PRJNA732448
Next generation sequencing of genome wide CRISPR knockout screens for alpha Synuclein oligomers
alpha Synuclein misfolding and aggregation are observed in several neurodegenerative diseases. The oligomeric form has been regarded as the most toxic species. However, the molecular mechanisms controlling alpha Synuclein oligomerization are still elusive. Here, we performed genome wide CRISPR Cas9 loss of function screening in human HEK293 cells for negative regulators of alpha Synuclein oligomerization by using an established system, which drives bimolecular GFP fluorescence complementation to visualize alpha Synuclein oligomerization directly in living cells.