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Dissecting the first transcriptional divergence during human embryonic development. | LitMetric

AI Article Synopsis

  • The trophoblast cell lineage, which forms part of the early embryo, differentiates during the blastocyst stage into the trophectoderm and inner cell mass.
  • Research using advanced mRNA amplification techniques reveals that human trophectoderm expresses key genes like ABCG2, known for protecting the embryo from harmful substances, and a variety of Laminins.
  • A network of 13 transcription factors essential for the trophectoderm's development was identified, and this regulatory circuitry can also be recreated in lab models of trophoblast differentiation.

Article Abstract

The trophoblast cell lineage is specified early at the blastocyst stage, leading to the emergence of the trophectoderm and the pluripotent cells of the inner cell mass. Using a double mRNA amplification technique and a comparison with transcriptome data on pluripotent stem cells, placenta, germinal and adult tissues, we report here some essential molecular features of the human mural trophectoderm. In addition to genes known for their role in placenta (CGA, PGF, ALPPL2 and ABCG2), human trophectoderm also strongly expressed Laminins, such as LAMA1, and the GAGE Cancer/Testis genes. The very high level of ABCG2 expression in trophectoderm, 7.9-fold higher than in placenta, suggests a major role of this gene in shielding the very early embryo from xenobiotics. Several genes, including CCKBR and DNMT3L, were specifically up-regulated only in trophectoderm, indicating that the trophoblast cell lineage shares with the germinal lineage a transient burst of DNMT3L expression. A trophectoderm core transcriptional regulatory circuitry formed by 13 tightly interconnected transcription factors (CEBPA, GATA2, GATA3, GCM1, KLF5, MAFK, MSX2, MXD1, PPARD, PPARG, PPP1R13L, TFAP2C and TP63), was found to be induced in trophectoderm and maintained in placenta. The induction of this network could be recapitulated in an in vitro trophoblast differentiation model.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3285757PMC
http://dx.doi.org/10.1007/s12015-011-9301-3DOI Listing

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