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The trafficking protein Tmed2/p24beta(1) is required for morphogenesis of the mouse embryo and placenta.

During vesicular transport between the endoplasmic reticulum and the Golgi, members of the TMED/p24 protein family form hetero-oligomeric complexes that facilitate protein-cargo recognition as well as vesicle budding. In addition, they regulate each other's level of expression. Despite analyses of TMED/p24 protein distribution in mammalian cells, yeast, and C. elegans, little is known about the role of this family in vertebrate embryogenesis. We report the presence of a single point mutation in Tmed2/p24beta(1) in a mutant mouse line, 99J, identified in an ENU mutagenesis screen for recessive developmental abnormalities. This mutation does not affect Tmed2/p24beta(1) mRNA levels but results in loss of TMED2/p24beta(1) protein. Prior to death at mid-gestation, 99J homozygous mutant embryos exhibit developmental delay, abnormal rostral-caudal elongation, randomized heart looping, and absence of the labyrinth layer of the placenta. We find that Tmed2/p24beta(1) is normally expressed in tissues showing morphological defects in 99J mutant embryos and that these affected tissues lack the TMED2/p24beta(1) oligomerization partners, TMED7/p24gamma(3) and TMED10/p24delta(1). Our data reveal a requirement for TMED2/p24beta(1) protein in the morphogenesis of the mouse embryo and placenta.

Pubmed ID: 20178780


  • Jerome-Majewska LA
  • Achkar T
  • Luo L
  • Lupu F
  • Lacy E


Developmental biology

Publication Data

May 1, 2010

Associated Grants

  • Agency: NICHD NIH HHS, Id: U01 HD043478
  • Agency: NICHD NIH HHS, Id: U01 HD043478-05

Mesh Terms

  • Animals
  • Embryo, Mammalian
  • Endoplasmic Reticulum
  • Female
  • Gene Expression Regulation, Developmental
  • Mice
  • Mice, Inbred C57BL
  • Morphogenesis
  • Mutation
  • Placenta
  • Pregnancy
  • Vesicular Transport Proteins