Chopra Vivek Sarojkumar, Srinivasan Arumugam, Kumar Ram Parikshan, Mishra Krishnaveni, Basquin Denis, Docquier Mylène, Seum Carole, Pauli Daniel, Mishra Rakesh Kumar
Center for Cellular and Molecular Biology, Uppal Road, Hyderabad, 500007, India.
Dev Biol. 2008 May 15;317(2):660-70. doi: 10.1016/j.ydbio.2008.02.008. Epub 2008 Feb 15.
The GAGA factor (GAF), encoded by the Trithorax like gene (Trl) is a multifunctional protein involved in gene activation, Polycomb-dependent repression, chromatin remodeling and is a component of chromatin domain boundaries. Although first isolated as transcriptional activator of the Drosophila homeotic gene Ultrabithorax (Ubx), the molecular basis of this GAF activity is unknown. Here we show that dmTAF3 (also known as BIP2 and dTAF(II)155), a component of TFIID, interacts directly with GAF. We generated mutations in dmTAF3 and show that, in Trl mutant background, they affect transcription of Ubx leading to enhancement of Ubx phenotype. These results reveal that the gene activation pathway involving GAF is through its direct interaction with dmTAF3.
由类三胸节基因（Trl）编码的GAGA因子（GAF）是一种多功能蛋白质，参与基因激活、多梳蛋白依赖性抑制、染色质重塑，并且是染色质结构域边界的一个组成部分。尽管GAF最初是作为果蝇同源异型基因超双胸（Ubx）的转录激活因子被分离出来的，但其这种活性的分子基础尚不清楚。在此我们表明，TFIID的一个组成部分dmTAF3（也称为BIP2和dTAF（II）155）直接与GAF相互作用。我们在dmTAF3中产生了突变，并表明，在Trl突变背景下，这些突变会影响Ubx的转录，导致Ubx表型增强。这些结果揭示，涉及GAF的基因激活途径是通过其与dmTAF3的直接相互作用实现的。
