Placental defects lead to embryonic lethality in mice lacking the Formin and PCP proteins Daam1 and Daam2
Genre
Journal ArticleDate
2020-04-01Author
Nakaya, MAGudmundsson, KO
Komiya, Y
Keller, JR
Habas, R
Yamaguchi, TP
Ajima, R
Subject
Actin CytoskeletonAdaptor Proteins, Signal Transducing
Animals
Carrier Proteins
Cell Polarity
Cytoskeleton
Embryonic Development
Female
Formins
Gene Expression Regulation, DevelopmentalMaleMiceMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsPlacentaPlacentationPregnancyWnt Signaling Pathwayrho GTP-Binding Proteins
Permanent link to this record
http://hdl.handle.net/20.500.12613/4489Metadata
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10.1371/journal.pone.0232025Abstract
This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. The actin cytoskeleton plays a central role in establishing cell polarity and shape during embryonic morphogenesis. Daam1, a member of the Formin family of actin cytoskeleton regulators, is a Dvl2-binding protein that functions in the Wnt/Planar Cell Polarity (PCP) pathway. To examine the role of the Daam proteins in mammalian development, we generated Daam-deficient mice by gene targeting and found that Daam1, but not Daam2, is necessary for fetal survival. Embryonic development of Daam1 mutants was delayed most likely due to functional defects in the labyrinthine layer of the placenta. Examination of Daam2 and Daam1/2 double mutants revealed that Daam1 and Daam2 are functionally redundant during placental development. Of note, neural tube closure defects (NTD), which are observed in several mammalian PCP mutants, are not observed in Wnt5a or Daam1 single mutants, but arise in Daam1;Wnt5a double mutants. These findings demonstrate a unique function for Daam genes in placental development and are consistent with a role for Daam1 in the Wnt/PCP pathway in mammals.Citation to related work
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