Understanding the Degradation Pathway and Kinetics of Tau Protein in Human Neuroglioma Cells Utilizing dCAS9-KRAB

Presenter

Todd Yau

Campus

UMass Amherst

Sponsor

Jennifer Rauch, Department of Biochemistry and Molecular Biology, UMass Amherst

Schedule

Session 4, 2:30 PM - 3:15 PM [Schedule by Time][Poster Grid for Time/Location]

Location

Poster Board A34, Campus Center Auditorium, Row 2 (A21-A40) [Poster Location Map]

Abstract

The microtubule associated protein tau (“tau”) has been associated with neurodegenerative diseases wherein tau is known to disassociate from microtubules and form neurofibrillary tangles (NFTs) that spread in neurons of the central nervous system. The spread of tau aggregates has been linked to pathology in Alzheimer’s disease and frontotemporal dementia. While the exact mechanism of cell-to-cell spreading is unknown we seek to understand the cellular mechanisms that govern tau spread between and within cells. To better understand this process, we have manipulated genes associated with the endosomal pathway normally associated with the engulfment and degradation of extracellular proteins. Utilizing CRISPR/dCas9KRAB knockdowns in neuroglioma cells and a split nanoluciferase tagged tau we show how endosomal markers, mutant tau, and phosphorylated tau affects degradation kinetics.

Keywords

Alzheimer's Disease, Tau, Neurodegeneration, In Vitro, CRISPR

Research Area

Biological Organisms

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