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Mesodermal development in mouse embryos mutant for fibronectin
Author(s) -
GeorgesLabouesse Elisabeth N.,
George Elizabeth L.,
Rayburn Helen,
Hynes Richard O.
Publication year - 1996
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/(sici)1097-0177(199610)207:2<145::aid-aja3>3.0.co;2-h
Subject(s) - notochord , biology , brachyury , somite , mesoderm , morphogenesis , microbiology and biotechnology , fibronectin , phenotype , mutant , genetics , embryo , embryonic stem cell , embryogenesis , gene , extracellular matrix
Three independent mutations were made by homologous recombination in two different regions of the fibronectin (FN) gene; all three appeared to be functional null mutations. The embryonic lethal phenotypes of these mutations were indistinguishable; all three FN mutant strains show mesodermal defects and fail to develop notochord or somites. Nevertheless analysis with lineage markers ( Brachyury, sonic hedgehog, Notch‐1, and mox‐1 ) showed that both the notochord and the somite lineages were induced at the correct times and places. Furthermore, notochord precursor cells showed extensive cell migration in the absence of FN. However, neither notochord nor somites condensed properly in the absence of FN. These results show that specification of notochordal and somitic mesodermal lineages and significant cell migration are independent of fibronectin but that correct morphogenesis of these structures is FN‐dependent. © 1996 Wiley‐Liss, Inc.