AI Article Synopsis

  • The study focuses on how the anterior-posterior axis in mouse embryos is established through the formation and migration of distal visceral endoderm (DVE).
  • It reveals that bone morphogenetic protein (BMP) signaling has two crucial roles: supporting the differentiation of primitive endoderm into embryonic visceral endoderm at an early stage and inhibiting DVE formation later on.
  • Additionally, a factor called Activin helps in DVE development by creating a specific region where Smad2 is active and Smad1 is inactive, indicating a balance of signaling between these two pathways.

Article Abstract

The anterior-posterior axis of the mouse embryo is established by formation of distal visceral endoderm (DVE) and its subsequent migration. The precise mechanism of DVE formation has remained unknown, however. Here we show that bone morphogenetic protein (BMP) signaling plays dual roles in DVE formation. BMP signaling is required at an early stage for differentiation of the primitive endoderm into the embryonic visceral endoderm (VE), whereas it inhibits DVE formation, restricting it to the distal region, at a later stage. A Smad2-activating factor such as Activin also contributes to DVE formation by generating a region of VE positive for the Smad2 signal and negative for Smad1 signal. DVE is thus formed at the distal end of the embryo, the only region of VE negative for the Smad1 signal and positive for Smad2 signal. An inverse relation between the level of phosphorylated Smad1 and that of phosphorylated Smad2 in VE suggests an involvement of antagonism between Smad1- and Smad2-mediated signaling.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2654303PMC
http://dx.doi.org/10.1083/jcb.200808044DOI Listing

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