Smad-interacting protein-1 (Zfhx1b) acts upstream of Wnt signaling in the mouse hippocampus and controls its formation

被引:75
作者
Miquelajauregui, Amaya
Van de Putte, Tom
Polyakov, Alexander
Nityanandam, Anjana
Boppana, Sridhar
Seuntjens, Eve
Karabinos, Anton
Higashi, Yujiro
Huylebroeck, Danny
Tarabykin, Victor
机构
[1] Max Planck Inst Expt Med, D-37075 Gottingen, Germany
[2] Univ Ghent VIB, Dept Mol Biol Celgen, BE-9000 Ghent, Belgium
[3] Univ Ghent VIB, Mol Biol Lab, BE-9000 Ghent, Belgium
[4] Katholieke Univ Leuven, Dept Human Genet, B-3000 Louvain, Belgium
[5] Osaka Univ, Grad Sch Frontier Biosci, Osaka 5650871, Japan
关键词
development; sfrp1; knockout; telencephalon; cortex;
D O I
10.1073/pnas.0609863104
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Smad-interacting protein-1 (Sip1) [Zinc finger homeobox (Zfhx1b)] is a transcription factor implicated in the genesis of Mowat-Wilson syndrome in humans. Sip1 expression in the dorsal telencephalon of mouse embryos was documented from E12.5. We inactivated the gene specifically in cortical precursors. This resulted in the lack of the entire hippocampal formation. Sip1 mutant mice exhibited death of differentiating cells and decreased proliferation in the region of the prospective hippocampus and dentate gyrus. The expression of the Wnt antagonist Sfrp1 was ectopically activated, whereas the activity of the noncanonical Wnt effector, JNK, was down-regulated in the embryonic hippocampus of mutant mice. In cortical cells, Sip1 protein was detected on the promoter of Sfrp1 gene and both genes showed a mutually exclusive pattern of expression suggesting that Sfrp1 expression is negatively regulated by Sip1. Sip1 is therefore essential to the development of the hippocampus and dentate gyrus, and is able to modulate Wnt signaling in these regions.
引用
收藏
页码:12919 / 12924
页数:6
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