Mikita T, Kurama M, Schindler U
Tularik Inc., South San Francisco, CA 94080, USA.
J Immunol. 1998 Aug 15;161(4):1822-8.
Transcription of the Ig H chain germline transcripts is a prerequisite for class switching. Expression of the epsilon germline transcript is induced by IL-4 and requires the integrity of a composite IL-4 response element. The element is bound by the IL-4-inducible transcription factor Stat6 and one or more members of the CAAT/enhancer-binding protein (C/EBP) family, a constitutively expressed class of transcription factors. Here, we show that Stat6 and C/EBP beta cooperate to synergistically activate transcription from the epsilon element. The effect was most pronounced in lymphoid cells, and the activation domains of both proteins were required to achieve this synergy. Although other members of the C/EBP family are able to bind the element, very little cooperativity was seen with C/EBP alpha and none with C/EBP gamma. In fact, C/EBP gamma was able to inhibit IL-4-induced reporter activity. Stat6 and C/EBP beta bind the IL-4 response element simultaneously. The fast dissociation rate apparent when Stat6 binds this DNA element alone is slowed when C/EBP beta binds at the neighboring site. These data suggest a mechanism whereby C/EBP beta stabilizes Stat6 binding at this element, thereby increasing the likelihood that both of their activation domains will interact, possibly with other factors, to activate transcription in an IL-4-dependent manner.
免疫球蛋白重链种系转录本的转录是类别转换的前提条件。ε种系转录本的表达由白细胞介素-4诱导,并且需要复合白细胞介素-4反应元件的完整性。该元件由白细胞介素-4诱导型转录因子Stat6以及CCAAT/增强子结合蛋白(C/EBP)家族的一个或多个成员结合,C/EBP家族是一类组成性表达的转录因子。在此,我们表明Stat6和C/EBPβ协同作用以协同激活ε元件的转录。这种效应在淋巴细胞中最为明显,并且两种蛋白的激活结构域对于实现这种协同作用都是必需的。尽管C/EBP家族的其他成员能够结合该元件,但与C/EBPα几乎没有协同作用,与C/EBPγ则完全没有协同作用。事实上,C/EBPγ能够抑制白细胞介素-4诱导的报告基因活性。Stat6和C/EBPβ同时结合白细胞介素-4反应元件。当Stat6单独结合该DNA元件时明显的快速解离速率,在C/EBPβ结合到相邻位点时会减慢。这些数据提示了一种机制,即C/EBPβ稳定Stat6在该元件上的结合,从而增加它们两个的激活结构域相互作用(可能与其他因子)以白细胞介素-4依赖方式激活转录的可能性。