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Amniotic ectoderm expansion occurs via distinct modes and requires SMAD5-mediated signalling.

08:00 EDT 8th June 2018 | BioPortfolio

Summary of "Amniotic ectoderm expansion occurs via distinct modes and requires SMAD5-mediated signalling."

Upon gastrulation, the mammalian conceptus transforms rapidly from a simple bilayer into a multi-layered embryo enveloped by its extraembryonic membranes. Impaired development of the amnion, the innermost membrane, causes major malformations. To clarify the origin of the mouse amnion, we used single cell-labelling and clonal analysis. We identified four clone types with distinct clonal growth patterns in amniotic ectoderm (AmEc). Two main types have progenitors in extreme proximal-anterior epiblast. Early descendants initiate and expand AmEc posteriorly, while descendants of cells remaining anteriorly later expand AmEc from its anterior side. Amniogenesis is abnormal in embryos deficient in the BMP signalling effector SMAD5, with delayed closure of the proamniotic canal, and aberrant amnion and folding morphogenesis. Transcriptomics of individual mutant amnions isolated before visible malformations, and tetraploid chimera analysis, revealed two amnion defect sets. We attribute them to impairment of progenitors of the two main cell populations in AmEc and to compromised cuboidal-to-squamous transition of anterior AmEc. In both cases, SMAD5 is critical for expanding AmEc rapidly into a stretchable squamous sheet to accommodate exocoelom expansion, axial growth and folding morphogenesis.

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This article was published in the following journal.

Name: Development (Cambridge, England)
ISSN: 1477-9129
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