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Nodal and Bone morphogenetic protein 5 interact in murine mesoderm formation and implantation
Author(s) -
Pfendler Kristina C.,
Yoon JoonWon,
Taborn Gregory U.,
Kuehn Michael R.,
Iannaccone Philip M.
Publication year - 2000
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/1526-968x(200009)28:1<1::aid-gene10>3.0.co;2-x
Subject(s) - nodal , gastrulation , mesoderm , nodal signaling , ectoderm , biology , mutant , embryo , endoderm , phenotype , germ layer , genetics , microbiology and biotechnology , embryogenesis , embryonic stem cell , gene , induced pluripotent stem cell
Summary: Mice mutant for the TGF‐β family member, nodal , lack mesoderm and die between E8.5 and E9.5. The short ear‐lethal ( se l ) mutation, a deletion that eliminates Bmp‐5 , causes a strikingly similar gastrulation defect. Here we analyze se l ;nodal compound mutants and find a dosage effect. Embryos homozygous for one mutation show distinct gastrulation stage defects that depend on whether they are heterozygous or homozygous for the other mutation. Embryos mutant for nodal or se l ;nodal compound mutants fail to execute an antigenic shift indicative of mesoderm differentiation and ectoderm cells are shunted into an apoptotic pathway. Furthermore, we find a novel phenotype in se l ;nodal double mutant litters, in which two to four genetically different embryos are contained within the same deciduum. Both the gastrulation and implantation phenotypes can also arise in short ear‐viable ( se v ) and se v ;nodal mutant mice. These data indicate that loss of Bmp‐5 may underlie the se l gastrulation phenotype and suggest that nodal and Bmp‐5 interact during murine mesoderm formation. Our data also reveal an unsuspected role for Bmp‐5 in implantation and the decidual response in the mouse. genesis 28:1–14, 2000. © 2000 Wiley‐Liss, Inc.