Optical induction of autophagy via Transcription factor EB (TFEB) reduces pathological tau in neurons

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ID: 270969
2020
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Abstract
Pathological accumulation of microtubule associated protein tau in neurons is a major neuropathological hallmark of Alzheimer’s disease (AD) and related tauopathies. Several attempts have been made to promote clearance of pathological tau (p-Tau) from neurons. Transcription factor EB (TFEB) has shown to clear p-Tau from neurons via autophagy. However, sustained TFEB activation and autophagy can create burden on cellular bioenergetics and can be deleterious. Here, we modified previously described two-plasmid systems of Light Activated Protein (LAP) from bacterial transcription factor—EL222 and Light Responsive Element (LRE) to encode TFEB. Upon blue-light (465 nm) illumination, the conformation changes in LAP induced LRE-driven expression of TFEB, its nuclear entry, TFEB-mediated expression of autophagy-lysosomal genes and clearance of p-Tau from neuronal cells and AD patient-derived human iPSC-neurons. Turning the blue-light off reversed the expression of TFEB-target genes and attenuated p-Tau clearance. Together, these results suggest that optically regulated TFEB expression unlocks the potential of opto-therapeutics to treat AD and other dementias.
Reference Key
binder2020plosoptical Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Jessica L. Binder, Praveen Chander, Vojo Deretic, Jason P. Weick, Kiran Bhaskar
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Journal PloS one
Year 2020
DOI
10.1371/journal.pone.0230026
URL
http://dx.plos.org/10.1371/journal.pone.0230026
Keywords
neurons gene expression alzheimer's disease light phosphorylation transcription factors autophagic cell death luciferase

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