Riss Anne, Scheer Elisabeth, Joint Mathilde, Trowitzsch Simon, Berger Imre, Tora László
From the Cellular Signaling and Nuclear Dynamics Program and.
Proteomics platform, Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS UMR 7104, INSERM U964, Université de Strasbourg, BP 10142, 67404 Illkirch Cedex, CU de Strasbourg, France and.
J Biol Chem. 2015 Nov 27;290(48):28997-9009. doi: 10.1074/jbc.M115.668533. Epub 2015 Oct 14.
Histone acetyl transferases (HATs) play a crucial role in eukaryotes by regulating chromatin architecture and locus specific transcription. GCN5 (KAT2A) is a member of the GNAT (Gcn5-related N-acetyltransferase) family of HATs. In metazoans this enzyme is found in two functionally distinct coactivator complexes, SAGA (Spt Ada Gcn5 acetyltransferase) and ATAC (Ada Two A-containing). These two multiprotein complexes comprise complex-specific and shared subunits, which are organized in functional modules. The HAT module of ATAC is composed of GCN5, ADA2a, ADA3, and SGF29, whereas in the SAGA HAT module ADA2b is present instead of ADA2a. To better understand how the activity of human (h) hGCN5 is regulated in the two related, but different, HAT complexes we carried out in vitro HAT assays. We compared the activity of hGCN5 alone with its activity when it was part of purified recombinant hATAC or hSAGA HAT modules or endogenous hATAC or hSAGA complexes using histone tail peptides and full-length histones as substrates. We demonstrated that the subunit environment of the HAT complexes into which GCN5 incorporates determines the enhancement of GCN5 activity. On histone peptides we show that all the tested GCN5-containing complexes acetylate mainly histone H3K14. Our results suggest a stronger influence of ADA2b as compared with ADA2a on the activity of GCN5. However, the lysine acetylation specificity of GCN5 on histone tails or full-length histones was not changed when incorporated in the HAT modules of ATAC or SAGA complexes. Our results thus demonstrate that the catalytic activity of GCN5 is stimulated by subunits of the ADA2a- or ADA2b-containing HAT modules and is further increased by incorporation of the distinct HAT modules in the ATAC or SAGA holo-complexes.
组蛋白乙酰转移酶(HATs)通过调节染色质结构和基因座特异性转录在真核生物中发挥关键作用。GCN5(KAT2A)是HATs的GNAT(Gcn5相关N-乙酰转移酶)家族的成员。在多细胞动物中,这种酶存在于两种功能不同的共激活因子复合物中,即SAGA(Spt Ada Gcn5乙酰转移酶)和ATAC(含Ada Two A)。这两种多蛋白复合物包含复合物特异性和共享亚基,它们被组织成功能模块。ATAC的HAT模块由GCN5、ADA2a、ADA3和SGF29组成,而在SAGA HAT模块中,存在的是ADA2b而非ADA2a。为了更好地理解人(h)hGCN5的活性在这两种相关但不同的HAT复合物中是如何被调节的,我们进行了体外HAT测定。我们使用组蛋白尾肽和全长组蛋白作为底物,比较了单独的hGCN5的活性与其作为纯化的重组hATAC或hSAGA HAT模块的一部分以及内源性hATAC或hSAGA复合物时的活性。我们证明,GCN5所整合到的HAT复合物的亚基环境决定了GCN5活性的增强。在组蛋白肽上,我们表明所有测试的含GCN5的复合物主要乙酰化组蛋白H3K14。我们的结果表明,与ADA2a相比,ADA2b对GCN5的活性影响更强。然而,当GCN5整合到ATAC或SAGA复合物的HAT模块中时,其在组蛋白尾或全长组蛋白上的赖氨酸乙酰化特异性并未改变。因此,我们的结果表明,GCN5的催化活性受到含ADA2a或ADA2b的HAT模块亚基的刺激,并且通过将不同的HAT模块整合到ATAC或SAGA全复合物中而进一步增加。