Fátima Gasset-Rosa

TL;DR: It is shown that TDP-43 at its endogenous level undergoes liquid-liquid phase separation (LLPS) within nuclei in multiple cell types and identifies a neuronal cell death mechanism that can be initiated by transient-stress-induced cytosolic de-mixing of T DP-43.

TL;DR: Overall, the findings identify polyglutamine-dependent inhibition of nucleocytoplasmic transport and alteration of nuclear integrity as a central component of Huntington's disease.

TL;DR: It is reported that a hyper‐amyloidogenic functional variant of RepA, fused to a red fluorescent protein, causes an amyloid proteinopathy in Escherichia coli with the following features: in the presence of multiple copies of the specific DNA sequence opsp, WH1(A31V) accumulates as cytoplasmatic inclusions segregated from the nucleoid.

TL;DR: The bacterial RepA‐WH1 prionoid provides key qualitative and quantitative clues on the biology of intracellular amyloid proteinopathies and in vivo the coexistence of two strain‐like types of amyloids within a genetically identical population and a controlled homogeneous environment is identified.

TL;DR: It is found that the handcuffed RepA assemblies, either reconstructed in vitro or in plasmids clustering at the bacterial nucleoid, are amyloidogenic, the first protein amyloids directly dealing with DNA.