Department of Chemistry, Michigan State University, East Lansing, Michigan, 48824.
Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan, 48824.
Protein Sci. 2019 Jul;28(7):1262-1275. doi: 10.1002/pro.3629. Epub 2019 May 8.
ATPases associated with diverse cellular activities (AAA+) proteases utilize ATP hydrolysis to actively unfold native or misfolded proteins and translocate them into a protease chamber for degradation. This basic mechanism yields diverse cellular consequences, including the removal of misfolded proteins, control of regulatory circuits, and remodeling of protein conformation. Among various bacterial AAA+ proteases, FtsH is only membrane-integrated and plays a key role in membrane protein quality control. Previously, we have shown that FtsH has substantial unfoldase activity for degrading membrane proteins overcoming a dual energetic burden of substrate unfolding and membrane dislocation. Here, we asked how efficiently FtsH utilizes ATP hydrolysis to degrade membrane proteins. To answer this question, we measured degradation rates of the model membrane substrate GlpG at various ATP hydrolysis rates in the lipid bilayers. We find that the dependence of degradation rates on ATP hydrolysis rates is highly nonlinear: (i) FtsH cannot degrade GlpG until it reaches a threshold ATP hydrolysis rate; (ii) after exceeding the threshold, the degradation rates steeply increase and saturate at the ATP hydrolysis rates far below the maxima. During the steep increase, FtsH efficiently utilizes ATP hydrolysis for degradation, consuming only 40-60% of the total ATP cost measured at the maximal ATP hydrolysis rates. This behavior does not fundamentally change against water-soluble substrates as well as upon addition of the macromolecular crowding agent Ficoll 70. The Hill analysis shows that the nonlinearity stems from coupling of three to five ATP hydrolysis events to degradation, which represents unique cooperativity compared to other AAA+ proteases including ClpXP, HslUV, Lon, and proteasomes.
与多种细胞活动相关的 ATP 酶(AAA+)蛋白酶利用 ATP 水解来主动展开天然或错误折叠的蛋白质,并将它们转运到蛋白酶腔中进行降解。这种基本机制产生了多种细胞后果,包括去除错误折叠的蛋白质、控制调节回路和重塑蛋白质构象。在各种细菌 AAA+蛋白酶中,FtsH 仅整合在膜上,在膜蛋白质量控制中起着关键作用。以前,我们已经表明,FtsH 具有大量的展开酶活性,可用于降解膜蛋白,克服底物展开和膜移位的双重能量负担。在这里,我们询问 FtsH 如何有效地利用 ATP 水解来降解膜蛋白。为了回答这个问题,我们在脂质双层中的各种 ATP 水解速率下测量了模型膜底物 GlpG 的降解速率。我们发现,降解速率对 ATP 水解速率的依赖性非常非线性:(i)FtsH 不能降解 GlpG,除非它达到一个阈值 ATP 水解速率;(ii)超过阈值后,降解速率急剧增加,并在远低于最大 ATP 水解速率的 ATP 水解速率下饱和。在急剧增加期间,FtsH 有效地利用 ATP 水解进行降解,仅消耗在最大 ATP 水解速率下测量的总 ATP 成本的 40-60%。这种行为在水溶性底物以及添加大分子拥挤剂 Ficoll 70 时并没有根本改变。Hill 分析表明,这种非线性源于三个到五个 ATP 水解事件与降解的偶联,与其他 AAA+蛋白酶(包括 ClpXP、HslUV、Lon 和蛋白酶体)相比,这种偶联具有独特的协同性。