Muroi Sawako, Naoe Yoshinori, Miyamoto Chizuko, Akiyama Kaori, Ikawa Tomokatsu, Masuda Kyoko, Kawamoto Hiroshi, Taniuchi Ichiro
Laboratory for Transcriptional Regulation, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan.
Nat Immunol. 2008 Oct;9(10):1113-21. doi: 10.1038/ni.1650. Epub 2008 Sep 7.
CD4 and the transcription factor ThPOK are essential for the differentiation of major histocompatibility complex class II-restricted thymocytes into the helper T cell lineage; their genes (Cd4 and Zbtb7b (called 'ThPOK' here)) are repressed by transcriptional silencer elements in cytotoxic T cells. The molecular mechanisms regulating expression of these genes during helper T cell lineage differentiation remain unknown. Here we showed that inefficient upregulation of ThPOK, induced by removal of the proximal enhancer from the ThPOK locus, resulted in the transdifferentiation of helper lineage-specified cells into the cytotoxic T cell lineage. Furthermore, direct antagonism by ThPOK of the Cd4 and ThPOK silencers generated two regulatory loops that initially inhibited Cd4 downregulation and later stabilized ThPOK expression. Our results show how an initial lineage-specification signal can be amplified and stabilized during the lineage-commitment process.
CD4和转录因子ThPOK对于主要组织相容性复合体II类限制性胸腺细胞分化为辅助性T细胞谱系至关重要;它们的基因(Cd4和Zbtb7b,此处称为“ThPOK”)在细胞毒性T细胞中被转录沉默元件所抑制。在辅助性T细胞谱系分化过程中调节这些基因表达的分子机制仍然未知。在此我们表明,通过从ThPOK基因座去除近端增强子诱导的ThPOK低效上调,导致辅助性谱系指定细胞转分化为细胞毒性T细胞谱系。此外,ThPOK对Cd4和ThPOK沉默子的直接拮抗作用产生了两个调节环,最初抑制Cd4下调,随后稳定ThPOK表达。我们的结果显示了初始谱系指定信号在谱系承诺过程中如何被放大和稳定。