Hombauer Hans, Weismann David, Mudrak Ingrid, Stanzel Claudia, Fellner Thomas, Lackner Daniel H, Ogris Egon
Department of Medical Biochemistry, Max F. Perutz Laboratories, Medical University of Vienna, Vienna, Austria.
PLoS Biol. 2007 Jun;5(6):e155. doi: 10.1371/journal.pbio.0050155.
Protein phosphatase 2A (PP2A) is a prime example of the multisubunit architecture of protein serine/threonine phosphatases. Until substrate-specific PP2A holoenzymes assemble, a constitutively active, but nonspecific, catalytic C subunit would constitute a risk to the cell. While it has been assumed that the severe proliferation impairment of yeast lacking the structural PP2A subunit, TPD3, is due to the unrestricted activity of the C subunit, we recently obtained evidence for the existence of the C subunit in a low-activity conformation that requires the RRD/PTPA proteins for the switch into the active conformation. To study whether and how maturation of the C subunit is coupled with holoenzyme assembly, we analyzed PP2A biogenesis in yeast. Here we show that the generation of the catalytically active C subunit depends on the physical and functional interaction between RRD2 and the structural subunit, TPD3. The phenotype of the tpd3Delta strain is therefore caused by impaired, rather than increased, PP2A activity. TPD3/RRD2-dependent C subunit maturation is under the surveillance of the PP2A methylesterase, PPE1, which upon malfunction of PP2A biogenesis, prevents premature generation of the active C subunit and holoenzyme assembly by counteracting the untimely methylation of the C subunit. We propose a novel model of PP2A biogenesis in which a tightly controlled activation cascade protects cells from untargeted activity of the free catalytic PP2A subunit.
蛋白磷酸酶2A(PP2A)是蛋白丝氨酸/苏氨酸磷酸酶多亚基结构的一个典型例子。在底物特异性PP2A全酶组装之前,组成型活性但非特异性的催化C亚基对细胞构成风险。虽然一直认为缺乏结构PP2A亚基TPD3的酵母严重增殖受损是由于C亚基不受限制的活性,但我们最近获得证据表明,C亚基以低活性构象存在,需要RRD/PTPA蛋白才能转换为活性构象。为了研究C亚基的成熟是否以及如何与全酶组装相关联,我们分析了酵母中的PP2A生物合成。在这里我们表明,催化活性C亚基的产生取决于RRD2与结构亚基TPD3之间的物理和功能相互作用。因此,tpd3Delta菌株的表型是由PP2A活性受损而非增加引起的。TPD3/RRD2依赖性C亚基成熟受到PP2A甲酯酶PPE1的监测,当PP2A生物合成出现故障时,PPE1通过抵消C亚基的过早甲基化来防止活性C亚基和全酶组装过早产生。我们提出了一种新的PP2A生物合成模型,其中严格控制的激活级联可保护细胞免受游离催化PP2A亚基的非靶向活性影响。