Placental Failure in Mice Lacking the Homeobox Gene Dlx3

Dlx3 is a homeodomain transcription factor and a member of the vertebrate Distal-less family. Targeted deletion of the mouse Dlx3 gene results in embryonic death between day 9.5 and day 10 because of placental defects that alter the development of the labyrinthine layer. In situ hybridization reveal...

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Published inProceedings of the National Academy of Sciences - PNAS Vol. 96; no. 1; pp. 162 - 167
Main Authors Morasso, Maria I., Grinberg, Alexander, Robinson, Gertraud, Sargent, Thomas D., Mahon, Kathleen A.
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences of the United States of America 05.01.1999
National Acad Sciences
The National Academy of Sciences
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Summary:Dlx3 is a homeodomain transcription factor and a member of the vertebrate Distal-less family. Targeted deletion of the mouse Dlx3 gene results in embryonic death between day 9.5 and day 10 because of placental defects that alter the development of the labyrinthine layer. In situ hybridization reveals that the Dlx3 gene is initially expressed in ectoplacental cone cells and chorionic plate, and later in the labyrinthine trophoblast of the chorioallantoic placenta, where major defects are observed in the Dlx3 - / - embryos. The expression of structural genes, such as 4311 and PL-1, which were used as markers to follow the fate of different derivatives of the placenta, was not affected in the Dlx3-null embryos. However, by day 10.5 of development, expression of the paired-like homeodomain gene Esx1 was strongly down-regulated in affected placenta tissue, suggesting that Dlx3 is required for the maintenance of Esx1 expression, normal placental morphogenesis, and embryonic survival.
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To whom reprint requests should be addressed at present address: Laboratory of Skin Biology, Building 6, Room 134, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda MD 20892. e-mail: morasso@nih.gov.
Communicated by Igor B. Dawid, National Institute of Child Health and Human Development, Bethesda, MD
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.96.1.162