A TAG1-APP signalling pathway through Fe65 negatively modulates neurogenesis

被引：171

作者：

Ma, Quan-Hong ^{[1
,2
,3
,4
]}

Futagawa, Toshitaka ^{[2
,5
]}

Yang, Wu-Lin ^{[2
]}

Jiang, Xiao-Dan ^{[6
]}

Zeng, Li ^{[1
]}

Takeda, Yasuo ^{[5
]}

Xu, Ru-Xiang ^{[6
]}

Bagnard, Dominique ^{[4
]}

Schachner, Melitta ^{[3
,7
]}

Furley, Andrew J. ^{[8
]}

Karagogeos, Domna ^{[9
,10
]}

Watanabe, Kazutada ^{[11
]}

Dawe, Gavin S. ^{[12
]}

Xiao, Zhi-Cheng ^{[1
,2
,13
]}

机构：

[1] Inst Mol & Cell Biol, Singapore 138673, Singapore

[2] Singapore Gen Hosp, Dept Clin Res, Singapore 169608, Singapore

[3] Univ Hamburg, Zentrum Mol Neurobiol, D-20251 Hamburg, Germany

[4] Ctr Neurochim, INSERM, U Physiopathol Syst Nerveux 575, F-67084 Strasbourg, France

[5] Kagoshima Univ, Dept Clin Pharm & Parmacol, Grad Sch Med & Dent Sci, Kagoshima 8908520, Japan

[6] So Med Univ, Zhujiang Hosp, Neuromed Inst, Guangzhou 510282, Peoples R China

[7] Rutgers State Univ, Keck Ctr Collaborat Neurosci, Piscataway, NJ 08854 USA

[8] Univ Sheffield, Ctr Dev Genet, Sch Med & Biomed Sci, Sheffield S10 2TN, S Yorkshire, England

[9] Inst Mol Biol & Biotechnol, Iraklion 71110, Crete, Greece

[10] Univ Crete, Sch Med, Iraklion 71110, Crete, Greece

[11] Nagaoka Univ Technol, Dept Bioengn, Nagaoka, Niigata 9402188, Japan

[12] Natl Univ Singapore, Dept Pharmacol, Singapore 117597, Singapore

[13] Natl Univ Singapore, Dept Anat, Yong Loo Lin Sch Med, Singapore 117597, Singapore

来源：

NATURE CELL BIOLOGY | 2008年 / 10卷 / 03期

基金：

英国医学研究理事会;

关键词：

D O I：

10.1038/ncb1690

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The release of amyloid precursor protein (APP) intracellular domain (AICD) may be triggered by extracellular cues through gamma-secretase-dependent cleavage. AICD binds to Fe65, which may have a role in AICD-dependent signalling; however, the functional ligand has not been characterized. In this study, we have identified TAG1 as a functional ligand of APP. We found that, through an extracellular interaction with APP, TAG1 increased AICD release and triggered Fe65-dependent activity in gamma-secretase-dependent manner. TAG1, APP and Fe65 colocalized in the neural stem cell niche of the fetal ventricular zone. Neural precursor cells from TAG1(-/-), APP(-/-) and TAG1(-/-); APP(-/-) mice had aberrantly enhanced neurogenesis, which was significantly reversed in TAG1(-/-) mice by TAG1 or AICD but not by AICD mutated at the Fe65 binding site. Notably, TAG1 reduced normal neurogenesis in Fe65(+/+) mice. Abnormally enhanced neurogenesis also occurred in Fe65(-/-) mice but could not be reversed by TAG1. These results describe a TAG1-APP signalling pathway that negatively modulates neurogenesis through Fe65.

引用

页码：283 / U29

页数：28

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