pages (from-to)3551-3560
Number of pages10
Issue number21
Publication statusPublished - 1 Nov 2010


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