Amniotic ectoderm expansion in mouse occurs via distinct modes and requires SMAD5-mediated signalling
| Autor: | Nathan Criem, Agata Stryjewska, Marina Naval Sanchez, Ljuba C. Ponomarev, Susana M. Chuva de Sousa Lopes, Mariya P. Dobreva, Danny Huylebroeck, Kirstie A. Lawson, An Zwijsen, Stein Aerts, Vanesa Abon Escalona, Paulo N. G. Pereira |
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| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
Smad5 Protein
0301 basic medicine animal structures CLONAL ANALYSIS Morphogenesis Ectoderm Biology Bone morphogenetic protein BMP-SMAD Mice GENOMIC FEATURES 03 medical and health sciences Clonal analysis PRIMORDIAL GERM-CELLS BMP2 EXPRESSION medicine Animals Conceptus RNA-SEQ Amnion Molecular Biology EXTRAEMBRYONIC ECTODERM Science & Technology ANTERIOR VISCERAL ENDODERM Stem Cells EMBRYO Extra-embryonic-embryonic interface Correction DEFECTS Chorion Cell biology Gastrulation Extra-embryonic ectoderm 030104 developmental biology medicine.anatomical_structure Amnion fate map Epiblast MORPHOGENESIS embryonic structures Life Sciences & Biomedicine Developmental biology Research Article Signal Transduction Developmental Biology |
| Zdroj: | Development, 145(13) |
| Popis: | Upon gastrulation, the mammalian conceptus transforms rapidly from a simple bilayer into a multilayered embryo enveloped by its extra-embryonic 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. Two main types have progenitors in extreme proximal-anterior epiblast. Early descendants initiate and expand amniotic ectoderm posteriorly, while descendants of cells remaining anteriorly later expand amniotic ectoderm from its anterior side. Amniogenesis is abnormal in embryos deficient in the bone morphogenetic protein (BMP) signalling effector SMAD5, with delayed closure of the proamniotic canal, and aberrant amnion and folding morphogenesis. Transcriptomics of individual Smad5 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 amniotic ectoderm and to compromised cuboidal-to-squamous transition of anterior amniotic ectoderm. In both cases, SMAD5 is crucial for expanding amniotic ectoderm rapidly into a stretchable squamous sheet to accommodate exocoelom expansion, axial growth and folding morphogenesis. ispartof: DEVELOPMENT vol:145 issue:13 ispartof: location:England status: published |
| Databáze: | OpenAIRE |
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