Anomaly in autophagy pathway proteins lead to aberrant protein aggregation in neuronal cells, which is the common etiology of neurodegenerative disorders, such as Alzheimer’s and Parkinson’s. Ion channel proteins expressed on the ER, endosomes, and lysosomes have been implicated in maintaining the ionic balance of internal cellular compartments. Their function is relatively less understood due to their inaccessibility to available biophysical methods.

We hypothesize that specific ER- and endo-lysosome resident Ca2+ ion channels play key roles in autophagy and their ion channel and non-ion channel roles are critical for the progression of autophagy. In our lab, we are investigating the role of 2 specific intracellular ion channels TRPML3 and TPC2 in a cellular model of autophagy for the development of potential therapeutics against neurodegenerative disorders. We employ an array of automated RNAseq pipeline, in silico structural biology studies, patch-clamp electrophysiology and calcium imaging studies to investigate the direct role of TRPML3 and TPC2 in autophagy, their interaction with ARGs, and structure-function relationship in the context of neurodegenerative and lysosomal storage disorders.