Active complex formation of type I and type II activin and TGF beta receptors in vivo as studied by overexpression in zebrafish embryos

被引：9

作者：

deVries, CJM

deBoer, J

Joore, J

Strahle, U

vanAchterberg, TAE

Huylebroeck, D

Verschueren, K

Miyazono, K

vandenEijndenvanRaaij, AJM

Zivkovic, D

机构：

[1] NETHERLANDS INST DEV BIOL,HUBRECHT LAB,3584 CT UTRECHT,NETHERLANDS

[2] IGBMC,ILLKIRCH GRAFFENS,FRANCE

[3] UNIV LOUVAIN,CELGEN,MOLEC BIOL LAB,LOUVAIN,BELGIUM

[4] FLANDERS INTERUNIV INST BIOTECHNOL,DEPT CELL GROWTH DIFFERENTIAT & DEV,LOUVAIN,BELGIUM

[5] LUDWIG INST CANC RES,CTR BIOMED,S-75124 UPPSALA,SWEDEN

来源：

MECHANISMS OF DEVELOPMENT | 1996年 / 54卷 / 02期

关键词：

zebrafish; activin receptors; axis formation;

D O I：

10.1016/0925-4773(95)00480-7

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

We have investigated the involvement of activin receptors and TGF beta type I receptor in zebrafish development. Overexpression of either full-length or a truncated form of mouse ActR-IIA interferes with the development. Different splice variants of mouse ActR-IIB have distinct effects; ActR-IIB4 induces abnormal embryos, whereas ActR-IIB2 does not. Activin and TGF beta type I receptors can induce axis duplications. Go-expression of ActR-IA or ActR-IB with the type II activin receptors results in a synergistic increase of the frequency of axis duplication. Moreover, ActR-IIB2 is synergistic with ActR-IA and ActR-IB, demonstrating that ActR-IIB2 can interact with the zebrafish ligand. Overexpression of TGF beta R-I with ActR-IIA or ActR-IIB4 results in a synergistic increase in frequency of abnormal embryos, whereas in combination with ActR-IIB2 no such increase occurs.

引用

页码：225 / 236

页数：12

共 57 条

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