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First published online 27 April 2005
doi: 10.1242/dev.01844
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1 Laboratory for Embryonic Induction, RIKEN Center for Developmental Biology,
2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan
2 Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka,
Suita, Osaka 565-0871, Japan
3 Department of Neurology, Graduate School of Medicine, Osaka University, D-4,
2-2 Yamadaoka, Suita, Osaka 565-0871, Japan
4 Laboratory for Animal Resources and Genetic Engineering (LARGE), RIKEN Center
for Developmental Biology, 2-2-3 Minatojimaminamimachi, Chuo-ku, Kobe, Hyogo
650-0047, Japan
5 Division of Bioscience, Graduate School of Environmental Earth Science,
Hokkaido University, North 10 West 8, Sapporo 060-0810, Japan
6 Department of Genetics, Cell Biology, and Development, University of
Minnesota, Minneapolis, MN 55455, USA
7 Laboratory for Genome Exploration Research Group, Genomic Sciences Center,
RIKEN, Yokohama, Kanagawa 230-0045, Japan
8 Laboratory of Mammalian Genes and Development, National Institute of Child
Health and Human Development, National Institutes of Health, Bethesda, MD
20892, USA
9 Department of Molecular Genetics, The University of Texas M. D. Anderson
Cancer Center, Huston, TX 77030, USA
10 Center for Advanced Science and Technology, Hokkaido University, North 10 West
8, Sapporo 060-0810, Japan
* Author for correspondence (e-mail: sasaki{at}cdb.riken.jp)
Accepted 1 April 2005
The transcriptional activity of LIM-homeodomain (LIM-HD) proteins is regulated by their interactions with various factors that bind to the LIM domain. We show that reduced expression of single-stranded DNA-binding protein 1 (Ssdp1), which encodes a co-factor of LIM domain interacting protein 1 (Ldb1), in the mouse mutant headshrinker (hsk) disrupts anterior head development by partially mimicking Lim1 mutants. Although the anterior visceral endoderm and the anterior definitive endoderm, which together comprise the head organizer, were able to form normally in Ssdp1hsk/hsk mutants, development of the prechordal plate was compromised. Head development is partially initiated in Ssdp1hsk/hsk mutants, but neuroectoderm tissue anterior to the midbrain-hindbrain boundary is lost, without a concomitant increase in apoptosis. Cell proliferation is globally reduced in Ssdp1hsk/hsk mutants, and approximately half also exhibit smaller body size, similar to the phenotype observed in Lim1 and Ldb1 mutants. We also show that Ssdp1 contains an activation domain and is able to enhance transcriptional activation through a Lim1-Ldb1 complex in transfected cells, and that Ssdp1 interacts genetically with Lim1 and Ldb1 in both head development and body growth. These results suggest that Ssdp1 regulates the development of late head organizer tissues and body growth by functioning as an essential activator component of a Lim1 complex through interaction with Ldb1.
Key words: Ssdp1, Head organizer, Prechordal plate, Headshrinker, Lim1, Ldb1, Cell proliferation, Mouse
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