Increased G3BP2-Tau interaction in tauopathies is a natural defense against Tau aggregation

Neuron. 2023 Sep 6;111(17):2660-2674.e9. doi: 10.1016/j.neuron.2023.05.033. Epub 2023 Jun 28.

Abstract

Many RNA-binding proteins (RBPs), particularly those associated with RNA granules, promote pathological protein aggregation in neurodegenerative diseases. Here, we demonstrate that G3BP2, a core component of stress granules, directly interacts with Tau and inhibits Tau aggregation. In the human brain, the interaction of G3BP2 and Tau is dramatically increased in multiple tauopathies, and it is independent of neurofibrillary tangle (NFT) formation in Alzheimer's disease (AD). Surprisingly, Tau pathology is significantly elevated upon loss of G3BP2 in human neurons and brain organoids. Moreover, we found that G3BP2 masks the microtubule-binding region (MTBR) of Tau, thereby inhibiting Tau aggregation. Our study defines a novel role for RBPs as a line of defense against Tau aggregation in tauopathies.

Keywords: Alzheimer’s disease; G3BP2; RBP; Tau aggregation; tauopathies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism
  • Alzheimer Disease* / metabolism
  • Brain / metabolism
  • Humans
  • Neurons / metabolism
  • RNA-Binding Proteins / metabolism
  • Tauopathies* / metabolism
  • tau Proteins / metabolism

Substances

  • tau Proteins
  • RNA-Binding Proteins
  • G3BP2 protein, human
  • Adaptor Proteins, Signal Transducing