Identification of SWI•SNF complex subunit BAF60a as a determinant of the transactivation potential of Fos/Jun dimers
Identification of SWI•SNF complex subunit BAF60a as a determinant of the transactivation potential of Fos/Jun dimers
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DOI：
10.1074/jbc.m009633200
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发表时间：
2001-01-26
影响因子：
4.8
通讯作者：
Iba, H
中科院分区：
文献类型：
--
作者：
Ito, T;Yamauchi, M;Iba, H
Fos家族蛋白与Jun家族蛋白形成稳定的异源二聚体，每个异源二聚体通过AP-1结合位点显示出独特的反式激活潜能，调节细胞的生长、分化和发育。然而，二聚体特异性的分子机制和促进反式激活的分子仍然不清楚。在这里，我们证明了BAF60a，SWI.SNF染色质重塑复合体的一个亚单位，是Fos/Jun二聚体反式激活潜力的决定因素。BAF60a分别使用c-Fos和c-Jun的两个不同接口与Fos/Jun异二聚体的特定子集结合。只有当有功能的SWI.SNF复合体存在时，c-Fos/c-Jun(与BAF60a高亲和力)才能诱导内源性AP-1调控的基因，如胶原酶和c-Met，而Fra-2/Jund(对BAF60a无亲和力)则不能。这些结果表明，特定的Fos/Jun二聚体通过BAF60a招募SWI.SNF复合体启动转录。
Fos family proteins form stable heterodimers with Jun family proteins, and each heterodimer shows distinctive transactivating potential for regulating cellular growth, differentiation, and development via AP-1 binding sites. However, the molecular mechanism underlying dimer specificity and the molecules that facilitate transactivation remain undefined. Here, we show that BAF60a, a subunit of the SWI.SNF chromatin remodeling complex, is a determinant of the transactivation potential of Fos/Jun dimers. BAF60a binds to a specific subset of Fos/Jun heterodimers using two different interfaces for c-Fos and c-Jun, respectively. Only when the functional SWI.SNF complex is present, can c-Fos/c-Jun (high affinity to BAF60a) but not Fra-2/JunD (no affinity to BAF60a) induce the endogenous AP-1-regulated genes such as collagenase and c-met, These results indicate that a specific subset of Fos/Jun dimers recruits SWI.SNF complex via BAF60a to initiate transcription.