The placenta is a feto-maternal organ of primarily fetal origin. Labyrinth and junctional zones of the placenta are fetal-derived while the decidual zone is maternally derived. A fully vascularized placenta ensures adequate fetal and maternal nutrient and gas exchange thus placental defects could affect embryonic development. While there are a large number of mouse strains that are embryonic lethal, whether these are embryonic or placentation defects had previously not been comprehensively studied. In this report, Perez-Garcia et al. demonstrate the importance of placental development by identifying that placental dysmorphologies are associated with more than half of tested strains with embryonic lethality. When a strain is embryonic lethal prior to E14.5, placental defects were found in nearly all strains.
To separate whether placentation defects are independent of embryonic defects, candidate genes were tested for in vitro placentation using trophoblast stem cells, finding that two of three embryonic lethal gene deletions in the trophoblasts also had defective markers of stem cell renewal and in vitro differentiation into mature placental tissues. To test these findings in an in vivo system, the authors used conditional knockouts to demonstrate that for one of the three genes tested, embryonic development was partially normalized when placental gene expression was intact but embryonic tissues were ablated. This report highlights the importance of proper placentation and how placental development or lack thereof can alter embryonic development. This argues for a broader consideration of placental development when considering the embryonic lethality of some variants.
The placenta is a feto-maternal organ of primarily fetal origin. Labyrinth and junctional zones of the placenta are fetal-derived while the decidual zone is maternally derived. A fully vascularized placenta ensures adequate fetal and maternal nutrient and gas exchange thus placental defects could affect embryonic development. While there are a large number of mouse strains that are embryonic lethal, whether these are embryonic or placentation defects had previously not been comprehensively studied. In this report, Perez-Garcia et al. demonstrate the importance of placental development by identifying that placental dysmorphologies are associated with more than half of tested strains with embryonic lethality. When a strain is embryonic lethal prior to E14.5, placental defects were found in nearly all strains.
To separate whether placentation defects are independent of embryonic defects, candidate genes were tested for in vitro placentation using trophoblast stem cells, finding that two of three embryonic lethal gene deletions in the trophoblasts also had defective markers of stem cell renewal and in vitro differentiation into mature placental tissues. To test these findings in an in vivo system, the authors used conditional knockouts to demonstrate that for one of the three genes tested, embryonic development was partially normalized when placental gene expression was intact but embryonic tissues were ablated. This report highlights the importance of proper placentation and how placental development or lack thereof can alter embryonic development. This argues for a broader consideration of placental development when considering the embryonic lethality of some variants.
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