Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152, Martinsried, Germany.
Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, USA.
Nat Commun. 2023 Feb 2;14(1):560. doi: 10.1038/s41467-023-36058-2.
Amyloid-like aggregates of the microtubule-associated protein Tau are associated with several neurodegenerative disorders including Alzheimer's disease. The existence of cellular machinery for the removal of such aggregates has remained unclear, as specialized disaggregase chaperones are thought to be absent in mammalian cells. Here we show in cell culture and in neurons that the hexameric ATPase valosin-containing protein (VCP) is recruited to ubiquitylated Tau fibrils, resulting in their efficient disaggregation. Aggregate clearance depends on the functional cooperation of VCP with heat shock 70 kDa protein (Hsp70) and the ubiquitin-proteasome machinery. While inhibition of VCP activity stabilizes large Tau aggregates, disaggregation by VCP generates seeding-active Tau species as byproduct. These findings identify VCP as a core component of the machinery for the removal of neurodegenerative disease aggregates and suggest that its activity can be associated with enhanced aggregate spreading in tauopathies.
微管相关蛋白 Tau 的淀粉样样聚集物与包括阿尔茨海默病在内的几种神经退行性疾病有关。尽管人们认为哺乳动物细胞中缺乏专门的解聚酶伴侣,但对于是否存在用于去除此类聚集物的细胞机制仍不清楚。在这里,我们在细胞培养物和神经元中表明,六聚体 ATP 酶泛素结合酶(VCP)被招募到泛素化 Tau 纤维上,从而有效地将其解聚。聚集物的清除取决于 VCP 与热休克 70kDa 蛋白(Hsp70)和泛素-蛋白酶体机制的功能合作。虽然 VCP 活性的抑制会稳定大的 Tau 聚集物,但 VCP 的解聚会产生作为副产物的具有种子活性的 Tau 物质。这些发现将 VCP 鉴定为用于去除神经退行性疾病聚集物的机制的核心组成部分,并表明其活性可能与 Tau 病中聚集物扩散的增强有关。