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...

Full description

Saved in:
Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1999-01, Vol.96 (1), p.162-167
Main Authors: Morasso, Maria I., Grinberg, Alexander, Robinson, Gertraud, Sargent, Thomas D., Mahon, Kathleen A.
Format: Article
Language:English
Subjects:
Allantois
Animals
Antigens, Differentiation
Biological Sciences
Cell Lineage
Chorion
Developmental biology
DNA
DNA probes
Embryos
Female
Gene Targeting
Genes
Genes, Homeobox
Genetic Vectors
Giant cells
Homeodomain Proteins
In Situ Hybridization
Mice
Mice, Mutant Strains
Placenta
Placenta - pathology
Pregnancy
Proto-Oncogene Proteins - biosynthesis
Transcription Factors - biosynthesis
Transcription Factors - deficiency
Transcription Factors - genetics
Trophoblasts
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.96.1.162