Regulation of cell fate decision of undifferentiated spermatogonia by GDNF

被引：1034

作者：

Meng, XJ

Lindahl, M

Hyvönen, ME

Parvinen, M

de Rooij, DG

Hess, MW

Raatikainen-Ahokas, A

Sainio, K

Rauvala, H

Lakso, M

Pichel, JG

Westphal, H

Saarma, M

Sariola, H

机构：

[1] Univ Helsinki, Inst Biotechnol, Viikki Bioctr, Res Program Dev Biol, FIN-00014 Helsinki, Finland

[2] Univ Helsinki, Inst Biotechnol, Viikki Bioctr, Res Program Mol Neurobiol, FIN-00014 Helsinki, Finland

[3] Univ Helsinki, Inst Biotechnol, Transgen Unit, FIN-00014 Helsinki, Finland

[4] Univ Helsinki, Dept Biosci, FIN-00014 Helsinki, Finland

[5] Univ Turku, Dept Anat, FIN-20520 Turku, Finland

[6] Univ Utrecht, Med Ctr, Dept Cell Biol, NL-3584 CX Utrecht, Netherlands

[7] Hosp Merida, Unidad Invest, Badajoz 06800, Spain

[8] NICHHD, Bethesda, MD 20892 USA

来源：

SCIENCE | 2000年 / 287卷 / 5457期

关键词：

D O I：

10.1126/science.287.5457.1489

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：

The molecular control of self-renewal and differentiation of stem cells has remained enigmatic. Transgenic Loss-of-function and overexpression models now show that the dosage of glial cell Line-derived neurotrophic factor (GDNF), produced by Sertoli cells, regulates cell fate decisions of undifferentiated spermatogonial cells that include the stem cells for spermatogenesis. Gene-targeted mice with one GDNF-null allele show depletion of stem cell reserves, whereas mice overexpressing GDNF show accumulation of undifferentiated spermatogonia. They are unable to respond properly to differentiation signals and undergo apoptosis upon retinoic acid treatment. Nonmetastatic testicular tumors are regularly formed in older GDNF-overexpressing mice. Thus, GDNF contributes to paracrine regulation of spermatogonial self-renewal and differentiation.

引用

页码：1489 / 1493

页数：5

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