JunB can substitute for Jun in mouse development and cell proliferation

被引:124
作者
Passegué, E [1 ]
Jochum, W [1 ]
Behrens, A [1 ]
Ricci, R [1 ]
Wagner, EF [1 ]
机构
[1] Res Inst Mol Pathol, A-1030 Vienna, Austria
关键词
D O I
10.1038/ng790
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The Jun and JunB components of the AP-1 transcription factor are known to have antagonistic functions. Here we show, by a knock-in strategy and a transgenic complementation approach, that Junb can substitute for absence of Jun during mouse development. Junb can rescue both liver and cardiac defects in Jun-null mice in a manner dependent on gene dosage. JunB restores the expression of genes regulated by Jun/Fos, but not those regulated by Jun/ATF, thereby rescuing Jun-dependent defects in vivo as well as in primary fibroblasts and fetal hepatoblasts in vitro. Thus, the transcriptionally less active JunB has the potential to substitute for Jun, indicating that the spatial and temporal regulation of expression of the transcription factor AP-1 may be more important than the coding sequence of its components.
引用
收藏
页码:158 / 166
页数:9
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